DRUG INTERACTIONS

7 Due to CNS effects, use caution when administering with other centrally-acting drugs.

Avoid alcohol.

( 7.1 ) Due to hypotensive effects, hypotensive effects of other drugs with this potential may be enhanced.

( 7.2 ) Effects of levodopa and dopamine agonists may be antagonized.

( 7.3 ) Cimetidine and ranitidine increase the bioavailability of risperidone.

( 7.5 ) Clozapine may decrease clearance of risperidone.

( 7.6 ) Fluoxetine and paroxetine increase plasma concentrations of risperidone.

( 7.10 ) Carbamazepine and other enzyme inducers decrease plasma concentrations of risperidone.

( 7.11 ) 7.1 Centrally-Acting Drugs and Alcohol Given the primary CNS effects of risperidone, caution should be used when RISPERDAL ® is taken in combination with other centrally-acting drugs and alcohol.

7.2 Drugs with Hypotensive Effects Because of its potential for inducing hypotension, RISPERDAL ® may enhance the hypotensive effects of other therapeutic agents with this potential.

7.3 Levodopa and Dopamine Agonists RISPERDAL ® may antagonize the effects of levodopa and dopamine agonists.

7.4 Amitriptyline Amitriptyline did not affect the pharmacokinetics of risperidone or risperidone and 9-hydroxyrisperidone combined.

7.5 Cimetidine and Ranitidine Cimetidine and ranitidine increased the bioavailability of risperidone by 64% and 26%, respectively.

However, cimetidine did not affect the AUC of risperidone and 9-hydroxyrisperidone combined, whereas ranitidine increased the AUC of risperidone and 9-hydroxyrisperidone combined by 20%.

7.6 Clozapine Chronic administration of clozapine with RISPERDAL ® may decrease the clearance of risperidone.

7.7 Lithium Repeated oral doses of RISPERDAL ® (3 mg twice daily) did not affect the exposure (AUC) or peak plasma concentrations (C max ) of lithium (n=13).

7.8 Valproate Repeated oral doses of RISPERDAL ® (4 mg once daily) did not affect the pre-dose or average plasma concentrations and exposure (AUC) of valproate (1000 mg/day in three divided doses) compared to placebo (n=21).

However, there was a 20% increase in valproate peak plasma concentration (C max ) after concomitant administration of RISPERDAL ® .

7.9 Digoxin RISPERDAL ® (0.25 mg twice daily) did not show a clinically relevant effect on the pharmacokinetics of digoxin.

7.10 Drugs That Inhibit CYP 2D6 and Other CYP Isozymes Risperidone is metabolized to 9-hydroxyrisperidone by CYP 2D6, an enzyme that is polymorphic in the population and that can be inhibited by a variety of psychotropic and other drugs [see Clinical Pharmacology (12.3) ] .

Drug interactions that reduce the metabolism of risperidone to 9-hydroxyrisperidone would increase the plasma concentrations of risperidone and lower the concentrations of 9-hydroxyrisperidone.

Analysis of clinical studies involving a modest number of poor metabolizers (n≅70) does not suggest that poor and extensive metabolizers have different rates of adverse effects.

No comparison of effectiveness in the two groups has been made.

In vitro studies showed that drugs metabolized by other CYP isozymes, including 1A1, 1A2, 2C9, 2C19, and 3A4, are only weak inhibitors of risperidone metabolism.

Fluoxetine and Paroxetine Fluoxetine (20 mg once daily) and paroxetine (20 mg once daily) have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

When either concomitant fluoxetine or paroxetine is initiated or discontinued, the physician should re-evaluate the dosing of RISPERDAL ® .

The effects of discontinuation of concomitant fluoxetine or paroxetine therapy on the pharmacokinetics of risperidone and 9-hydroxyrisperidone have not been studied.

Erythromycin There were no significant interactions between RISPERDAL ® and erythromycin.

7.11 Carbamazepine and Other Enzyme Inducers Carbamazepine co-administration decreased the steady-state plasma concentrations of risperidone and 9-hydroxyrisperidone by about 50%.

Plasma concentrations of carbamazepine did not appear to be affected.

The dose of RISPERDAL ® may need to be titrated accordingly for patients receiving carbamazepine, particularly during initiation or discontinuation of carbamazepine therapy.

Co-administration of other known enzyme inducers (e.g., phenytoin, rifampin, and phenobarbital) with RISPERDAL ® may cause similar decreases in the combined plasma concentrations of risperidone and 9-hydroxyrisperidone, which could lead to decreased efficacy of RISPERDAL ® treatment.

7.12 Drugs Metabolized by CYP 2D6 In vitro studies indicate that risperidone is a relatively weak inhibitor of CYP 2D6.

Therefore, RISPERDAL ® is not expected to substantially inhibit the clearance of drugs that are metabolized by this enzymatic pathway.

In drug interaction studies, RISPERDAL ® did not significantly affect the pharmacokinetics of donepezil and galantamine, which are metabolized by CYP 2D6.

OVERDOSAGE

10 10.1 Human Experience Premarketing experience included eight reports of acute RISPERDAL ® overdosage with estimated doses ranging from 20 to 300 mg and no fatalities.

In general, reported signs and symptoms were those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness and sedation, tachycardia and hypotension, and extrapyramidal symptoms.

One case, involving an estimated overdose of 240 mg, was associated with hyponatremia, hypokalemia, prolonged QT, and widened QRS.

Another case, involving an estimated overdose of 36 mg, was associated with a seizure.

Postmarketing experience includes reports of acute RISPERDAL ® overdosage, with estimated doses of up to 360 mg.

In general, the most frequently reported signs and symptoms are those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness, sedation, tachycardia, hypotension, and extrapyramidal symptoms.

Other adverse reactions reported since market introduction related to RISPERDAL ® overdose include prolonged QT interval and convulsions.

Torsade de pointes has been reported in association with combined overdose of RISPERDAL ® and paroxetine.

10.2 Management of Overdosage In case of acute overdosage, establish and maintain an airway and ensure adequate oxygenation and ventilation.

Gastric lavage (after intubation, if patient is unconscious) and administration of activated charcoal together with a laxative should be considered.

Because of the rapid disintegration of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets, pill fragments may not appear in gastric contents obtained with lavage.

The possibility of obtundation, seizures, or dystonic reaction of the head and neck following overdose may create a risk of aspiration with induced emesis.

Cardiovascular monitoring should commence immediately and should include continuous electrocardiographic monitoring to detect possible arrhythmias.

If antiarrhythmic therapy is administered, disopyramide, procainamide, and quinidine carry a theoretical hazard of QT-prolonging effects that might be additive to those of risperidone.

Similarly, it is reasonable to expect that the alpha-blocking properties of bretylium might be additive to those of risperidone, resulting in problematic hypotension.

There is no specific antidote to RISPERDAL ® .

Therefore, appropriate supportive measures should be instituted.

The possibility of multiple drug involvement should be considered.

Hypotension and circulatory collapse should be treated with appropriate measures, such as intravenous fluids and/or sympathomimetic agents (epinephrine and dopamine should not be used, since beta stimulation may worsen hypotension in the setting of risperidone-induced alpha blockade).

In cases of severe extrapyramidal symptoms, anticholinergic medication should be administered.

Close medical supervision and monitoring should continue until the patient recovers.

DESCRIPTION

11 RISPERDAL ® contains risperidone, a psychotropic agent belonging to the chemical class of benzisoxazole derivatives.

The chemical designation is 3-[2-[4-(6-fluoro-1,2-benzisoxazol-3-yl)-1-piperidinyl]ethyl]-6,7,8,9-tetrahydro-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one.

Its molecular formula is C 23 H 27 FN 4 O 2 and its molecular weight is 410.49.

The structural formula is: Risperidone is a white to slightly beige powder.

It is practically insoluble in water, freely soluble in methylene chloride, and soluble in methanol and 0.1 N HCl.

RISPERDAL ® Tablets are available in 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green) strengths.

RISPERDAL ® tablets contain the following inactive ingredients: colloidal silicon dioxide, hypromellose, lactose, magnesium stearate, microcrystalline cellulose, propylene glycol, sodium lauryl sulfate, and starch (corn).

The 0.25 mg, 0.5 mg, 2 mg, 3 mg, and 4 mg tablets also contain talc and titanium dioxide.

The 0.25 mg tablets contain yellow iron oxide; the 0.5 mg tablets contain red iron oxide; the 2 mg tablets contain FD&C Yellow No.

6 Aluminum Lake; the 3 mg and 4 mg tablets contain D&C Yellow No.

10; the 4 mg tablets contain FD&C Blue No.

2 Aluminum Lake.

RISPERDAL ® is also available as a 1 mg/mL oral solution.

RISPERDAL ® Oral Solution contains the following inactive ingredients: tartaric acid, benzoic acid, sodium hydroxide, and purified water.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in 0.5 mg (light coral), 1 mg (light coral), 2 mg (coral), 3 mg (coral), and 4 mg (coral) strengths.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain the following inactive ingredients: Amberlite ® resin, gelatin, mannitol, glycine, simethicone, carbomer, sodium hydroxide, aspartame, red ferric oxide, and peppermint oil.

In addition, the 2 mg, 3 mg, and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain xanthan gum.

Chemical Structure

CLINICAL STUDIES

14 14.1 Schizophrenia Adults Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of schizophrenia was established in four short-term (4- to 8-week) controlled trials of psychotic inpatients who met DSM-III-R criteria for schizophrenia.

Several instruments were used for assessing psychiatric signs and symptoms in these studies, among them the Brief Psychiatric Rating Scale (BPRS), a multi-item inventory of general psychopathology traditionally used to evaluate the effects of drug treatment in schizophrenia.

The BPRS psychosis cluster (conceptual disorganization, hallucinatory behavior, suspiciousness, and unusual thought content) is considered a particularly useful subset for assessing actively psychotic schizophrenic patients.

A second traditional assessment, the Clinical Global Impression (CGI), reflects the impression of a skilled observer, fully familiar with the manifestations of schizophrenia, about the overall clinical state of the patient.

In addition, the Positive and Negative Syndrome Scale (PANSS) and the Scale for Assessing Negative Symptoms (SANS) were employed.

The results of the trials follow: (1)In a 6-week, placebo-controlled trial (n=160) involving titration of RISPERDAL ® in doses up to 10 mg/day (twice-daily schedule), RISPERDAL ® was generally superior to placebo on the BPRS total score, on the BPRS psychosis cluster, and marginally superior to placebo on the SANS.

(2)In an 8-week, placebo-controlled trial (n=513) involving 4 fixed doses of RISPERDAL ® (2 mg/day, 6 mg/day, 10 mg/day, and 16 mg/day, on a twice-daily schedule), all 4 RISPERDAL ® groups were generally superior to placebo on the BPRS total score, BPRS psychosis cluster, and CGI severity score; the 3 highest RISPERDAL ® dose groups were generally superior to placebo on the PANSS negative subscale.

The most consistently positive responses on all measures were seen for the 6 mg dose group, and there was no suggestion of increased benefit from larger doses.

(3)In an 8-week, dose comparison trial (n=1356) involving 5 fixed doses of RISPERDAL ® (1 mg/day, 4 mg/day, 8 mg/day, 12 mg/day, and 16 mg/day, on a twice-daily schedule), the four highest RISPERDAL ® dose groups were generally superior to the 1 mg RISPERDAL ® dose group on BPRS total score, BPRS psychosis cluster, and CGI severity score.

None of the dose groups were superior to the 1 mg group on the PANSS negative subscale.

The most consistently positive responses were seen for the 4 mg dose group.

(4)In a 4-week, placebo-controlled dose comparison trial (n=246) involving 2 fixed doses of RISPERDAL ® (4 and 8 mg/day on a once-daily schedule), both RISPERDAL ® dose groups were generally superior to placebo on several PANSS measures, including a response measure (>20% reduction in PANSS total score), PANSS total score, and the BPRS psychosis cluster (derived from PANSS).

The results were generally stronger for the 8 mg than for the 4 mg dose group.

Long-Term Efficacy In a longer-term trial, 365 adult outpatients predominantly meeting DSM-IV criteria for schizophrenia and who had been clinically stable for at least 4 weeks on an antipsychotic medication were randomized to RISPERDAL ® (2–8 mg/day) or to an active comparator, for 1 to 2 years of observation for relapse.

Patients receiving RISPERDAL ® experienced a significantly longer time to relapse over this time period compared to those receiving the active comparator.

Pediatrics The efficacy of RISPERDAL ® in the treatment of schizophrenia in adolescents aged 13–17 years was demonstrated in two short-term (6 and 8 weeks), double-blind controlled trials.

All patients met DSM-IV diagnostic criteria for schizophrenia and were experiencing an acute episode at time of enrollment.

In the first trial (study #1), patients were randomized into one of three treatment groups: RISPERDAL ® 1–3 mg/day (n = 55, mean modal dose = 2.6 mg), RISPERDAL ® 4–6 mg/day (n = 51, mean modal dose = 5.3 mg), or placebo (n = 54).

In the second trial (study #2), patients were randomized to either RISPERDAL ® 0.15–0.6 mg/day (n = 132, mean modal dose = 0.5 mg) or RISPERDAL ® 1.5–6 mg/day (n = 125, mean modal dose = 4 mg).

In all cases, study medication was initiated at 0.5 mg/day (with the exception of the 0.15–0.6 mg/day group in study #2, where the initial dose was 0.05 mg/day) and titrated to the target dosage range by approximately Day 7.

Subsequently, dosage was increased to the maximum tolerated dose within the target dose range by Day 14.

The primary efficacy variable in all studies was the mean change from baseline in total PANSS score.

Results of the studies demonstrated efficacy of RISPERDAL ® in all dose groups from 1–6 mg/day compared to placebo, as measured by significant reduction of total PANSS score.

The efficacy on the primary parameter in the 1–3 mg/day group was comparable to the 4–6 mg/day group in study #1, and similar to the efficacy demonstrated in the 1.5–6 mg/day group in study #2.

In study #2, the efficacy in the 1.5–6 mg/day group was statistically significantly greater than that in the 0.15–0.6 mg/day group.

Doses higher than 3 mg/day did not reveal any trend towards greater efficacy.

14.2 Bipolar Mania – Monotherapy Adults The efficacy of RISPERDAL ® in the treatment of acute manic or mixed episodes was established in two short-term (3-week) placebo-controlled trials in patients who met the DSM-IV criteria for Bipolar I Disorder with manic or mixed episodes.

These trials included patients with or without psychotic features.

The primary rating instrument used for assessing manic symptoms in these trials was the Young Mania Rating Scale (YMRS), an 11-item clinician-rated scale traditionally used to assess the degree of manic symptomatology (irritability, disruptive/aggressive behavior, sleep, elevated mood, speech, increased activity, sexual interest, language/thought disorder, thought content, appearance, and insight) in a range from 0 (no manic features) to 60 (maximum score).

The primary outcome in these trials was change from baseline in the YMRS total score.

The results of the trials follow: (1)In one 3-week placebo-controlled trial (n=246), limited to patients with manic episodes, which involved a dose range of RISPERDAL ® 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 4.1 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

(2)In another 3-week placebo-controlled trial (n=286), which involved a dose range of 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 5.6 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

Pediatrics The efficacy of RISPERDAL ® in the treatment of mania in children or adolescents with Bipolar I disorder was demonstrated in a 3-week, randomized, double-blind, placebo-controlled, multicenter trial including patients ranging in ages from 10 to 17 years who were experiencing a manic or mixed episode of bipolar I disorder.

Patients were randomized into one of three treatment groups: RISPERDAL ® 0.5–2.5 mg/day (n = 50, mean modal dose = 1.9 mg), RISPERDAL ® 3–6 mg/day (n = 61, mean modal dose = 4.7 mg), or placebo (n = 58).

In all cases, study medication was initiated at 0.5 mg/day and titrated to the target dosage range by Day 7, with further increases in dosage to the maximum tolerated dose within the targeted dose range by Day 10.

The primary rating instrument used for assessing efficacy in this study was the mean change from baseline in the total YMRS score.

Results of this study demonstrated efficacy of RISPERDAL ® in both dose groups compared with placebo, as measured by significant reduction of total YMRS score.

The efficacy on the primary parameter in the 3–6 mg/day dose group was comparable to the 0.5–2.5 mg/day dose group.

Doses higher than 2.5 mg/day did not reveal any trend towards greater efficacy.

14.3 Bipolar Mania – Combination Therapy The efficacy of RISPERDAL ® with concomitant lithium or valproate in the treatment of acute manic or mixed episodes was established in one controlled trial in adult patients who met the DSM-IV criteria for Bipolar I Disorder.

This trial included patients with or without psychotic features and with or without a rapid-cycling course.

(1)In this 3-week placebo-controlled combination trial, 148 in- or outpatients on lithium or valproate therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® , placebo, or an active comparator, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.8 mg/day), combined with lithium or valproate (in a therapeutic range of 0.6 mEq/L to 1.4 mEq/L or 50 mcg/mL to 120 mcg/mL, respectively) was superior to lithium or valproate alone in the reduction of YMRS total score.

(2)In a second 3-week placebo-controlled combination trial, 142 in- or outpatients on lithium, valproate, or carbamazepine therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® or placebo, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.7 mg/day), combined with lithium, valproate, or carbamazepine (in therapeutic ranges of 0.6 mEq/L to 1.4 mEq/L for lithium, 50 mcg/mL to 125 mcg/mL for valproate, or 4–12 mcg/mL for carbamazepine, respectively) was not superior to lithium, valproate, or carbamazepine alone in the reduction of YMRS total score.

A possible explanation for the failure of this trial was induction of risperidone and 9-hydroxyrisperidone clearance by carbamazepine, leading to subtherapeutic levels of risperidone and 9-hydroxyrisperidone.

14.4 Irritability Associated with Autistic Disorder Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of irritability associated with autistic disorder was established in two 8-week, placebo-controlled trials in children and adolescents (aged 5 to 16 years) who met the DSM-IV criteria for autistic disorder.

Over 90% of these subjects were under 12 years of age and most weighed over 20 kg (16–104.3 kg).

Efficacy was evaluated using two assessment scales: the Aberrant Behavior Checklist (ABC) and the Clinical Global Impression – Change (CGI-C) scale.

The primary outcome measure in both trials was the change from baseline to endpoint in the Irritability subscale of the ABC (ABC-I).

The ABC-I subscale measured the emotional and behavioral symptoms of autism, including aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods.

The CGI-C rating at endpoint was a co-primary outcome measure in one of the studies.

The results of these trials are as follows: (1)In one of the 8-week, placebo-controlled trials, children and adolescents with autistic disorder (n=101), aged 5 to 16 years, received twice daily doses of placebo or RISPERDAL ® 0.5–3.5 mg/day on a weight-adjusted basis.

RISPERDAL ® , starting at 0.25 mg/day or 0.5 mg/day depending on baseline weight (< 20 kg and ≥ 20 kg, respectively) and titrated to clinical response (mean modal dose of 1.9 mg/day, equivalent to 0.06 mg/kg/day), significantly improved scores on the ABC-I subscale and on the CGI-C scale compared with placebo.

(2)In the other 8-week, placebo-controlled trial in children with autistic disorder (n=55), aged 5 to 12 years, RISPERDAL ® 0.02 to 0.06 mg/kg/day given once or twice daily, starting at 0.01 mg/kg/day and titrated to clinical response (mean modal dose of 0.05 mg/kg/day, equivalent to 1.4 mg/day), significantly improved scores on the ABC-I subscale compared with placebo.

Long-Term Efficacy Following completion of the first 8-week double-blind study, 63 patients entered an open-label study extension where they were treated with RISPERDAL ® for 4 or 6 months (depending on whether they received RISPERDAL ® or placebo in the double-blind study).

During this open-label treatment period, patients were maintained on a mean modal dose of RISPERDAL ® of 1.8–2.1 mg/day (equivalent to 0.05 – 0.07 mg/kg/day).

Patients who maintained their positive response to RISPERDAL ® (response was defined as ≥ 25% improvement on the ABC-I subscale and a CGI-C rating of ‘much improved’ or ‘very much improved’) during the 4–6 month open-label treatment phase for about 140 days, on average, were randomized to receive RISPERDAL ® or placebo during an 8-week, double-blind withdrawal study (n=39 of the 63 patients).

A pre-planned interim analysis of data from patients who completed the withdrawal study (n=32), undertaken by an independent Data Safety Monitoring Board, demonstrated a significantly lower relapse rate in the RISPERDAL ® group compared with the placebo group.

Based on the interim analysis results, the study was terminated due to demonstration of a statistically significant effect on relapse prevention.

Relapse was defined as ≥ 25% worsening on the most recent assessment of the ABC-I subscale (in relation to baseline of the randomized withdrawal phase).

HOW SUPPLIED

16 /STORAGE AND HANDLING RISPERDAL ® (risperidone) Tablets RISPERDAL ® (risperidone) Tablets are imprinted ” JANSSEN ” on one side and either “R1”, or “R3” according to their respective strengths.

1 mg white, capsule-shaped tablets: bottles of 15 NDC 21695-113-15 3 mg yellow, capsule-shaped tablets: bottles of 30 NDC 21695-115-30 and bottles of 60 NDC 21695-113-60.

Storage and Handling RISPERDAL ® Tablets should be stored at controlled room temperature 15°–25°C (59°–77°F).

Protect from light and moisture.

Keep out of reach of children.

RECENT MAJOR CHANGES

Warnings and Precautions, Leukopenia, Neutropenia, and Agranulocytosis ( 5.8 ) 07/2009

GERIATRIC USE

8.5 Geriatric Use Clinical studies of RISPERDAL ® in the treatment of schizophrenia did not include sufficient numbers of patients aged 65 and over to determine whether or not they respond differently than younger patients.

Other reported clinical experience has not identified differences in responses between elderly and younger patients.

In general, a lower starting dose is recommended for an elderly patient, reflecting a decreased pharmacokinetic clearance in the elderly, as well as a greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy [see Clinical Pharmacology (12.3) and Dosage and Administration (2.4 , 2.5) ] .

While elderly patients exhibit a greater tendency to orthostatic hypotension, its risk in the elderly may be minimized by limiting the initial dose to 0.5 mg twice daily followed by careful titration [see Warnings and Precautions (5.7) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

This drug is substantially excreted by the kidneys, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.

Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see Dosage and Administration (2.4) ] .

Concomitant use with Furosemide in Elderly Patients with Dementia-Related Psychosis In two of four placebo-controlled trials in elderly patients with dementia-related psychosis, a higher incidence of mortality was observed in patients treated with furosemide plus RISPERDAL ® when compared to patients treated with RISPERDAL ® alone or with placebo plus furosemide.

No pathological mechanism has been identified to explain this finding, and no consistent pattern for cause of death was observed.

An increase of mortality in elderly patients with dementia-related psychosis was seen with the use of RISPERDAL ® regardless of concomitant use with furosemide.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See Boxed Warning and Warnings and Precautions (5.1) ]

DOSAGE FORMS AND STRENGTHS

3 RISPERDAL ® Tablets are available in the following strengths and colors: 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green).

All are capsule shaped, and imprinted with “JANSSEN” on one side and either “Ris 0.25”, “Ris 0.5”, “R1”, “R2”, “R3”, or “R4” on the other side according to their respective strengths.

RISPERDAL ® Oral Solution is available in a 1 mg/mL strength.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in the following strengths, colors, and shapes: 0.5 mg (light coral, round), 1 mg (light coral, square), 2 mg (coral, square), 3 mg (coral, round), and 4 mg (coral, round).

All are biconvex and etched on one side with “R0.5”, “R1”, “R2”, “R3”, or “R4” according to their respective strengths.

Tablets: 0.25 mg, 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 ) Oral solution: 1 mg/mL ( 3 ) Orally disintegrating tablets: 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of action of RISPERDAL ® , as with other drugs used to treat schizophrenia, is unknown.

However, it has been proposed that the drug’s therapeutic activity in schizophrenia is mediated through a combination of dopamine Type 2 (D 2 ) and serotonin Type 2 (5HT 2 ) receptor antagonism.

RISPERDAL ® is a selective monoaminergic antagonist with high affinity (Ki of 0.12 to 7.3 nM) for the serotonin Type 2 (5HT 2 ), dopamine Type 2 (D 2 ), α 1 and α 2 adrenergic, and H 1 histaminergic receptors.

RISPERDAL ® acts as an antagonist at other receptors, but with lower potency.

RISPERDAL ® has low to moderate affinity (Ki of 47 to 253 nM) for the serotonin 5HT 1C , 5HT 1D , and 5HT 1A receptors, weak affinity (Ki of 620 to 800 nM) for the dopamine D 1 and haloperidol-sensitive sigma site, and no affinity (when tested at concentrations >10 -5 M) for cholinergic muscarinic or β 1 and β 2 adrenergic receptors.

INDICATIONS AND USAGE

1 RISPERDAL® is an atypical antipsychotic agent indicated for: Treatment of schizophrenia in adults and adolescents aged 13–17 years ( 1.1 ) Alone, or in combination with lithium or valproate, for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults, and alone in children and adolescents aged 10–17 years ( 1.2 ) Treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years ( 1.3 ) 1.1 Schizophrenia Adults RISPERDAL ® (risperidone) is indicated for the acute and maintenance treatment of schizophrenia [see Clinical Studies (14.1) ] .

Adolescents RISPERDAL ® is indicated for the treatment of schizophrenia in adolescents aged 13–17 years [see Clinical Studies (14.1) ] .

1.2 Bipolar Mania Monotherapy – Adults and Pediatrics RISPERDAL ® is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults and in children and adolescents aged 10–17 years [see Clinical Studies (14.2) ] .

Combination Therapy – Adults The combination of RISPERDAL ® with lithium or valproate is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder [ see Clinical Studies (14.3) ] .

1.3 Irritability Associated with Autistic Disorder Pediatrics RISPERDAL ® is indicated for the treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years, including symptoms of aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods [see Clinical Studies (14.4) ] .

PEDIATRIC USE

8.4 Pediatric Use The efficacy and safety of RISPERDAL ® in the treatment of schizophrenia were demonstrated in 417 adolescents, aged 13 – 17 years, in two short-term (6 and 8 weeks, respectively) double-blind controlled trials [see Indications and Usage (1.1) , Adverse Reactions (6.1) , and Clinical Studies (14.1) ].

Additional safety and efficacy information was also assessed in one long-term (6-month) open-label extension study in 284 of these adolescent patients with schizophrenia.

Safety and effectiveness of RISPERDAL ® in children less than 13 years of age with schizophrenia have not been established.

The efficacy and safety of RISPERDAL ® in the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in 169 children and adolescent patients, aged 10 – 17 years, were demonstrated in one double-blind, placebo-controlled, 3-week trial [see Indications and Usage (1.2) , Adverse Reactions (6.2) , and Clinical Studies (14.2) ] .

Safety and effectiveness of RISPERDAL ® in children less than 10 years of age with bipolar disorder have not been established.

The efficacy and safety of RISPERDAL ® in the treatment of irritability associated with autistic disorder were established in two 8-week, double-blind, placebo-controlled trials in 156 children and adolescent patients, aged 5 to 16 years [see Indications and Usage (1.3) , Adverse Reactions (6.3) and Clinical Studies (14.4) ] .

Additional safety information was also assessed in a long-term study in patients with autistic disorder, or in short- and long-term studies in more than 1200 pediatric patients with psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania who were of similar age and weight, and who received similar dosages of RISPERDAL ® as patients treated for irritability associated with autistic disorder.

The safety and effectiveness of RISPERDAL ® in pediatric patients less than 5 years of age with autistic disorder have not been established.

Tardive Dyskinesia In clinical trials in 1885 children and adolescents treated with RISPERDAL ® , 2 (0.1%) patients were reported to have tardive dyskinesia, which resolved on discontinuation of RISPERDAL ® treatment [see also Warnings and Precautions (5.4) ] .

Weight Gain In a long-term, open-label extension study in adolescent patients with schizophrenia, weight increase was reported as a treatment-emergent adverse event in 14% of patients.

In 103 adolescent patients with schizophrenia, a mean increase of 9.0 kg was observed after 8 months of RISPERDAL ® treatment.

The majority of that increase was observed within the first 6 months.

The average percentiles at baseline and 8 months, respectively, were 56 and 72 for weight, 55 and 58 for height, and 51 and 71 for body mass index.

In long-term, open-label trials (studies in patients with autistic disorder or other psychiatric disorders), a mean increase of 7.5 kg after 12 months of RISPERDAL ® treatment was observed, which was higher than the expected normal weight gain (approximately 3 to 3.5 kg per year adjusted for age, based on Centers for Disease Control and Prevention normative data).

The majority of that increase occurred within the first 6 months of exposure to RISPERDAL ® .

The average percentiles at baseline and 12 months, respectively, were 49 and 60 for weight, 48 and 53 for height, and 50 and 62 for body mass index.

In one 3-week, placebo-controlled trial in children and adolescent patients with acute manic or mixed episodes of bipolar I disorder, increases in body weight were higher in the RISPERDAL ® groups than the placebo group, but not dose related (1.90 kg in the RISPERDAL ® 0.5–2.5 mg group, 1.44 kg in the RISPERDAL ® 3–6 mg group, and 0.65 kg in the placebo group).

A similar trend was observed in the mean change from baseline in body mass index.

When treating pediatric patients with RISPERDAL ® for any indication, weight gain should be assessed against that expected with normal growth.

[See also Adverse Reactions (6.7) ] Somnolence Somnolence was frequently observed in placebo-controlled clinical trials of pediatric patients with autistic disorder.

Most cases were mild or moderate in severity.

These events were most often of early onset with peak incidence occurring during the first two weeks of treatment, and transient with a median duration of 16 days.

Somnolence was the most commonly observed adverse event in the clinical trial of bipolar disorder in children and adolescents, as well as in the schizophrenia trials in adolescents.

As was seen in the autistic disorder trials, these events were most often of early onset and transient in duration.

[See also Adverse Reactions (6.1 , 6.2 , 6.3) ] Patients experiencing persistent somnolence may benefit from a change in dosing regimen [ see Dosage and Administration (2.1 , 2.2 , 2.3) ] .

Hyperprolactinemia, Growth, and Sexual Maturation RISPERDAL ® has been shown to elevate prolactin levels in children and adolescents as well as in adults [se e Warnings and Precautions (5.6) ] .

In double-blind, placebo-controlled studies of up to 8 weeks duration in children and adolescents (aged 5 to 17 years) with autistic disorder or psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania, 49% of patients who received RISPERDAL ® had elevated prolactin levels compared to 2% of patients who received placebo.

Similarly, in placebo-controlled trials in children and adolescents (aged 10 to 17 years) with bipolar disorder, or adolescents (aged 13 to 17 years) with schizophrenia, 82–87% of patients who received RISPERDAL ® had elevated levels of prolactin compared to 3–7% of patients on placebo.

Increases were dose-dependent and generally greater in females than in males across indications.

In clinical trials in 1885 children and adolescents, galactorrhea was reported in 0.8% of RISPERDAL ® -treated patients and gynecomastia was reported in 2.3% of RISPERDAL ® -treated patients.

The long-term effects of RISPERDAL ® on growth and sexual maturation have not been fully evaluated.

PREGNANCY

8.1 Pregnancy Pregnancy Category C.

The teratogenic potential of risperidone was studied in three Segment II studies in Sprague-Dawley and Wistar rats (0.63–10 mg/kg or 0.4 to 6 times the maximum recommended human dose [MRHD] on a mg/m 2 basis) and in one Segment II study in New Zealand rabbits (0.31–5 mg/kg or 0.4 to 6 times the MRHD on a mg/m 2 basis).

The incidence of malformations was not increased compared to control in offspring of rats or rabbits given 0.4 to 6 times the MRHD on a mg/m 2 basis.

In three reproductive studies in rats (two Segment III and a multigenerational study), there was an increase in pup deaths during the first 4 days of lactation at doses of 0.16–5 mg/kg or 0.1 to 3 times the MRHD on a mg/m 2 basis.

It is not known whether these deaths were due to a direct effect on the fetuses or pups or to effects on the dams.

There was no no-effect dose for increased rat pup mortality.

In one Segment III study, there was an increase in stillborn rat pups at a dose of 2.5 mg/kg or 1.5 times the MRHD on a mg/m 2 basis.

In a cross-fostering study in Wistar rats, toxic effects on the fetus or pups, as evidenced by a decrease in the number of live pups and an increase in the number of dead pups at birth (Day 0), and a decrease in birth weight in pups of drug-treated dams were observed.

In addition, there was an increase in deaths by Day 1 among pups of drug-treated dams, regardless of whether or not the pups were cross-fostered.

Risperidone also appeared to impair maternal behavior in that pup body weight gain and survival (from Day 1 to 4 of lactation) were reduced in pups born to control but reared by drug-treated dams.

These effects were all noted at the one dose of risperidone tested, i.e., 5 mg/kg or 3 times the MRHD on a mg/m 2 basis.

Placental transfer of risperidone occurs in rat pups.

There are no adequate and well-controlled studies in pregnant women.

However, there was one report of a case of agenesis of the corpus callosum in an infant exposed to risperidone in utero .

The causal relationship to RISPERDAL ® therapy is unknown.

Reversible extrapyramidal symptoms in the neonate were observed following postmarketing use of RISPERDAL ® during the last trimester of pregnancy.

RISPERDAL ® should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

NUSRING MOTHERS

8.3 Nursing Mothers In animal studies, risperidone and 9-hydroxyrisperidone are excreted in milk.

Risperidone and 9-hydroxyrisperidone are also excreted in human breast milk.

Therefore, women receiving RISPERDAL ® should not breast-feed.

BOXED WARNING

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

Analyses of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients.

Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature.

Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.

The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear.

RISPERDAL ® (risperidone) is not approved for the treatment of patients with dementia-related psychosis.

[See Warnings and Precautions (5.1) ] WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS See full prescribing information for complete boxed warning.

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis.

( 5.1 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Cerebrovascular events, including stroke, in elderly patients with dementia-related psychosis.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis ( 5.2 ) Neuroleptic Malignant Syndrome ( 5.3 ) Tardive dyskinesia ( 5.4 ) Hyperglycemia and diabetes mellitus ( 5.5 ) Hyperprolactinemia ( 5.6 ) Orthostatic hypotension ( 5.7 ) Leukopenia, Neutropenia, and Agranulocytosis: has been reported with antipsychotics, including risperidone.

Patients with a history of a clinically significant low white blood cell count (WBC) or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

( 5.8 ) Potential for cognitive and motor impairment ( 5.9 ) Seizures ( 5.10 ) Dysphagia ( 5.11 ) Priapism ( 5.12 ) Thrombotic Thrombocytopenic Purpura (TTP) ( 5.13 ) Disruption of body temperature regulation ( 5.14 ) Antiemetic Effect ( 5.15 ) Suicide ( 5.16 ) Increased sensitivity in patients with Parkinson’s disease or those with dementia with Lewy bodies ( 5.17 ) Diseases or conditions that could affect metabolism or hemodynamic responses ( 5.17 ) 5.1 Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® (risperidone) is not approved for the treatment of dementia-related psychosis [see Boxed Warning ] .

5.2 Cerebrovascular Adverse Events, Including Stroke, in Elderly Patients with Dementia-Related Psychosis Cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, were reported in patients (mean age 85 years; range 73–97) in trials of risperidone in elderly patients with dementia-related psychosis.

In placebo-controlled trials, there was a significantly higher incidence of cerebrovascular adverse events in patients treated with risperidone compared to patients treated with placebo.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See also Boxed Warnings and Warnings and Precautions (5.1) ] 5.3 Neuroleptic Malignant Syndrome (NMS) A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with antipsychotic drugs.

Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).

Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis), and acute renal failure.

The diagnostic evaluation of patients with this syndrome is complicated.

In arriving at a diagnosis, it is important to identify cases in which the clinical presentation includes both serious medical illness (e.g., pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and symptoms (EPS).

Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever, and primary central nervous system pathology.

The management of NMS should include: (1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; (2) intensive symptomatic treatment and medical monitoring; and (3) treatment of any concomitant serious medical problems for which specific treatments are available.

There is no general agreement about specific pharmacological treatment regimens for uncomplicated NMS.

If a patient requires antipsychotic drug treatment after recovery from NMS, the potential reintroduction of drug therapy should be carefully considered.

The patient should be carefully monitored, since recurrences of NMS have been reported.

5.4 Tardive Dyskinesia A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs.

Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.

Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.

The risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase.

However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses.

There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.

Antipsychotic treatment, itself, however, may suppress (or partially suppress) the signs and symptoms of the syndrome and thereby may possibly mask the underlying process.

The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown.

Given these considerations, RISPERDAL ® should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.

Chronic antipsychotic treatment should generally be reserved for patients who suffer from a chronic illness that: (1) is known to respond to antipsychotic drugs, and (2) for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.

In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

The need for continued treatment should be reassessed periodically.

If signs and symptoms of tardive dyskinesia appear in a patient treated with RISPERDAL ® , drug discontinuation should be considered.

However, some patients may require treatment with RISPERDAL ® despite the presence of the syndrome.

5.5 Hyperglycemia and Diabetes Mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics including RISPERDAL ® .

Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population.

Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse events is not completely understood.

However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse events in patients treated with the atypical antipsychotics.

Precise risk estimates for hyperglycemia-related adverse events in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics should be monitored regularly for worsening of glucose control.

Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment.

Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should undergo fasting blood glucose testing.

In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of the suspect drug.

5.6 Hyperprolactinemia As with other drugs that antagonize dopamine D 2 receptors, RISPERDAL ® elevates prolactin levels and the elevation persists during chronic administration.

RISPERDAL ® is associated with higher levels of prolactin elevation than other antipsychotic agents.

Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion.

This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is contemplated in a patient with previously detected breast cancer.

An increase in pituitary gland, mammary gland, and pancreatic islet cell neoplasia (mammary adenocarcinomas, pituitary and pancreatic adenomas) was observed in the risperidone carcinogenicity studies conducted in mice and rats [see Non-Clinical Toxicology (13.1) ] .

Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans; the available evidence is considered too limited to be conclusive at this time.

5.7 Orthostatic Hypotension RISPERDAL ® may induce orthostatic hypotension associated with dizziness, tachycardia, and in some patients, syncope, especially during the initial dose-titration period, probably reflecting its alpha-adrenergic antagonistic properties.

Syncope was reported in 0.2% (6/2607) of RISPERDAL ® -treated patients in Phase 2 and 3 studies in adults with schizophrenia.

The risk of orthostatic hypotension and syncope may be minimized by limiting the initial dose to 2 mg total (either once daily or 1 mg twice daily) in normal adults and 0.5 mg twice daily in the elderly and patients with renal or hepatic impairment [see Dosage and Administration (2.1 , 2.4) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

A dose reduction should be considered if hypotension occurs.

RISPERDAL ® should be used with particular caution in patients with known cardiovascular disease (history of myocardial infarction or ischemia, heart failure, or conduction abnormalities), cerebrovascular disease, and conditions which would predispose patients to hypotension, e.g., dehydration and hypovolemia.

Clinically significant hypotension has been observed with concomitant use of RISPERDAL ® and antihypertensive medication.

5.8 Leukopenia, Neutropenia, and Agranulocytosis Class Effect: In clinical trial and/or postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to antipsychotic agents, including RISPERDAL ® .

Agranulocytosis has also been reported.

Possible risk factors for leukopenia/neutropenia include pre-existing low white blood cell count (WBC) and history of drug-induced leukopenia/neutropenia.

Patients with a history of a clinically significant low WBC or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

Patients with clinically significant neutropenia should be carefully monitored for fever or other symptoms or signs of infection and treated promptly if such symptoms or signs occur.

Patients with severe neutropenia (absolute neutrophil count <1000/mm 3 ) should discontinue RISPERDAL ® and have their WBC followed until recovery.

5.9 Potential for Cognitive and Motor Impairment Somnolence was a commonly reported adverse event associated with RISPERDAL ® treatment, especially when ascertained by direct questioning of patients.

This adverse event is dose-related, and in a study utilizing a checklist to detect adverse events, 41% of the high-dose patients (RISPERDAL ® 16 mg/day) reported somnolence compared to 16% of placebo patients.

Direct questioning is more sensitive for detecting adverse events than spontaneous reporting, by which 8% of RISPERDAL ® 16 mg/day patients and 1% of placebo patients reported somnolence as an adverse event.

Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely.

5.10 Seizures During premarketing testing in adult patients with schizophrenia, seizures occurred in 0.3% (9/2607) of RISPERDAL ® -treated patients, two in association with hyponatremia.

RISPERDAL ® should be used cautiously in patients with a history of seizures.

5.11 Dysphagia Esophageal dysmotility and aspiration have been associated with antipsychotic drug use.

Aspiration pneumonia is a common cause of morbidity and mortality in patients with advanced Alzheimer’s dementia.

RISPERDAL ® and other antipsychotic drugs should be used cautiously in patients at risk for aspiration pneumonia.

[See also Boxed Warning and Warnings and Precautions (5.1) ] 5.12 Priapism Rare cases of priapism have been reported.

While the relationship of the events to RISPERDAL ® use has not been established, other drugs with alpha-adrenergic blocking effects have been reported to induce priapism, and it is possible that RISPERDAL ® may share this capacity.

Severe priapism may require surgical intervention.

5.13 Thrombotic Thrombocytopenic Purpura (TTP) A single case of TTP was reported in a 28 year-old female patient receiving oral RISPERDAL ® in a large, open premarketing experience (approximately 1300 patients).

She experienced jaundice, fever, and bruising, but eventually recovered after receiving plasmapheresis.

The relationship to RISPERDAL ® therapy is unknown.

5.14 Body Temperature Regulation Disruption of body temperature regulation has been attributed to antipsychotic agents.

Both hyperthermia and hypothermia have been reported in association with oral RISPERDAL ® use.

Caution is advised when prescribing for patients who will be exposed to temperature extremes.

5.15 Antiemetic Effect Risperidone has an antiemetic effect in animals; this effect may also occur in humans, and may mask signs and symptoms of overdosage with certain drugs or of conditions such as intestinal obstruction, Reye’s syndrome, and brain tumor.

5.16 Suicide The possibility of a suicide attempt is inherent in patients with schizophrenia and bipolar mania, including children and adolescent patients, and close supervision of high-risk patients should accompany drug therapy.

Prescriptions for RISPERDAL ® should be written for the smallest quantity of tablets, consistent with good patient management, in order to reduce the risk of overdose.

5.17 Use in Patients with Concomitant Illness Clinical experience with RISPERDAL ® in patients with certain concomitant systemic illnesses is limited.

Patients with Parkinson’s Disease or Dementia with Lewy Bodies who receive antipsychotics, including RISPERDAL ® , are reported to have an increased sensitivity to antipsychotic medications.

Manifestations of this increased sensitivity have been reported to include confusion, obtundation, postural instability with frequent falls, extrapyramidal symptoms, and clinical features consistent with the neuroleptic malignant syndrome.

Caution is advisable in using RISPERDAL ® in patients with diseases or conditions that could affect metabolism or hemodynamic responses.

RISPERDAL ® has not been evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or unstable heart disease.

Patients with these diagnoses were excluded from clinical studies during the product’s premarket testing.

Increased plasma concentrations of risperidone and 9-hydroxyrisperidone occur in patients with severe renal impairment (creatinine clearance <30 mL/min/1.73 m 2 ), and an increase in the free fraction of risperidone is seen in patients with severe hepatic impairment.

A lower starting dose should be used in such patients [ see Dosage and Administration (2.4) ] .

5.18 Monitoring: Laboratory Tests No specific laboratory tests are recommended.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION Physicians are advised to discuss the following issues with patients for whom they prescribe RISPERDAL ® : 17.1 Orthostatic Hypotension Patients should be advised of the risk of orthostatic hypotension, especially during the period of initial dose titration [see Warnings and Precautions (5.7) ] .

17.2 Interference with Cognitive and Motor Performance Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely [see Warnings and Precautions (5.9) ] .

17.3 Pregnancy Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy [see Use in Specific Populations (8.1) ] .

17.4 Nursing Patients should be advised not to breast-feed an infant if they are taking RISPERDAL ® [see Use in Specific Populations (8.3) ] .

17.5 Concomitant Medication Patients should be advised to inform their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs, since there is a potential for interactions [see Drug Interactions (7) ] .

17.6 Alcohol Patients should be advised to avoid alcohol while taking RISPERDAL ® [see Drug Interactions (7.1) ] .

17.7 Phenylketonurics Phenylalanine is a component of aspartame.

Each 4 mg RISPERDAL ® M-TAB ® Orally Orally Disintegrating Tablet contains 0.14 mg phenylalanine.

DOSAGE AND ADMINISTRATION

2 Initial Dose Titration Target Dose Effective Dose Range Schizophrenia- adults ( 2.1 ) 2 mg/day 1–2 mg daily 4–8 mg daily 4–16 mg/day Schizophrenia – adolescents ( 2.1 ) 0.5mg/day 0.5– 1 mg daily 3mg/day 1–6 mg/day Bipolar mania – adults ( 2.2 ) 2–3 mg/day 1mg daily 1–6mg/day 1–6 mg/day Bipolar mania in children/adolescents ( 2.2 ) 0.5 mg/day 0.5–1mg daily 2.5mg/day 0.5–6 mg/day Irritability associated with autistic disorder ( 2.3 ) 0.25 mg/day (<20 kg) 0.5 mg/day (≥20 kg) 0.25–0.5 mg at ≥ 2 weeks 0.5 mg/day (<20 kg) 1 mg/day (≥20 kg) 0.5–3 mg/day 2.1 Schizophrenia Adults Usual Initial Dose RISPERDAL ® can be administered once or twice daily.

Initial dosing is generally 2 mg/day.

Dose increases should then occur at intervals not less than 24 hours, in increments of 1–2 mg/day, as tolerated, to a recommended dose of 4–8 mg/day.

In some patients, slower titration may be appropriate.

Efficacy has been demonstrated in a range of 4–16 mg/day [see Clinical Studies (14.1) ] .

However, doses above 6 mg/day for twice daily dosing were not demonstrated to be more efficacious than lower doses, were associated with more extrapyramidal symptoms and other adverse effects, and are generally not recommended.

In a single study supporting once-daily dosing, the efficacy results were generally stronger for 8 mg than for 4 mg.

The safety of doses above 16 mg/day has not been evaluated in clinical trials.

Maintenance Therapy While it is unknown how long a patient with schizophrenia should remain on RISPERDAL ® , the effectiveness of RISPERDAL ® 2 mg/day to 8 mg/day at delaying relapse was demonstrated in a controlled trial in patients who had been clinically stable for at least 4 weeks and were then followed for a period of 1 to 2 years [ see Clinical Studies (14.1) ] .

Patients should be periodically reassessed to determine the need for maintenance treatment with an appropriate dose.

Adolescents The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 3 mg/day.

Although efficacy has been demonstrated in studies of adolescent patients with schizophrenia at doses between 1 and 6 mg/day, no additional benefit was seen above 3 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

There are no controlled data to support the longer term use of RISPERDAL ® beyond 8 weeks in adolescents with schizophrenia.

The physician who elects to use RISPERDAL ® for extended periods in adolescents with schizophrenia should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

Reinitiation of Treatment in Patients Previously Discontinued Although there are no data to specifically address reinitiation of treatment, it is recommended that after an interval off RISPERDAL ® , the initial titration schedule should be followed.

Switching From Other Antipsychotics There are no systematically collected data to specifically address switching schizophrenic patients from other antipsychotics to RISPERDAL ® , or treating patients with concomitant antipsychotics.

While immediate discontinuation of the previous antipsychotic treatment may be acceptable for some schizophrenic patients, more gradual discontinuation may be most appropriate for others.

The period of overlapping antipsychotic administration should be minimized.

When switching schizophrenic patients from depot antipsychotics, initiate RISPERDAL ® therapy in place of the next scheduled injection.

The need for continuing existing EPS medication should be re-evaluated periodically.

2.2 Bipolar Mania Usual Dose Adults RISPERDAL ® should be administered on a once-daily schedule, starting with 2 mg to 3 mg per day.

Dosage adjustments, if indicated, should occur at intervals of not less than 24 hours and in dosage increments/decrements of 1 mg per day, as studied in the short-term, placebo-controlled trials.

In these trials, short-term (3 week) anti-manic efficacy was demonstrated in a flexible dosage range of 1–6 mg per day [see Clinical Studies (14.2 , 14.3) ] .

RISPERDAL ® doses higher than 6 mg per day were not studied.

Pediatrics The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 2.5 mg/day.

Although efficacy has been demonstrated in studies of pediatric patients with bipolar mania at doses between 0.5 and 6 mg/day, no additional benefit was seen above 2.5 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

Maintenance Therapy There is no body of evidence available from controlled trials to guide a clinician in the longer-term management of a patient who improves during treatment of an acute manic episode with RISPERDAL ® .

While it is generally agreed that pharmacological treatment beyond an acute response in mania is desirable, both for maintenance of the initial response and for prevention of new manic episodes, there are no systematically obtained data to support the use of RISPERDAL ® in such longer-term treatment (i.e., beyond 3 weeks).

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

2.3 Irritability Associated with Autistic Disorder – Pediatrics (Children and Adolescents) The safety and effectiveness of RISPERDAL ® in pediatric patients with autistic disorder less than 5 years of age have not been established.

The dosage of RISPERDAL ® should be individualized according to the response and tolerability of the patient.

The total daily dose of RISPERDAL ® can be administered once daily, or half the total daily dose can be administered twice daily.

Dosing should be initiated at 0.25 mg per day for patients < 20 kg and 0.5 mg per day for patients ≥ 20 kg.

After a minimum of four days from treatment initiation, the dose may be increased to the recommended dose of 0.5 mg per day for patients < 20 kg and 1 mg per day for patients ≥ 20 kg.

This dose should be maintained for a minimum of 14 days.

In patients not achieving sufficient clinical response, dose increases may be considered at ≥ 2-week intervals in increments of 0.25 mg per day for patients < 20 kg or 0.5 mg per day for patients ≥ 20 kg.

Caution should be exercised with dosage for smaller children who weigh less than 15 kg.

In clinical trials, 90% of patients who showed a response (based on at least 25% improvement on ABC-I, [see Clinical Studies (14.4) ] ) received doses of RISPERDAL ® between 0.5 mg and 2.5 mg per day.

The maximum daily dose of RISPERDAL ® in one of the pivotal trials, when the therapeutic effect reached plateau, was 1 mg in patients 45 kg.

No dosing data is available for children who weighed less than 15 kg.

Once sufficient clinical response has been achieved and maintained, consideration should be given to gradually lowering the dose to achieve the optimal balance of efficacy and safety.

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

Patients experiencing persistent somnolence may benefit from a once-daily dose administered at bedtime or administering half the daily dose twice daily, or a reduction of the dose.

2.4 Dosage in Special Populations The recommended initial dose is 0.5 mg twice daily in patients who are elderly or debilitated, patients with severe renal or hepatic impairment, and patients either predisposed to hypotension or for whom hypotension would pose a risk.

Dosage increases in these patients should be in increments of no more than 0.5 mg twice daily.

Increases to dosages above 1.5 mg twice daily should generally occur at intervals of at least 1 week.

In some patients, slower titration may be medically appropriate.

Elderly or debilitated patients, and patients with renal impairment, may have less ability to eliminate RISPERDAL ® than normal adults.

Patients with impaired hepatic function may have increases in the free fraction of risperidone, possibly resulting in an enhanced effect [see Clinical Pharmacology (12.3) ] .

Patients with a predisposition to hypotensive reactions or for whom such reactions would pose a particular risk likewise need to be titrated cautiously and carefully monitored [see Warnings and Precautions (5.2 , 5.7 , 5.17) ] .

If a once-daily dosing regimen in the elderly or debilitated patient is being considered, it is recommended that the patient be titrated on a twice-daily regimen for 2–3 days at the target dose.

Subsequent switches to a once-daily dosing regimen can be done thereafter.

2.5 Co-Administration of RISPERDAL ® with Certain Other Medications Co-administration of carbamazepine and other enzyme inducers (e.g., phenytoin, rifampin, phenobarbital) with RISPERDAL ® would be expected to cause decreases in the plasma concentrations of the sum of risperidone and 9-hydroxyrisperidone combined, which could lead to decreased efficacy of RISPERDAL ® treatment.

The dose of RISPERDAL ® needs to be titrated accordingly for patients receiving these enzyme inducers, especially during initiation or discontinuation of therapy with these inducers [see Drug Interactions (7.11) ] .

Fluoxetine and paroxetine have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

The dose of RISPERDAL ® needs to be titrated accordingly when fluoxetine or paroxetine is co-administered [see Drug Interactions (7.10) ] .

2.6 Administration of RISPERDAL ® Oral Solution RISPERDAL ® Oral Solution can be administered directly from the calibrated pipette, or can be mixed with a beverage prior to administration.

RISPERDAL ® Oral Solution is compatible in the following beverages: water, coffee, orange juice, and low-fat milk; it is NOT compatible with either cola or tea.

2.7 Directions for Use of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets Tablet Accessing RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg are supplied in blister packs of 4 tablets each.

Do not open the blister until ready to administer.

For single tablet removal, separate one of the four blister units by tearing apart at the perforations.

Bend the corner where indicated.

Peel back foil to expose the tablet.

DO NOT push the tablet through the foil because this could damage the tablet.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg are supplied in a child-resistant pouch containing a blister with 1 tablet each.

The child-resistant pouch should be torn open at the notch to access the blister.

Do not open the blister until ready to administer.

Peel back foil from the side to expose the tablet.

DO NOT push the tablet through the foil, because this could damage the tablet.

Tablet Administration Using dry hands, remove the tablet from the blister unit and immediately place the entire RISPERDAL ® M-TAB ® Orally Disintegrating Tablet on the tongue.

The RISPERDAL ® M-TAB ® Orally Disintegrating Tablet should be consumed immediately, as the tablet cannot be stored once removed from the blister unit.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets disintegrate in the mouth within seconds and can be swallowed subsequently with or without liquid.

Patients should not attempt to split or to chew the tablet.

Generic Name: MIRTAZAPINE
Brand Name: REMERON
  • Substance Name(s):
  • MIRTAZAPINE

DRUG INTERACTIONS

7 Table 5 includes clinically important drug interactions with REMERON/REMERONSolTab [see Clinical Pharmacology (12.3) ].

Table 5: Clinically Important Drug Interactions with REMERON/REMERONSolTab Monoamine Oxidase Inhibitors (MAOIs) Clinical Impact The concomitant use of serotonergic drugs, including REMERON/REMERONSolTab, and MAOIs increases the risk of serotonin syndrome.

Intervention REMERON/REMERONSolTab is contraindicated in patients taking MAOIs, including MAOIs such as linezolid or intravenous methylene blue [see Dosage and Administration (2.4) , Contraindications (4) , Warnings and Precautions (5.3) ].

Examples selegiline, tranylcypromine, isocarboxazid, phenelzine, linezolid, methylene blue Other Serotonergic Drugs Clinical Impact The concomitant use of serotonergic drugs with REMERON/REMERONSolTab increases the risk of serotonin syndrome.

Intervention Monitor patients for signs and symptoms of serotonin syndrome, particularly during treatment initiation and dosage increases.

If serotonin syndrome occurs, consider discontinuation of REMERON/REMERONSolTab and/or concomitant serotonergic drugs [see Warnings and Precautions (5.3) ].

Examples SSRIs, SNRIs, triptans, tricyclic antidepressants, fentanyl, lithium, amphetamines, St.

John’s Wort, tramadol, tryptophan, buspirone Strong CYP3A Inducers Clinical Impact The concomitant use of strong CYP3A inducers with REMERON/REMERONSolTab decreases the plasma concentration of mirtazapine [see Clinical Pharmacology (12.3) ] .

Intervention Increase the dose of REMERON/REMERONSolTab if needed with concomitant CYP3A inducer use.

Conversely, a decrease in dosage of REMERON/REMERONSolTab may be needed if the CYP3A inducer is discontinued [see Dosage and Administration (2.5) ].

Examples phenytoin, carbamazepine, rifampin Strong CYP3A Inhibitors Clinical Impact The concomitant use of strong CYP3A inhibitors with REMERON/REMERONSolTab may increase the plasma concentration of mirtazapine [see Clinical Pharmacology (12.3) ] .

Intervention Decrease the dose of REMERON/REMERONSolTab if needed with concomitant strong CYP3A inhibitor use.

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if the CYP3A inhibitor is discontinued [see Dosage and Administration (2.5) ].

Examples itraconazole, ritonavir, nefazodone Cimetidine Clinical Impact The concomitant use of cimetidine, a CYP1A2, CYP2D6, and CYP3A inhibitor, with REMERON/REMERONSolTab may increase the plasma concentration of mirtazapine [see Clinical Pharmacology (12.3) ].

Intervention Decrease the dose of REMERON/REMERONSolTab if needed with concomitant cimetidine use.

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if cimetidine is discontinued [see Dosage and Administration (2.5) ] .

Benzodiazepines and Alcohol Clinical Impact The concomitant use of benzodiazepines or alcohol with REMERON/REMERONSolTab increases the impairment of cognitive and motor skills produced by REMERON/REMERONSolTab alone.

Intervention Avoid concomitant use of benzodiazepines and alcohol with REMERON/REMERONSolTab [see Warnings and Precautions (5.7) , Clinical Pharmacology (12.3) ] ] .

Examples diazepam, alprazolam, alcohol Drugs that Prolong QTc Interval Clinical Impact The concomitant use of other drugs which prolong the QTc interval with REMERON/REMERONSolTab, increase the risk of QT prolongation and/or ventricular arrhythmias (e.g., Torsades de Pointes).

Intervention Use caution when using REMERON/REMERONSolTab concomitantly with drugs that prolong the QTc interval [see Warnings and Precautions (5.5) , Clinical Pharmacology (12.3) ].

Warfarin Clinical Impact The concomitant use of warfarin with REMERON/REMERONSolTab may result in an increase in INR [see Clinical Pharmacology (12.3) ] .

Intervention Monitor INR during concomitant use of warfarin with REMERON/REMERONSolTab.

Strong CYP3A inducers: Dosage increase may be needed for REMERON/REMERONSolTab with concomitant use of strong CYP3A inducers.

( 2.5 , 7 ) Strong CYP3A inhibitors : Dosage decrease may be needed when REMERON/REMERONSolTab is coadministered with strong CYP3A inhibitors.

( 2.5 , 7 ) Cimetidine: Dosage decrease may be needed when REMERON/REMERONSolTab is coadministered with cimetidine.

( 2.5 , 7 ) Warfarin : Monitor INR during concomitant use.

( 7 )

OVERDOSAGE

10 Human Experience In premarketing clinical studies, there were reports of REMERON overdose alone or in combination with other pharmacological agents.

Signs and symptoms reported in association with overdose included disorientation, drowsiness, impaired memory, and tachycardia.

Based on postmarketing reports, serious outcomes (including fatalities) may occur at dosages higher than the recommended doses, especially with mixed overdoses.

In these cases, QT prolongation and Torsades de Pointes have also been reported [see Warnings and Precautions (5.5) , Adverse Reactions (6.2) , and Drug Interactions (7) ].

Overdose Management No specific antidotes for mirtazapine are known.

Contact Poison Control (1-800-222-1222) for the latest recommendations.

DESCRIPTION

11 REMERON and REMERONSolTab contain mirtazapine.

Mirtazapine has a tetracyclic chemical structure and belongs to the piperazino-azepine group of compounds.

It is designated 1,2,3,4,10,14b-hexahydro-2-methylpyrazino [2,1-a] pyrido [2,3-c][2] benzazepine and has the empirical formula of C 17 H 19 N 3 .

Its molecular weight is 265.35.

The structural formula is the following and it is the racemic mixture: Mirtazapine is a white to creamy white crystalline powder which is practically insoluble in water.

REMERON is available for oral administration as scored film-coated tablets containing 15 or 30 mg of mirtazapine Each tablet contains the following inactive ingredients: colloidal silicon dioxide anhydrous, corn starch, ferric oxide (yellow), hydroxypropyl cellulose, hypromellose, magnesium stearate, lactose monohydrate, polyethylene glycol 8000, and titanium dioxide.

The 30 mg tablets also contain ferric oxide (red).

REMERONSolTab is available for oral administration as an orally disintegrating tablet containing 15, 30, or 45 mg of mirtazapine.

REMERONSolTab also contains the following inactive ingredients: aspartame, citric acid anhydrous fine granular, crospovidone, hypromellose, magnesium stearate, mannitol, granular mannitol 2080, microcrystalline cellulose, natural and artificial orange flavor, polymethacrylate (Eudragit E100), povidone, sodium bicarbonate, and sugar spheres (composed of starch and sucrose).

Chemical Structure

CLINICAL STUDIES

14 The efficacy of REMERON as a treatment for major depressive disorder was established in 4 placebo-controlled, 6-week trials in adult outpatients meeting DSM-III criteria for major depressive disorder.

Patients were titrated with REMERON from a dose range of 5 mg to 35 mg/day.

The mean mirtazapine dose for patients who completed these 4 studies ranged from 21 to 32 mg/day.

Overall, these studies demonstrated REMERON to be superior to placebo on at least 3 of the following 4 measures: 21-Item Hamilton Depression Rating Scale (HDRS) total score; HDRS Depressed Mood Item; CGI Severity score; and Montgomery and Asberg Depression Rating Scale (MADRS).

Superiority of REMERON over placebo was also found for certain factors of the HDRS, including anxiety/somatization factor and sleep disturbance factor.

Examination of age and gender subsets of the population did not reveal any differential responsiveness on the basis of these subgroupings.

In a longer-term study, patients meeting (DSM-IV) criteria for major depressive disorder who had responded during an initial 8 to 12 weeks of acute treatment on REMERON were randomized to continuation of REMERON or placebo for up to 40 weeks of observation for relapse.

Response during the open phase was defined as having achieved a HAM-D 17 total score of ≤8 and a CGI-Improvement score of 1 or 2 at 2 consecutive visits beginning with week 6 of the 8 to 12 weeks in the open-label phase of the study.

Relapse during the double-blind phase was determined by the individual investigators.

Patients receiving continued REMERON treatment experienced significantly lower relapse rates over the subsequent 40 weeks compared to those receiving placebo.

This pattern was demonstrated in both male and female patients.

HOW SUPPLIED

16 /STORAGE AND HANDLING REMERON tablets are supplied as: Tablet Strength Tablet Color/Shape Tablet Markings Package Configuration NDC Code 15 mg Yellow, oval tablet Scored with “Organon” debossed on one side and ” T 3 Z ” on other side, on both sides of score line Bottle / 30 count 0052-0105-30 15 mg Yellow, oval tablet Scored with “MSD” debossed on one side and ” T 3 Z ” on other side, on both sides of score line Bottle / 30 count 0052-4364-01 30 mg Red-brown, oval tablet Scored with “Organon” debossed on one side and ” T 5 Z ” on other side, on both sides of score line Bottle / 30 count 0052-0107-30 30 mg Red-brown, oval tablet Scored with “MSD” debossed on one side and ” T 5 Z ” on other side, on both sides of score line Bottle / 30 count 0052-4365-01 Storage Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].

Protect from light and moisture.

REMERONSolTab orally disintegrating tablets are supplied as: Tablet Strength Tablet Color/Shape Tablet Markings Package Configuration NDC Code 15 mg White, round tablet ” T 1 Z ” debossed on one side.

Box of 5 × 6-unit dose blister packs/ 30 count 0052-0106-30 30 mg White, round tablet ” T 2 Z ” debossed on one side.

Box of 5 × 6-unit dose blister packs/30 count 0052-0108-30 45 mg White, round tablet ” T 4 Z ” debossed on one side Box of 5 × 6-unit dose blister packs/30 count 0052-0110-30 Storage Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].

Protect from light and moisture.

Use immediately upon opening individual tablet blister.

GERIATRIC USE

8.5 Geriatric Use Approximately 190 patients ≥65 years of age participated in clinical studies with REMERON.

REMERON/REMERONSolTab is known to be substantially excreted by the kidney (75%), and the risk of decreased clearance of this drug is greater in patients with impaired renal function.

Pharmacokinetic studies revealed a decreased clearance of mirtazapine in the elderly [see Clinical Pharmacology (12.3) ] .

Sedating drugs, including REMERON/REMERONSolTab, may cause confusion and over-sedation in the elderly.

Elderly patients may be at greater risk of developing hyponatremia.

Caution is indicated when administering REMERON/REMERONSolTab to elderly patients [see Warnings and Precautions (5.11) , (5.14) and Clinical Pharmacology (12.3) ] .

In general, dose selection for an elderly patient should be conservative, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.

DOSAGE FORMS AND STRENGTHS

3 REMERON is supplied as: 15 mg tablets: Oval, scored, yellow, with “Organon” debossed on one side and ” T 3 Z ” on the other side, on both sides of the score line 15 mg tablets: Oval, scored, yellow, with “MSD” debossed on one side and ” T 3 Z ” on the other side, on both sides of the score line 30 mg tablets: Oval, scored, red-brown, with “Organon” debossed on one side and ” T 5 Z ” on the other side, on both sides of the score line 30 mg tablets: Oval, scored, red-brown, with “MSD” debossed on one side and ” T 5 Z ” on the other side, on both sides of the score line REMERONSolTab is supplied as: 15 mg orally disintegrating tablets: Round, white, with ” T 1 Z ” debossed on one side 30 mg orally disintegrating tablets: Round, white, with ” T 2 Z ” debossed on one side 45 mg orally disintegrating tablets: Round, white, with ” T 4 Z ” debossed on one side Tablets : 15 mg scored and 30 mg scored.

( 3 ) Orally disintegrating tablets : 15 mg, 30 mg, and 45 mg.

( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of action of mirtazapine for the treatment of major depressive disorder, is unclear.

However, its efficacy could be mediated through its activity as an antagonist at central presynaptic α 2 -adrenergic inhibitory autoreceptors and heteroreceptors and enhancing central noradrenergic and serotonergic activity.

INDICATIONS AND USAGE

1 REMERON/REMERONSolTab are indicated for the treatment of major depressive disorder (MDD) in adults [see Clinical Studies (14) ] .

REMERON/REMERONSolTab is indicated for the treatment of major depressive disorder (MDD) in adults.

( 1 )

PEDIATRIC USE

8.4 Pediatric Use The safety and effectiveness of REMERON/REMERONSolTab have not been established in pediatric patients with MDD.

Two placebo-controlled trials in 258 pediatric patients with MDD have been conducted with REMERON, and the data were insufficient to establish the safety and effectiveness of REMERON/REMERONSolTab in pediatric patients with MDD.

Antidepressants increased the risk of suicidal thoughts and behaviors in pediatric patients [see Boxed Warning and Warnings and Precautions (5.1) ] .

In an 8-week-long clinical trial in pediatric patients receiving doses between 15 to 45 mg per day, 49% of REMERON-treated patients had a weight gain of at least 7%, compared to 5.7% of placebo-treated patients.

The mean increase in weight was 4 kg (2 kg SD) for REMERON-treated patients versus 1 kg (2 kg SD) for placebo-treated patients [see Warnings and Precautions (5.6) ] .

PREGNANCY

8.1 Pregnancy Pregnancy Exposure Registry There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antidepressants during pregnancy.

Healthcare providers are encouraged to register patients by calling the National Pregnancy Registry for Antidepressants at 1-844-405-6185 or visiting online at https://womensmentalhealth.org/clinical-and-research-programs/pregnancyregistry/antidepressants/.

Risk Summary Prolonged experience with mirtazapine in pregnant women, based on published observational studies and postmarketing reports, has not reliably identified a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes.

There are risks associated with untreated depression in pregnancy (see Clinical Considerations ).

In animal reproduction studies, oral administration of mirtazapine to pregnant rats and rabbits during the period of organogenesis revealed no evidence of teratogenic effects up to 20 and 17 times the maximum recommended human dose (MRHD) of 45 mg, respectively, based on mg/m 2 body surface area.

However, in rats, there was an increase in postimplantation loss at 20 times the MRHD based on mg/m 2 body surface area.

Oral administration of mirtazapine to pregnant rats during pregnancy and lactation resulted in an increase in pup deaths and a decrease in pup birth weights at doses 20 times the MRHD based on mg/m 2 body surface area (see Data ).

The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

All pregnancies have a background risk of birth defect, loss, or other adverse outcomes.

In the U.S.

general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.

Clinical Considerations Disease-Associated Maternal and/or Embryo/Fetal Risk Women who discontinue antidepressants during pregnancy are more likely to experience a relapse of major depression than women who continue antidepressants.

This finding is from a prospective, longitudinal study that followed 201 pregnant women with a history of major depressive disorder who were euthymic and taking antidepressants at the beginning of pregnancy.

Consider the risk of untreated depression when discontinuing or changing treatment with antidepressant medication during pregnancy and postpartum.

Data Animal Data Mirtazapine was administered orally to pregnant rats and rabbits during the period of organogenesis at doses of 2.5, 15, and 100 mg/kg/day and 2.5, 10, and 40 mg/kg/day, respectively, which are up to 20 and 17 times the maximum recommended human dose (MRHD) of 45 mg based on mg/m 2 body surface area, respectively.

No evidence of teratogenic effects was observed.

However, in rats, there was an increase in postimplantation loss in dams treated with mirtazapine at 100 mg/kg/day which is 20 times the MRHD based on mg/m 2 body surface area.

Oral administration of mirtazapine at doses of 2.5, 15, and 100 mg/kg/day to pregnant rats during pregnancy and lactation resulted in an increase in pup deaths during the first 3 days of lactation and a decrease in pup birth weights at 20 times the MRHD based on mg/m 2 body surface area.

The cause of these deaths is not known.

The no effect dose level is 3 times the MRHD based on mg/m 2 body surface area.

BOXED WARNING

WARNING: SUICIDAL THOUGHTS AND BEHAVIORS Antidepressants increased the risk of suicidal thoughts and behaviors in pediatric and young adult patients in short-term studies.

Closely monitor all antidepressant-treated patients for clinical worsening, and for emergence of suicidal thoughts and behaviors [see Warnings and Precautions (5.1) ] .

REMERON/REMERONSolTab is not approved for use in pediatric patients [see Use in Specific Populations (8.4) ].

WARNING: SUICIDAL THOUGHTS AND BEHAVIORS See full prescribing information for complete boxed warning.

Increased risk of suicidal thoughts and behavior in pediatric and young adult patients taking antidepressants.

Closely monitor all antidepressant-treated patients for clinical worsening and emergence of suicidal thoughts and behaviors.

REMERON/REMERONSolTab is not approved for use in pediatric patients.

( 5.1 , 8.4 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Agranulocytosis : If sore throat, fever, stomatitis or signs of infection occur, along with a low white blood cell count, treatment with REMERON/REMERONSolTab should be discontinued and the patient should be closely monitored.

( 5.2 ) Serotonin Syndrome : Increased risk when co-administered with other serotonergic drugs (e.g., SSRI, SNRI, triptans), but also when taken alone.

If it occurs, discontinue REMERON/REMERONSolTab and initiate supportive treatment.

( 2.4 , 4 , 5.3 , 7 ) Angle-Closure Glaucoma : Angle closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressants.

( 5.4 ) QT Prolongation : Use REMERON/REMERONSolTab with caution in patients with risk factors for QT prolongation.

( 5.5 , 7 ) Increased Appetite/Weight Gain : REMERON/REMERONSolTab has been associated with increased appetite and weight gain.

( 5.6 ) Somnolence : May impair judgment, thinking and/or motor skills.

Use with caution when engaging in activities requiring alertness, such as driving or operating machinery.

( 5.7 , 7 ) Activation of Mania/Hypomania : Screen patients for bipolar disorder prior to initiating treatment.

( 2.3 , 5.8 ) Seizures : Use with caution in patients with a seizure disorder.

( 5.9 ) Elevated Cholesterol/Triglycerides : Has been reported with REMERON use.

( 5.10 ) Hyponatremia : May occur as a result of treatment with serotonergic antidepressants, including REMERON/REMERONSolTab.

( 5.11 ) Transaminase Elevations : Clinically significant elevations have occurred.

Use with caution in patients with impaired hepatic function.

( 5.12 ) 5.1 Suicidal Thoughts and Behaviors in Adolescents and Young Adults In pooled analyses of placebo-controlled trials of antidepressant drugs (SSRIs and other antidepressant classes) that included approximately 77,000 adult patients and 4,500 pediatric patients, the incidence of suicidal thoughts and behaviors in antidepressant-treated patients age 24 years and younger was greater than in placebo-treated patients.

There was considerable variation in risk of suicidal thoughts and behaviors among drugs, but there was an increased risk identified in young patients for most drugs studied.

There were differences in absolute risk of suicidal thoughts and behaviors across the different indications, with the highest incidence in patients with MDD.

The drug-placebo differences in the number of cases of suicidal thoughts and behaviors per 1000 patients treated are provided in Table 1.

Table 1: Risk Differences of the Number of Patients with Suicidal Thoughts and Behavior in the Pooled Placebo-Controlled Trials of Antidepressants in Pediatric and Adult Patients Age Range Drug-Placebo Difference in Number of Patients with Suicidal Thoughts or Behaviors per 1000 Patients Treated Increases Compared to Placebo <18 years old 14 additional patients 18–24 years old 5 additional patients Decreases Compared to Placebo 25–64 years old 1 fewer patient ≥65 years old 6 fewer patients It is unknown whether the risk of suicidal thoughts and behaviors in children, adolescents, and young adults extends to longer-term use, i.e., beyond four months.

However, there is substantial evidence from placebo-controlled maintenance trials in adults with MDD that antidepressants delay the recurrence of depression and that depression itself is a risk factor for suicidal thoughts and behaviors.

Monitor all antidepressant-treated patients for any indication of clinical worsening and emergence of suicidal thoughts and behaviors, especially during the initial few months of drug therapy, and at times of dosage changes.

Counsel family members or caregivers of patients to monitor for changes in behavior and to alert the healthcare provider.

Consider changing the therapeutic regimen, including possibly discontinuing REMERON/REMERONSolTab, in patients whose depression is persistently worse, or who are experiencing emergent suicidal thoughts or behaviors.

5.2 Agranulocytosis In premarketing clinical trials, 2 (1 with Sjögren’s Syndrome) out of 2796 patients treated with REMERON developed agranulocytosis [absolute neutrophil count (ANC) <500/mm 3 with associated signs and symptoms, e.g., fever, infection, etc.] and a third patient developed severe neutropenia (ANC <500/mm 3 without any associated symptoms).

For these 3 patients, onset of severe neutropenia was detected on days 61, 9, and 14 of treatment, respectively.

All 3 patients recovered after REMERON was stopped.

If a patient develops a sore throat, fever, stomatitis, or other signs of infection, along with a low white blood cell (WBC) count, treatment with REMERON/REMERONSolTab should be discontinued and the patient should be closely monitored.

5.3 Serotonin Syndrome Serotonergic antidepressants, including REMERON/REMERONSolTab, can precipitate serotonin syndrome, a potentially life-threatening condition.

The risk is increased with concomitant use of other serotonergic drugs (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, amphetamines, and St.

John’s Wort) and with drugs that impair metabolism of serotonin, i.e., MAOIs [see Contraindications (4) , Drug Interactions (7) ] .

Serotonin syndrome can also occur when these drugs are used alone.

Serotonin syndrome signs and symptoms may include mental status changes (e.g., agitation, hallucinations, delirium, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, dizziness, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea).

The concomitant use of REMERON/REMERONSolTab with MAOIs is contraindicated.

In addition, do not initiate REMERON/REMERONSolTab in a patient being treated with MAOIs such as linezolid or intravenous methylene blue.

No reports involved the administration of methylene blue by other routes (such as oral tablets or local tissue injection).

If it is necessary to initiate treatment with an MAOI such as linezolid or intravenous methylene blue in a patient taking REMERON/REMERONSolTab, discontinue REMERON/REMERONSolTab before initiating treatment with the MAOI [see Contraindications (4) , Drug Interactions (7) ] .

Monitor all patients taking REMERON/REMERONSolTab for the emergence of serotonin syndrome.

Discontinue treatment with REMERON/REMERONSolTab and any concomitant serotonergic agents immediately if the above symptoms occur, and initiate supportive symptomatic treatment.

If concomitant use of REMERON/REMERONSolTab with other serotonergic drugs is clinically warranted, inform patients of the increased risk for serotonin syndrome and monitor for symptoms.

5.4 Angle-Closure Glaucoma The pupillary dilation that occurs following use of many antidepressant drugs, including REMERON/REMERONSolTab, may trigger an angle-closure attack in a patient with anatomically narrow angles who does not have a patent iridectomy.

5.5 QT Prolongation and Torsades de Pointes The effect of REMERON (mirtazapine) on QTc interval was assessed in a clinical randomized trial with placebo and positive (moxifloxacin) controls involving 54 healthy volunteers using exposure response analysis.

This trial showed a positive relationship between mirtazapine concentrations and prolongation of the QTc interval.

However, the degree of QT prolongation observed with both 45 mg and 75 mg (1.67 times the maximum recommended daily dose) doses of mirtazapine was not at a level generally considered to be clinically meaningful.

During postmarketing use of mirtazapine, cases of QT prolongation, Torsades de Pointes, ventricular tachycardia, and sudden death, have been reported [see Adverse Reactions (6.1 , 6.2) ] .

The majority of reports occurred in association with overdose or in patients with other risk factors for QT prolongation, including concomitant use of QTc-prolonging medicines [see Drug Interactions (7) and Overdosage (10) ] .

Exercise caution when REMERON/REMERONSolTab is prescribed in patients with known cardiovascular disease or family history of QT prolongation, and in concomitant use with other drugs thought to prolong the QTc interval.

5.6 Increased Appetite and Weight Gain In U.S.

controlled clinical studies, appetite increase was reported in 17% of patients treated with REMERON, compared to 2% for placebo.

In these same trials, weight gain of ≥7% of body weight was reported in 7.5% of patients treated with mirtazapine, compared to 0% for placebo.

In a pool of premarketing U.S.

clinical studies, including many patients for long-term, open-label treatment, 8% of patients receiving REMERON discontinued for weight gain.

In an 8-week-long pediatric clinical trial of doses between 15 to 45 mg/day, 49% of REMERON-treated pediatric patients had a weight gain of at least 7%, compared to 5.7% of placebo-treated patients.

The safety and effectiveness of REMERON/REMERONSolTab in pediatric patients with MDD have not been established [see Use in Specific Populations (8.4) ] .

5.7 Somnolence In U.S.

controlled studies, somnolence was reported in 54% of patients treated with REMERON, compared to 18% for placebo.

In these studies, somnolence resulted in discontinuation for 10.4% of REMERON-treated patients, compared to 2.2% for placebo.

It is unclear whether tolerance develops to the somnolent effects of REMERON/REMERONSolTab.

Because of the potentially significant effects of REMERON/REMERONSolTab on impairment of performance, caution patients about engaging in activities that require alertness, including operating hazardous machinery and motor vehicles, until they are reasonably certain that REMERON/REMERONSolTab does not affect them adversely.

The concomitant use of benzodiazepines and alcohol with REMERON/REMERONSolTab should be avoided [see Drug Interactions (7) ] .

5.8 Activation of Mania or Hypomania In patients with bipolar disorder, treating a depressive episode with REMERON/REMERONSolTab or another antidepressant may precipitate a mixed/manic episode.

In controlled clinical trials, patients with bipolar disorder were generally excluded; however, symptoms of mania or hypomania were reported in 0.2% of patients treated with REMERON.

Prior to initiating treatment with REMERON/REMERONSolTab, screen patients for any personal or family history of bipolar disorder, mania, or hypomania.

5.9 Seizures REMERON/REMERONSolTab has not been systematically evaluated in patients with seizure disorders.

In premarketing clinical trials, 1 seizure was reported among the 2796 U.S.

and non-U.S.

patients treated with REMERON.

REMERON/REMERONSolTab should be prescribed with caution in patients with a seizure disorder.

5.10 Elevated Cholesterol and Triglycerides In U.S.

controlled studies, nonfasting cholesterol increases to ≥20% above the upper limits of normal were observed in 15% of patients treated with REMERON, compared to 7% for placebo.

In these same studies, nonfasting triglyceride increases to ≥500 mg/dL were observed in 6% of patients treated with REMERON, compared to 3% for placebo.

5.11 Hyponatremia Hyponatremia may occur as a result of treatment with serotonergic antidepressants, including REMERON/REMERONSolTab.

Cases with serum sodium lower than 110 mmol/L have been reported.

Signs and symptoms of hyponatremia include headache, difficulty concentrating, memory impairment, confusion, weakness, and unsteadiness, which may lead to falls.

Signs and symptoms associated with more severe or acute cases have included hallucination, syncope, seizure, coma, respiratory arrest, and death.

In many cases, this hyponatremia appears to be the result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

In patients with symptomatic hyponatremia, discontinue REMERON/REMERONSolTab and institute appropriate medical intervention.

Elderly patients, patients taking diuretics, and those who are volume-depleted may be at greater risk of developing hyponatremia [see Use in Specific Populations (8.5) ] .

5.12 Transaminase Elevations Clinically significant ALT (SGPT) elevations (≥3 times the upper limit of the normal range) were observed in 2.0% (8/424) of patients treated with REMERON in a pool of short-term, U.S.

controlled trials, compared to 0.3% (1/328) of placebo patients.

While some patients were discontinued for the ALT increases, in other cases, the enzyme levels returned to normal despite continued REMERON treatment.

REMERON/REMERONSolTab should be used with caution in patients with impaired hepatic function [see Use in Specific Populations (8.6) , Clinical Pharmacology (12.3) ] .

5.13 Discontinuation Syndrome There have been reports of adverse reactions upon the discontinuation of REMERON/REMERONSolTab (particularly when abrupt), including but not limited to the following: dizziness, abnormal dreams, sensory disturbances (including paresthesia and electric shock sensations), agitation, anxiety, fatigue, confusion, headache, tremor, nausea, vomiting, and sweating, or other symptoms which may be of clinical significance.

A gradual reduction in the dosage, rather than an abrupt cessation, is recommended [see Dosage and Administration (2.6) ].

5.14 Use in Patients with Concomitant Illness REMERON/REMERONSolTab has not been systematically evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or other significant heart disease.

REMERON was associated with significant orthostatic hypotension in early clinical pharmacology trials with normal volunteers.

Orthostatic hypotension was infrequently observed in clinical trials with depressed patients [see Adverse Reactions (6.1) ] .

REMERON/REMERONSolTab should be used with caution in patients with known cardiovascular or cerebrovascular disease that could be exacerbated by hypotension (history of myocardial infarction, angina, or ischemic stroke) and conditions that would predispose patients to hypotension (dehydration, hypovolemia, and treatment with antihypertensive medication).

5.15 Risks in Patients with Phenylketonuria Phenylalanine can be harmful to patients with phenylketonuria (PKU).

REMERONSolTab contains phenylalanine, a component of aspartame.

REMERONSolTab contains the following amount of phenylalanine: 2.6 mg in 15 mg orally disintegrating tablet, 5.2 mg in 30 mg orally disintegrating tablet, and 7.8 mg in 45 mg orally disintegrating tablet.

Before prescribing REMERONSolTab to a patient with PKU, consider the combined daily amount of phenylalanine from all sources, including REMERONSolTab.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION Advise the patient to read the FDA-approved patient labeling (Medication Guide).

Suicidal Thoughts and Behaviors Advise patients and caregivers to look for the emergence of suicidality, especially early during treatment and when the dosage is adjusted up or down, and instruct them to report such symptoms to the healthcare provider [see Boxed Warning and Warnings and Precautions (5.1) ].

Agranulocytosis Advise patients to contact their physician if they experience fever, chills, sore throat, mucous membrane ulceration, flu-like complaints, or other symptoms that might suggest infection [see Warnings and Precautions (5.2) ].

Serotonin Syndrome Caution patients about the risk of serotonin syndrome, particularly with the concomitant use of REMERON/REMERONSolTab with other serotonergic drugs including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, amphetamines, St.

John’s Wort, and with drugs that impair metabolism of serotonin (in particular, MAOIs, both those intended to treat psychiatric disorders and also others, such as linezolid).

Advise patients to contact their healthcare provider or report to the emergency room if they experience signs or symptoms of serotonin syndrome [see Dosage and Administration (2.4) , Contraindications (4) , Warnings and Precautions (5.3) , Drug Interactions (7) ].

QT Prolongation and Torsades de Pointes Inform patients to consult their physician immediately if they feel faint, lose consciousness, or have heart palpitations [see Warnings and Precautions (5.5) , Drug Interactions (7) , Overdosage (10) ].

Advise patients to inform physicians that they are taking REMERON/REMERONSolTab before any new drug is taken.

Somnolence Advise patients that REMERON/REMERONSolTab may impair judgment, thinking, and particularly, motor skills, because of its prominent sedative effect.

Caution patients about performing activities requiring mental alertness, such as operating hazardous machinery or operating a motor vehicle, until they are reasonably certain that REMERON/REMERONSolTab therapy does not adversely affect their ability to engage in such activities.

[see Warnings and Precautions (5.7) ].

Alcohol Advise patients to avoid alcohol while taking REMERON/REMERONSolTab [see Warnings and Precautions (5.7) , Drug Interactions (7) ].

Activation of Mania/Hypomania Advise patients and their caregivers to observe for signs of activation of mania/hypomania and instruct them to report such symptoms to the healthcare provider [see Warnings and Precautions (5.8) ] .

Discontinuation Syndrome Advise patients not to abruptly discontinue REMERON/REMERONSolTab and to discuss any tapering regimen with their healthcare provider.

Adverse reactions can occur when REMERON/REMERONSolTab is discontinued [see Dosage and Administration (2.6) , Warnings and Precautions (5.13) ].

Allergic Reactions Advise patients to notify their healthcare provider if they develop an allergic reaction such as rash, hives, swelling, or difficulty breathing [see Contraindications (4) , Adverse Reactions (6.2) ] .

Pregnancy Advise patients to notify their physician if they become pregnant or intend to become pregnant during REMERON/REMERONSolTab therapy.

Advise patients that there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to REMERON/REMERONSolTab during pregnancy [see Use in Specific Populations (8.1) ] .

Lactation Advise patients to notify their physician if they are breastfeeding an infant [see Use in Specific Populations (8.2) ].

Angle-Closure Glaucoma Patients should be advised that taking REMERON can cause mild pupillary dilation, which in susceptible individuals, can lead to an episode of angle-closure glaucoma.

Pre-existing glaucoma is almost always open-angle glaucoma because angle-closure glaucoma, when diagnosed, can be treated definitively with iridectomy.

Open-angle glaucoma is not a risk factor for angle-closure glaucoma.

Patients may wish to be examined to determine whether they are susceptible to angle-closure, and have a prophylactic procedure (e.g., iridectomy), if they are susceptible [see Warnings and Precautions (5.4) .] Patients with Phenylketonuria Inform patients with phenylketonuria that REMERONSolTab contains phenylalanine [see Warnings and Precautions (5.15) ].

DOSAGE AND ADMINISTRATION

2 Starting dose: 15-mg once daily; may increase up to maximum recommended dose of 45 mg once daily.

( 2.1 ) Administer orally once daily, preferably in the evening prior to sleep.

( 2.1 ) Administer REMERONSolTab immediately after removal from blister pack.

( 2.2 ) Reduce dose gradually when discontinuing REMERON/REMERONSolTab.

( 2.6 , 5.13 ) 2.1 Recommended Dosage The recommended starting dose of REMERON/REMERONSolTab is 15 mg once daily, administered orally, preferably in the evening prior to sleep.

If patients do not have an adequate response to the initial 15 mg dose, increase the dose up to a maximum of 45 mg per day.

Dose changes should not be made in intervals of less than 1 to 2 weeks to allow sufficient time for evaluation of response to a given dose [see Clinical Pharmacology (12.3) ] .

2.2 Administration of REMERONSolTab The tablet should remain in the blister pack until the patient is ready to take it.

The patient or caregiver should use dry hands to open the blister.

As soon as the blister is opened, the tablet should be removed and placed on the patient’s tongue.

Use REMERONSolTab immediately after removal from its blister; once removed, it cannot be stored.

The whole tablet should be placed on the tongue and allowed to disintegrate without chewing or crushing.

Do not attempt to split the tablet.

The tablet will disintegrate in saliva so that it can be swallowed.

2.3 Screen for Bipolar Disorder Prior to Starting REMERON/REMERONSolTab Prior to initiating treatment with REMERON/REMERONSolTab or another antidepressant, screen patients for a personal or family history of bipolar disorder, mania, or hypomania [see Warnings and Precautions (5.8) ].

2.4 Switching Patients to or from a Monoamine Oxidase Inhibitor Antidepressant At least 14 days must elapse between discontinuation of a monoamine oxidase inhibitor (MAOI) antidepressant and initiation of REMERON/REMERONSolTab.

In addition, at least 14 days must elapse after stopping REMERON/REMERONSolTab before starting an MAOI antidepressant [see Contraindications (4) and Warnings and Precautions (5.3) ] .

2.5 Dosage Modifications Due to Drug Interactions Strong CYP3A Inducers An increase in dosage of REMERON/REMERONSolTab may be needed with concomitant strong CYP3A inducer (e.g., carbamazepine, phenytoin, rifampin) use.

Conversely, a decrease in dosage of REMERON/REMERONSolTab may be needed if the CYP3A inducer is discontinued [see Drug Interactions (7) ].

Strong CYP3A Inhibitors A decrease in dosage of REMERON/REMERONSolTab may be needed with concomitant use of strong CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin).

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if the CYP3A4 inhibitor is discontinued [see Drug Interactions (7) ].

Cimetidine A decrease in dosage of REMERON/REMERONSolTab may be needed with concomitant use of cimetidine.

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if cimetidine is discontinued [see Drug Interactions (7) ].

2.6 Discontinuation of REMERON/REMERONSolTab Treatment Adverse reactions may occur upon discontinuation or dose reduction of REMERON/REMERONSolTab [see Warnings and Precautions (5.13) ] .

Gradually reduce the dosage of REMERON/REMERONSolTab rather than stopping abruptly whenever possible.

DRUG INTERACTIONS

7 Due to CNS effects, use caution when administering with other centrally-acting drugs.

Avoid alcohol.

( 7.1 ) Due to hypotensive effects, hypotensive effects of other drugs with this potential may be enhanced.

( 7.2 ) Effects of levodopa and dopamine agonists may be antagonized.

( 7.3 ) Cimetidine and ranitidine increase the bioavailability of risperidone.

( 7.5 ) Clozapine may decrease clearance of risperidone.

( 7.6 ) Fluoxetine and paroxetine increase plasma concentrations of risperidone.

( 7.10 ) Carbamazepine and other enzyme inducers decrease plasma concentrations of risperidone.

( 7.11 ) 7.1 Centrally-Acting Drugs and Alcohol Given the primary CNS effects of risperidone, caution should be used when RISPERDAL ® is taken in combination with other centrally-acting drugs and alcohol.

7.2 Drugs with Hypotensive Effects Because of its potential for inducing hypotension, RISPERDAL ® may enhance the hypotensive effects of other therapeutic agents with this potential.

7.3 Levodopa and Dopamine Agonists RISPERDAL ® may antagonize the effects of levodopa and dopamine agonists.

7.4 Amitriptyline Amitriptyline did not affect the pharmacokinetics of risperidone or risperidone and 9-hydroxyrisperidone combined.

7.5 Cimetidine and Ranitidine Cimetidine and ranitidine increased the bioavailability of risperidone by 64% and 26%, respectively.

However, cimetidine did not affect the AUC of risperidone and 9-hydroxyrisperidone combined, whereas ranitidine increased the AUC of risperidone and 9-hydroxyrisperidone combined by 20%.

7.6 Clozapine Chronic administration of clozapine with RISPERDAL ® may decrease the clearance of risperidone.

7.7 Lithium Repeated oral doses of RISPERDAL ® (3 mg twice daily) did not affect the exposure (AUC) or peak plasma concentrations (C max ) of lithium (n=13).

7.8 Valproate Repeated oral doses of RISPERDAL ® (4 mg once daily) did not affect the pre-dose or average plasma concentrations and exposure (AUC) of valproate (1000 mg/day in three divided doses) compared to placebo (n=21).

However, there was a 20% increase in valproate peak plasma concentration (C max ) after concomitant administration of RISPERDAL ® .

7.9 Digoxin RISPERDAL ® (0.25 mg twice daily) did not show a clinically relevant effect on the pharmacokinetics of digoxin.

7.10 Drugs That Inhibit CYP 2D6 and Other CYP Isozymes Risperidone is metabolized to 9-hydroxyrisperidone by CYP 2D6, an enzyme that is polymorphic in the population and that can be inhibited by a variety of psychotropic and other drugs [see Clinical Pharmacology (12.3) ] .

Drug interactions that reduce the metabolism of risperidone to 9-hydroxyrisperidone would increase the plasma concentrations of risperidone and lower the concentrations of 9-hydroxyrisperidone.

Analysis of clinical studies involving a modest number of poor metabolizers (n≅70) does not suggest that poor and extensive metabolizers have different rates of adverse effects.

No comparison of effectiveness in the two groups has been made.

In vitro studies showed that drugs metabolized by other CYP isozymes, including 1A1, 1A2, 2C9, 2C19, and 3A4, are only weak inhibitors of risperidone metabolism.

Fluoxetine and Paroxetine Fluoxetine (20 mg once daily) and paroxetine (20 mg once daily) have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

When either concomitant fluoxetine or paroxetine is initiated or discontinued, the physician should re-evaluate the dosing of RISPERDAL ® .

The effects of discontinuation of concomitant fluoxetine or paroxetine therapy on the pharmacokinetics of risperidone and 9-hydroxyrisperidone have not been studied.

Erythromycin There were no significant interactions between RISPERDAL ® and erythromycin.

7.11 Carbamazepine and Other Enzyme Inducers Carbamazepine co-administration decreased the steady-state plasma concentrations of risperidone and 9-hydroxyrisperidone by about 50%.

Plasma concentrations of carbamazepine did not appear to be affected.

The dose of RISPERDAL ® may need to be titrated accordingly for patients receiving carbamazepine, particularly during initiation or discontinuation of carbamazepine therapy.

Co-administration of other known enzyme inducers (e.g., phenytoin, rifampin, and phenobarbital) with RISPERDAL ® may cause similar decreases in the combined plasma concentrations of risperidone and 9-hydroxyrisperidone, which could lead to decreased efficacy of RISPERDAL ® treatment.

7.12 Drugs Metabolized by CYP 2D6 In vitro studies indicate that risperidone is a relatively weak inhibitor of CYP 2D6.

Therefore, RISPERDAL ® is not expected to substantially inhibit the clearance of drugs that are metabolized by this enzymatic pathway.

In drug interaction studies, RISPERDAL ® did not significantly affect the pharmacokinetics of donepezil and galantamine, which are metabolized by CYP 2D6.

OVERDOSAGE

10 10.1 Human Experience Premarketing experience included eight reports of acute RISPERDAL ® overdosage with estimated doses ranging from 20 to 300 mg and no fatalities.

In general, reported signs and symptoms were those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness and sedation, tachycardia and hypotension, and extrapyramidal symptoms.

One case, involving an estimated overdose of 240 mg, was associated with hyponatremia, hypokalemia, prolonged QT, and widened QRS.

Another case, involving an estimated overdose of 36 mg, was associated with a seizure.

Postmarketing experience includes reports of acute RISPERDAL ® overdosage, with estimated doses of up to 360 mg.

In general, the most frequently reported signs and symptoms are those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness, sedation, tachycardia, hypotension, and extrapyramidal symptoms.

Other adverse reactions reported since market introduction related to RISPERDAL ® overdose include prolonged QT interval and convulsions.

Torsade de pointes has been reported in association with combined overdose of RISPERDAL ® and paroxetine.

10.2 Management of Overdosage In case of acute overdosage, establish and maintain an airway and ensure adequate oxygenation and ventilation.

Gastric lavage (after intubation, if patient is unconscious) and administration of activated charcoal together with a laxative should be considered.

Because of the rapid disintegration of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets, pill fragments may not appear in gastric contents obtained with lavage.

The possibility of obtundation, seizures, or dystonic reaction of the head and neck following overdose may create a risk of aspiration with induced emesis.

Cardiovascular monitoring should commence immediately and should include continuous electrocardiographic monitoring to detect possible arrhythmias.

If antiarrhythmic therapy is administered, disopyramide, procainamide, and quinidine carry a theoretical hazard of QT-prolonging effects that might be additive to those of risperidone.

Similarly, it is reasonable to expect that the alpha-blocking properties of bretylium might be additive to those of risperidone, resulting in problematic hypotension.

There is no specific antidote to RISPERDAL ® .

Therefore, appropriate supportive measures should be instituted.

The possibility of multiple drug involvement should be considered.

Hypotension and circulatory collapse should be treated with appropriate measures, such as intravenous fluids and/or sympathomimetic agents (epinephrine and dopamine should not be used, since beta stimulation may worsen hypotension in the setting of risperidone-induced alpha blockade).

In cases of severe extrapyramidal symptoms, anticholinergic medication should be administered.

Close medical supervision and monitoring should continue until the patient recovers.

DESCRIPTION

11 RISPERDAL ® contains risperidone, a psychotropic agent belonging to the chemical class of benzisoxazole derivatives.

The chemical designation is 3-[2-[4-(6-fluoro-1,2-benzisoxazol-3-yl)-1-piperidinyl]ethyl]-6,7,8,9-tetrahydro-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one.

Its molecular formula is C 23 H 27 FN 4 O 2 and its molecular weight is 410.49.

The structural formula is: Risperidone is a white to slightly beige powder.

It is practically insoluble in water, freely soluble in methylene chloride, and soluble in methanol and 0.1 N HCl.

RISPERDAL ® Tablets are available in 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green) strengths.

RISPERDAL ® tablets contain the following inactive ingredients: colloidal silicon dioxide, hypromellose, lactose, magnesium stearate, microcrystalline cellulose, propylene glycol, sodium lauryl sulfate, and starch (corn).

The 0.25 mg, 0.5 mg, 2 mg, 3 mg, and 4 mg tablets also contain talc and titanium dioxide.

The 0.25 mg tablets contain yellow iron oxide; the 0.5 mg tablets contain red iron oxide; the 2 mg tablets contain FD&C Yellow No.

6 Aluminum Lake; the 3 mg and 4 mg tablets contain D&C Yellow No.

10; the 4 mg tablets contain FD&C Blue No.

2 Aluminum Lake.

RISPERDAL ® is also available as a 1 mg/mL oral solution.

RISPERDAL ® Oral Solution contains the following inactive ingredients: tartaric acid, benzoic acid, sodium hydroxide, and purified water.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in 0.5 mg (light coral), 1 mg (light coral), 2 mg (coral), 3 mg (coral), and 4 mg (coral) strengths.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain the following inactive ingredients: Amberlite ® resin, gelatin, mannitol, glycine, simethicone, carbomer, sodium hydroxide, aspartame, red ferric oxide, and peppermint oil.

In addition, the 2 mg, 3 mg, and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain xanthan gum.

Chemical Structure

CLINICAL STUDIES

14 14.1 Schizophrenia Adults Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of schizophrenia was established in four short-term (4- to 8-week) controlled trials of psychotic inpatients who met DSM-III-R criteria for schizophrenia.

Several instruments were used for assessing psychiatric signs and symptoms in these studies, among them the Brief Psychiatric Rating Scale (BPRS), a multi-item inventory of general psychopathology traditionally used to evaluate the effects of drug treatment in schizophrenia.

The BPRS psychosis cluster (conceptual disorganization, hallucinatory behavior, suspiciousness, and unusual thought content) is considered a particularly useful subset for assessing actively psychotic schizophrenic patients.

A second traditional assessment, the Clinical Global Impression (CGI), reflects the impression of a skilled observer, fully familiar with the manifestations of schizophrenia, about the overall clinical state of the patient.

In addition, the Positive and Negative Syndrome Scale (PANSS) and the Scale for Assessing Negative Symptoms (SANS) were employed.

The results of the trials follow: (1)In a 6-week, placebo-controlled trial (n=160) involving titration of RISPERDAL ® in doses up to 10 mg/day (twice-daily schedule), RISPERDAL ® was generally superior to placebo on the BPRS total score, on the BPRS psychosis cluster, and marginally superior to placebo on the SANS.

(2)In an 8-week, placebo-controlled trial (n=513) involving 4 fixed doses of RISPERDAL ® (2 mg/day, 6 mg/day, 10 mg/day, and 16 mg/day, on a twice-daily schedule), all 4 RISPERDAL ® groups were generally superior to placebo on the BPRS total score, BPRS psychosis cluster, and CGI severity score; the 3 highest RISPERDAL ® dose groups were generally superior to placebo on the PANSS negative subscale.

The most consistently positive responses on all measures were seen for the 6 mg dose group, and there was no suggestion of increased benefit from larger doses.

(3)In an 8-week, dose comparison trial (n=1356) involving 5 fixed doses of RISPERDAL ® (1 mg/day, 4 mg/day, 8 mg/day, 12 mg/day, and 16 mg/day, on a twice-daily schedule), the four highest RISPERDAL ® dose groups were generally superior to the 1 mg RISPERDAL ® dose group on BPRS total score, BPRS psychosis cluster, and CGI severity score.

None of the dose groups were superior to the 1 mg group on the PANSS negative subscale.

The most consistently positive responses were seen for the 4 mg dose group.

(4)In a 4-week, placebo-controlled dose comparison trial (n=246) involving 2 fixed doses of RISPERDAL ® (4 and 8 mg/day on a once-daily schedule), both RISPERDAL ® dose groups were generally superior to placebo on several PANSS measures, including a response measure (>20% reduction in PANSS total score), PANSS total score, and the BPRS psychosis cluster (derived from PANSS).

The results were generally stronger for the 8 mg than for the 4 mg dose group.

Long-Term Efficacy In a longer-term trial, 365 adult outpatients predominantly meeting DSM-IV criteria for schizophrenia and who had been clinically stable for at least 4 weeks on an antipsychotic medication were randomized to RISPERDAL ® (2–8 mg/day) or to an active comparator, for 1 to 2 years of observation for relapse.

Patients receiving RISPERDAL ® experienced a significantly longer time to relapse over this time period compared to those receiving the active comparator.

Pediatrics The efficacy of RISPERDAL ® in the treatment of schizophrenia in adolescents aged 13–17 years was demonstrated in two short-term (6 and 8 weeks), double-blind controlled trials.

All patients met DSM-IV diagnostic criteria for schizophrenia and were experiencing an acute episode at time of enrollment.

In the first trial (study #1), patients were randomized into one of three treatment groups: RISPERDAL ® 1–3 mg/day (n = 55, mean modal dose = 2.6 mg), RISPERDAL ® 4–6 mg/day (n = 51, mean modal dose = 5.3 mg), or placebo (n = 54).

In the second trial (study #2), patients were randomized to either RISPERDAL ® 0.15–0.6 mg/day (n = 132, mean modal dose = 0.5 mg) or RISPERDAL ® 1.5–6 mg/day (n = 125, mean modal dose = 4 mg).

In all cases, study medication was initiated at 0.5 mg/day (with the exception of the 0.15–0.6 mg/day group in study #2, where the initial dose was 0.05 mg/day) and titrated to the target dosage range by approximately Day 7.

Subsequently, dosage was increased to the maximum tolerated dose within the target dose range by Day 14.

The primary efficacy variable in all studies was the mean change from baseline in total PANSS score.

Results of the studies demonstrated efficacy of RISPERDAL ® in all dose groups from 1–6 mg/day compared to placebo, as measured by significant reduction of total PANSS score.

The efficacy on the primary parameter in the 1–3 mg/day group was comparable to the 4–6 mg/day group in study #1, and similar to the efficacy demonstrated in the 1.5–6 mg/day group in study #2.

In study #2, the efficacy in the 1.5–6 mg/day group was statistically significantly greater than that in the 0.15–0.6 mg/day group.

Doses higher than 3 mg/day did not reveal any trend towards greater efficacy.

14.2 Bipolar Mania – Monotherapy Adults The efficacy of RISPERDAL ® in the treatment of acute manic or mixed episodes was established in two short-term (3-week) placebo-controlled trials in patients who met the DSM-IV criteria for Bipolar I Disorder with manic or mixed episodes.

These trials included patients with or without psychotic features.

The primary rating instrument used for assessing manic symptoms in these trials was the Young Mania Rating Scale (YMRS), an 11-item clinician-rated scale traditionally used to assess the degree of manic symptomatology (irritability, disruptive/aggressive behavior, sleep, elevated mood, speech, increased activity, sexual interest, language/thought disorder, thought content, appearance, and insight) in a range from 0 (no manic features) to 60 (maximum score).

The primary outcome in these trials was change from baseline in the YMRS total score.

The results of the trials follow: (1)In one 3-week placebo-controlled trial (n=246), limited to patients with manic episodes, which involved a dose range of RISPERDAL ® 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 4.1 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

(2)In another 3-week placebo-controlled trial (n=286), which involved a dose range of 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 5.6 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

Pediatrics The efficacy of RISPERDAL ® in the treatment of mania in children or adolescents with Bipolar I disorder was demonstrated in a 3-week, randomized, double-blind, placebo-controlled, multicenter trial including patients ranging in ages from 10 to 17 years who were experiencing a manic or mixed episode of bipolar I disorder.

Patients were randomized into one of three treatment groups: RISPERDAL ® 0.5–2.5 mg/day (n = 50, mean modal dose = 1.9 mg), RISPERDAL ® 3–6 mg/day (n = 61, mean modal dose = 4.7 mg), or placebo (n = 58).

In all cases, study medication was initiated at 0.5 mg/day and titrated to the target dosage range by Day 7, with further increases in dosage to the maximum tolerated dose within the targeted dose range by Day 10.

The primary rating instrument used for assessing efficacy in this study was the mean change from baseline in the total YMRS score.

Results of this study demonstrated efficacy of RISPERDAL ® in both dose groups compared with placebo, as measured by significant reduction of total YMRS score.

The efficacy on the primary parameter in the 3–6 mg/day dose group was comparable to the 0.5–2.5 mg/day dose group.

Doses higher than 2.5 mg/day did not reveal any trend towards greater efficacy.

14.3 Bipolar Mania – Combination Therapy The efficacy of RISPERDAL ® with concomitant lithium or valproate in the treatment of acute manic or mixed episodes was established in one controlled trial in adult patients who met the DSM-IV criteria for Bipolar I Disorder.

This trial included patients with or without psychotic features and with or without a rapid-cycling course.

(1)In this 3-week placebo-controlled combination trial, 148 in- or outpatients on lithium or valproate therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® , placebo, or an active comparator, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.8 mg/day), combined with lithium or valproate (in a therapeutic range of 0.6 mEq/L to 1.4 mEq/L or 50 mcg/mL to 120 mcg/mL, respectively) was superior to lithium or valproate alone in the reduction of YMRS total score.

(2)In a second 3-week placebo-controlled combination trial, 142 in- or outpatients on lithium, valproate, or carbamazepine therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® or placebo, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.7 mg/day), combined with lithium, valproate, or carbamazepine (in therapeutic ranges of 0.6 mEq/L to 1.4 mEq/L for lithium, 50 mcg/mL to 125 mcg/mL for valproate, or 4–12 mcg/mL for carbamazepine, respectively) was not superior to lithium, valproate, or carbamazepine alone in the reduction of YMRS total score.

A possible explanation for the failure of this trial was induction of risperidone and 9-hydroxyrisperidone clearance by carbamazepine, leading to subtherapeutic levels of risperidone and 9-hydroxyrisperidone.

14.4 Irritability Associated with Autistic Disorder Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of irritability associated with autistic disorder was established in two 8-week, placebo-controlled trials in children and adolescents (aged 5 to 16 years) who met the DSM-IV criteria for autistic disorder.

Over 90% of these subjects were under 12 years of age and most weighed over 20 kg (16–104.3 kg).

Efficacy was evaluated using two assessment scales: the Aberrant Behavior Checklist (ABC) and the Clinical Global Impression – Change (CGI-C) scale.

The primary outcome measure in both trials was the change from baseline to endpoint in the Irritability subscale of the ABC (ABC-I).

The ABC-I subscale measured the emotional and behavioral symptoms of autism, including aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods.

The CGI-C rating at endpoint was a co-primary outcome measure in one of the studies.

The results of these trials are as follows: (1)In one of the 8-week, placebo-controlled trials, children and adolescents with autistic disorder (n=101), aged 5 to 16 years, received twice daily doses of placebo or RISPERDAL ® 0.5–3.5 mg/day on a weight-adjusted basis.

RISPERDAL ® , starting at 0.25 mg/day or 0.5 mg/day depending on baseline weight (< 20 kg and ≥ 20 kg, respectively) and titrated to clinical response (mean modal dose of 1.9 mg/day, equivalent to 0.06 mg/kg/day), significantly improved scores on the ABC-I subscale and on the CGI-C scale compared with placebo.

(2)In the other 8-week, placebo-controlled trial in children with autistic disorder (n=55), aged 5 to 12 years, RISPERDAL ® 0.02 to 0.06 mg/kg/day given once or twice daily, starting at 0.01 mg/kg/day and titrated to clinical response (mean modal dose of 0.05 mg/kg/day, equivalent to 1.4 mg/day), significantly improved scores on the ABC-I subscale compared with placebo.

Long-Term Efficacy Following completion of the first 8-week double-blind study, 63 patients entered an open-label study extension where they were treated with RISPERDAL ® for 4 or 6 months (depending on whether they received RISPERDAL ® or placebo in the double-blind study).

During this open-label treatment period, patients were maintained on a mean modal dose of RISPERDAL ® of 1.8–2.1 mg/day (equivalent to 0.05 – 0.07 mg/kg/day).

Patients who maintained their positive response to RISPERDAL ® (response was defined as ≥ 25% improvement on the ABC-I subscale and a CGI-C rating of ‘much improved’ or ‘very much improved’) during the 4–6 month open-label treatment phase for about 140 days, on average, were randomized to receive RISPERDAL ® or placebo during an 8-week, double-blind withdrawal study (n=39 of the 63 patients).

A pre-planned interim analysis of data from patients who completed the withdrawal study (n=32), undertaken by an independent Data Safety Monitoring Board, demonstrated a significantly lower relapse rate in the RISPERDAL ® group compared with the placebo group.

Based on the interim analysis results, the study was terminated due to demonstration of a statistically significant effect on relapse prevention.

Relapse was defined as ≥ 25% worsening on the most recent assessment of the ABC-I subscale (in relation to baseline of the randomized withdrawal phase).

HOW SUPPLIED

16 /STORAGE AND HANDLING RISPERDAL ® (risperidone) Tablets RISPERDAL ® (risperidone) Tablets are imprinted ” JANSSEN ” on one side and either “R1”, or “R3” according to their respective strengths.

1 mg white, capsule-shaped tablets: bottles of 15 NDC 21695-113-15 3 mg yellow, capsule-shaped tablets: bottles of 30 NDC 21695-115-30 and bottles of 60 NDC 21695-113-60.

Storage and Handling RISPERDAL ® Tablets should be stored at controlled room temperature 15°–25°C (59°–77°F).

Protect from light and moisture.

Keep out of reach of children.

RECENT MAJOR CHANGES

Warnings and Precautions, Leukopenia, Neutropenia, and Agranulocytosis ( 5.8 ) 07/2009

GERIATRIC USE

8.5 Geriatric Use Clinical studies of RISPERDAL ® in the treatment of schizophrenia did not include sufficient numbers of patients aged 65 and over to determine whether or not they respond differently than younger patients.

Other reported clinical experience has not identified differences in responses between elderly and younger patients.

In general, a lower starting dose is recommended for an elderly patient, reflecting a decreased pharmacokinetic clearance in the elderly, as well as a greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy [see Clinical Pharmacology (12.3) and Dosage and Administration (2.4 , 2.5) ] .

While elderly patients exhibit a greater tendency to orthostatic hypotension, its risk in the elderly may be minimized by limiting the initial dose to 0.5 mg twice daily followed by careful titration [see Warnings and Precautions (5.7) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

This drug is substantially excreted by the kidneys, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.

Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see Dosage and Administration (2.4) ] .

Concomitant use with Furosemide in Elderly Patients with Dementia-Related Psychosis In two of four placebo-controlled trials in elderly patients with dementia-related psychosis, a higher incidence of mortality was observed in patients treated with furosemide plus RISPERDAL ® when compared to patients treated with RISPERDAL ® alone or with placebo plus furosemide.

No pathological mechanism has been identified to explain this finding, and no consistent pattern for cause of death was observed.

An increase of mortality in elderly patients with dementia-related psychosis was seen with the use of RISPERDAL ® regardless of concomitant use with furosemide.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See Boxed Warning and Warnings and Precautions (5.1) ]

DOSAGE FORMS AND STRENGTHS

3 RISPERDAL ® Tablets are available in the following strengths and colors: 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green).

All are capsule shaped, and imprinted with “JANSSEN” on one side and either “Ris 0.25”, “Ris 0.5”, “R1”, “R2”, “R3”, or “R4” on the other side according to their respective strengths.

RISPERDAL ® Oral Solution is available in a 1 mg/mL strength.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in the following strengths, colors, and shapes: 0.5 mg (light coral, round), 1 mg (light coral, square), 2 mg (coral, square), 3 mg (coral, round), and 4 mg (coral, round).

All are biconvex and etched on one side with “R0.5”, “R1”, “R2”, “R3”, or “R4” according to their respective strengths.

Tablets: 0.25 mg, 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 ) Oral solution: 1 mg/mL ( 3 ) Orally disintegrating tablets: 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of action of RISPERDAL ® , as with other drugs used to treat schizophrenia, is unknown.

However, it has been proposed that the drug’s therapeutic activity in schizophrenia is mediated through a combination of dopamine Type 2 (D 2 ) and serotonin Type 2 (5HT 2 ) receptor antagonism.

RISPERDAL ® is a selective monoaminergic antagonist with high affinity (Ki of 0.12 to 7.3 nM) for the serotonin Type 2 (5HT 2 ), dopamine Type 2 (D 2 ), α 1 and α 2 adrenergic, and H 1 histaminergic receptors.

RISPERDAL ® acts as an antagonist at other receptors, but with lower potency.

RISPERDAL ® has low to moderate affinity (Ki of 47 to 253 nM) for the serotonin 5HT 1C , 5HT 1D , and 5HT 1A receptors, weak affinity (Ki of 620 to 800 nM) for the dopamine D 1 and haloperidol-sensitive sigma site, and no affinity (when tested at concentrations >10 -5 M) for cholinergic muscarinic or β 1 and β 2 adrenergic receptors.

INDICATIONS AND USAGE

1 RISPERDAL® is an atypical antipsychotic agent indicated for: Treatment of schizophrenia in adults and adolescents aged 13–17 years ( 1.1 ) Alone, or in combination with lithium or valproate, for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults, and alone in children and adolescents aged 10–17 years ( 1.2 ) Treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years ( 1.3 ) 1.1 Schizophrenia Adults RISPERDAL ® (risperidone) is indicated for the acute and maintenance treatment of schizophrenia [see Clinical Studies (14.1) ] .

Adolescents RISPERDAL ® is indicated for the treatment of schizophrenia in adolescents aged 13–17 years [see Clinical Studies (14.1) ] .

1.2 Bipolar Mania Monotherapy – Adults and Pediatrics RISPERDAL ® is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults and in children and adolescents aged 10–17 years [see Clinical Studies (14.2) ] .

Combination Therapy – Adults The combination of RISPERDAL ® with lithium or valproate is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder [ see Clinical Studies (14.3) ] .

1.3 Irritability Associated with Autistic Disorder Pediatrics RISPERDAL ® is indicated for the treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years, including symptoms of aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods [see Clinical Studies (14.4) ] .

PEDIATRIC USE

8.4 Pediatric Use The efficacy and safety of RISPERDAL ® in the treatment of schizophrenia were demonstrated in 417 adolescents, aged 13 – 17 years, in two short-term (6 and 8 weeks, respectively) double-blind controlled trials [see Indications and Usage (1.1) , Adverse Reactions (6.1) , and Clinical Studies (14.1) ].

Additional safety and efficacy information was also assessed in one long-term (6-month) open-label extension study in 284 of these adolescent patients with schizophrenia.

Safety and effectiveness of RISPERDAL ® in children less than 13 years of age with schizophrenia have not been established.

The efficacy and safety of RISPERDAL ® in the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in 169 children and adolescent patients, aged 10 – 17 years, were demonstrated in one double-blind, placebo-controlled, 3-week trial [see Indications and Usage (1.2) , Adverse Reactions (6.2) , and Clinical Studies (14.2) ] .

Safety and effectiveness of RISPERDAL ® in children less than 10 years of age with bipolar disorder have not been established.

The efficacy and safety of RISPERDAL ® in the treatment of irritability associated with autistic disorder were established in two 8-week, double-blind, placebo-controlled trials in 156 children and adolescent patients, aged 5 to 16 years [see Indications and Usage (1.3) , Adverse Reactions (6.3) and Clinical Studies (14.4) ] .

Additional safety information was also assessed in a long-term study in patients with autistic disorder, or in short- and long-term studies in more than 1200 pediatric patients with psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania who were of similar age and weight, and who received similar dosages of RISPERDAL ® as patients treated for irritability associated with autistic disorder.

The safety and effectiveness of RISPERDAL ® in pediatric patients less than 5 years of age with autistic disorder have not been established.

Tardive Dyskinesia In clinical trials in 1885 children and adolescents treated with RISPERDAL ® , 2 (0.1%) patients were reported to have tardive dyskinesia, which resolved on discontinuation of RISPERDAL ® treatment [see also Warnings and Precautions (5.4) ] .

Weight Gain In a long-term, open-label extension study in adolescent patients with schizophrenia, weight increase was reported as a treatment-emergent adverse event in 14% of patients.

In 103 adolescent patients with schizophrenia, a mean increase of 9.0 kg was observed after 8 months of RISPERDAL ® treatment.

The majority of that increase was observed within the first 6 months.

The average percentiles at baseline and 8 months, respectively, were 56 and 72 for weight, 55 and 58 for height, and 51 and 71 for body mass index.

In long-term, open-label trials (studies in patients with autistic disorder or other psychiatric disorders), a mean increase of 7.5 kg after 12 months of RISPERDAL ® treatment was observed, which was higher than the expected normal weight gain (approximately 3 to 3.5 kg per year adjusted for age, based on Centers for Disease Control and Prevention normative data).

The majority of that increase occurred within the first 6 months of exposure to RISPERDAL ® .

The average percentiles at baseline and 12 months, respectively, were 49 and 60 for weight, 48 and 53 for height, and 50 and 62 for body mass index.

In one 3-week, placebo-controlled trial in children and adolescent patients with acute manic or mixed episodes of bipolar I disorder, increases in body weight were higher in the RISPERDAL ® groups than the placebo group, but not dose related (1.90 kg in the RISPERDAL ® 0.5–2.5 mg group, 1.44 kg in the RISPERDAL ® 3–6 mg group, and 0.65 kg in the placebo group).

A similar trend was observed in the mean change from baseline in body mass index.

When treating pediatric patients with RISPERDAL ® for any indication, weight gain should be assessed against that expected with normal growth.

[See also Adverse Reactions (6.7) ] Somnolence Somnolence was frequently observed in placebo-controlled clinical trials of pediatric patients with autistic disorder.

Most cases were mild or moderate in severity.

These events were most often of early onset with peak incidence occurring during the first two weeks of treatment, and transient with a median duration of 16 days.

Somnolence was the most commonly observed adverse event in the clinical trial of bipolar disorder in children and adolescents, as well as in the schizophrenia trials in adolescents.

As was seen in the autistic disorder trials, these events were most often of early onset and transient in duration.

[See also Adverse Reactions (6.1 , 6.2 , 6.3) ] Patients experiencing persistent somnolence may benefit from a change in dosing regimen [ see Dosage and Administration (2.1 , 2.2 , 2.3) ] .

Hyperprolactinemia, Growth, and Sexual Maturation RISPERDAL ® has been shown to elevate prolactin levels in children and adolescents as well as in adults [se e Warnings and Precautions (5.6) ] .

In double-blind, placebo-controlled studies of up to 8 weeks duration in children and adolescents (aged 5 to 17 years) with autistic disorder or psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania, 49% of patients who received RISPERDAL ® had elevated prolactin levels compared to 2% of patients who received placebo.

Similarly, in placebo-controlled trials in children and adolescents (aged 10 to 17 years) with bipolar disorder, or adolescents (aged 13 to 17 years) with schizophrenia, 82–87% of patients who received RISPERDAL ® had elevated levels of prolactin compared to 3–7% of patients on placebo.

Increases were dose-dependent and generally greater in females than in males across indications.

In clinical trials in 1885 children and adolescents, galactorrhea was reported in 0.8% of RISPERDAL ® -treated patients and gynecomastia was reported in 2.3% of RISPERDAL ® -treated patients.

The long-term effects of RISPERDAL ® on growth and sexual maturation have not been fully evaluated.

PREGNANCY

8.1 Pregnancy Pregnancy Category C.

The teratogenic potential of risperidone was studied in three Segment II studies in Sprague-Dawley and Wistar rats (0.63–10 mg/kg or 0.4 to 6 times the maximum recommended human dose [MRHD] on a mg/m 2 basis) and in one Segment II study in New Zealand rabbits (0.31–5 mg/kg or 0.4 to 6 times the MRHD on a mg/m 2 basis).

The incidence of malformations was not increased compared to control in offspring of rats or rabbits given 0.4 to 6 times the MRHD on a mg/m 2 basis.

In three reproductive studies in rats (two Segment III and a multigenerational study), there was an increase in pup deaths during the first 4 days of lactation at doses of 0.16–5 mg/kg or 0.1 to 3 times the MRHD on a mg/m 2 basis.

It is not known whether these deaths were due to a direct effect on the fetuses or pups or to effects on the dams.

There was no no-effect dose for increased rat pup mortality.

In one Segment III study, there was an increase in stillborn rat pups at a dose of 2.5 mg/kg or 1.5 times the MRHD on a mg/m 2 basis.

In a cross-fostering study in Wistar rats, toxic effects on the fetus or pups, as evidenced by a decrease in the number of live pups and an increase in the number of dead pups at birth (Day 0), and a decrease in birth weight in pups of drug-treated dams were observed.

In addition, there was an increase in deaths by Day 1 among pups of drug-treated dams, regardless of whether or not the pups were cross-fostered.

Risperidone also appeared to impair maternal behavior in that pup body weight gain and survival (from Day 1 to 4 of lactation) were reduced in pups born to control but reared by drug-treated dams.

These effects were all noted at the one dose of risperidone tested, i.e., 5 mg/kg or 3 times the MRHD on a mg/m 2 basis.

Placental transfer of risperidone occurs in rat pups.

There are no adequate and well-controlled studies in pregnant women.

However, there was one report of a case of agenesis of the corpus callosum in an infant exposed to risperidone in utero .

The causal relationship to RISPERDAL ® therapy is unknown.

Reversible extrapyramidal symptoms in the neonate were observed following postmarketing use of RISPERDAL ® during the last trimester of pregnancy.

RISPERDAL ® should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

NUSRING MOTHERS

8.3 Nursing Mothers In animal studies, risperidone and 9-hydroxyrisperidone are excreted in milk.

Risperidone and 9-hydroxyrisperidone are also excreted in human breast milk.

Therefore, women receiving RISPERDAL ® should not breast-feed.

BOXED WARNING

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

Analyses of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients.

Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature.

Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.

The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear.

RISPERDAL ® (risperidone) is not approved for the treatment of patients with dementia-related psychosis.

[See Warnings and Precautions (5.1) ] WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS See full prescribing information for complete boxed warning.

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis.

( 5.1 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Cerebrovascular events, including stroke, in elderly patients with dementia-related psychosis.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis ( 5.2 ) Neuroleptic Malignant Syndrome ( 5.3 ) Tardive dyskinesia ( 5.4 ) Hyperglycemia and diabetes mellitus ( 5.5 ) Hyperprolactinemia ( 5.6 ) Orthostatic hypotension ( 5.7 ) Leukopenia, Neutropenia, and Agranulocytosis: has been reported with antipsychotics, including risperidone.

Patients with a history of a clinically significant low white blood cell count (WBC) or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

( 5.8 ) Potential for cognitive and motor impairment ( 5.9 ) Seizures ( 5.10 ) Dysphagia ( 5.11 ) Priapism ( 5.12 ) Thrombotic Thrombocytopenic Purpura (TTP) ( 5.13 ) Disruption of body temperature regulation ( 5.14 ) Antiemetic Effect ( 5.15 ) Suicide ( 5.16 ) Increased sensitivity in patients with Parkinson’s disease or those with dementia with Lewy bodies ( 5.17 ) Diseases or conditions that could affect metabolism or hemodynamic responses ( 5.17 ) 5.1 Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® (risperidone) is not approved for the treatment of dementia-related psychosis [see Boxed Warning ] .

5.2 Cerebrovascular Adverse Events, Including Stroke, in Elderly Patients with Dementia-Related Psychosis Cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, were reported in patients (mean age 85 years; range 73–97) in trials of risperidone in elderly patients with dementia-related psychosis.

In placebo-controlled trials, there was a significantly higher incidence of cerebrovascular adverse events in patients treated with risperidone compared to patients treated with placebo.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See also Boxed Warnings and Warnings and Precautions (5.1) ] 5.3 Neuroleptic Malignant Syndrome (NMS) A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with antipsychotic drugs.

Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).

Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis), and acute renal failure.

The diagnostic evaluation of patients with this syndrome is complicated.

In arriving at a diagnosis, it is important to identify cases in which the clinical presentation includes both serious medical illness (e.g., pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and symptoms (EPS).

Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever, and primary central nervous system pathology.

The management of NMS should include: (1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; (2) intensive symptomatic treatment and medical monitoring; and (3) treatment of any concomitant serious medical problems for which specific treatments are available.

There is no general agreement about specific pharmacological treatment regimens for uncomplicated NMS.

If a patient requires antipsychotic drug treatment after recovery from NMS, the potential reintroduction of drug therapy should be carefully considered.

The patient should be carefully monitored, since recurrences of NMS have been reported.

5.4 Tardive Dyskinesia A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs.

Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.

Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.

The risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase.

However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses.

There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.

Antipsychotic treatment, itself, however, may suppress (or partially suppress) the signs and symptoms of the syndrome and thereby may possibly mask the underlying process.

The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown.

Given these considerations, RISPERDAL ® should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.

Chronic antipsychotic treatment should generally be reserved for patients who suffer from a chronic illness that: (1) is known to respond to antipsychotic drugs, and (2) for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.

In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

The need for continued treatment should be reassessed periodically.

If signs and symptoms of tardive dyskinesia appear in a patient treated with RISPERDAL ® , drug discontinuation should be considered.

However, some patients may require treatment with RISPERDAL ® despite the presence of the syndrome.

5.5 Hyperglycemia and Diabetes Mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics including RISPERDAL ® .

Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population.

Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse events is not completely understood.

However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse events in patients treated with the atypical antipsychotics.

Precise risk estimates for hyperglycemia-related adverse events in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics should be monitored regularly for worsening of glucose control.

Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment.

Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should undergo fasting blood glucose testing.

In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of the suspect drug.

5.6 Hyperprolactinemia As with other drugs that antagonize dopamine D 2 receptors, RISPERDAL ® elevates prolactin levels and the elevation persists during chronic administration.

RISPERDAL ® is associated with higher levels of prolactin elevation than other antipsychotic agents.

Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion.

This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is contemplated in a patient with previously detected breast cancer.

An increase in pituitary gland, mammary gland, and pancreatic islet cell neoplasia (mammary adenocarcinomas, pituitary and pancreatic adenomas) was observed in the risperidone carcinogenicity studies conducted in mice and rats [see Non-Clinical Toxicology (13.1) ] .

Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans; the available evidence is considered too limited to be conclusive at this time.

5.7 Orthostatic Hypotension RISPERDAL ® may induce orthostatic hypotension associated with dizziness, tachycardia, and in some patients, syncope, especially during the initial dose-titration period, probably reflecting its alpha-adrenergic antagonistic properties.

Syncope was reported in 0.2% (6/2607) of RISPERDAL ® -treated patients in Phase 2 and 3 studies in adults with schizophrenia.

The risk of orthostatic hypotension and syncope may be minimized by limiting the initial dose to 2 mg total (either once daily or 1 mg twice daily) in normal adults and 0.5 mg twice daily in the elderly and patients with renal or hepatic impairment [see Dosage and Administration (2.1 , 2.4) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

A dose reduction should be considered if hypotension occurs.

RISPERDAL ® should be used with particular caution in patients with known cardiovascular disease (history of myocardial infarction or ischemia, heart failure, or conduction abnormalities), cerebrovascular disease, and conditions which would predispose patients to hypotension, e.g., dehydration and hypovolemia.

Clinically significant hypotension has been observed with concomitant use of RISPERDAL ® and antihypertensive medication.

5.8 Leukopenia, Neutropenia, and Agranulocytosis Class Effect: In clinical trial and/or postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to antipsychotic agents, including RISPERDAL ® .

Agranulocytosis has also been reported.

Possible risk factors for leukopenia/neutropenia include pre-existing low white blood cell count (WBC) and history of drug-induced leukopenia/neutropenia.

Patients with a history of a clinically significant low WBC or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

Patients with clinically significant neutropenia should be carefully monitored for fever or other symptoms or signs of infection and treated promptly if such symptoms or signs occur.

Patients with severe neutropenia (absolute neutrophil count <1000/mm 3 ) should discontinue RISPERDAL ® and have their WBC followed until recovery.

5.9 Potential for Cognitive and Motor Impairment Somnolence was a commonly reported adverse event associated with RISPERDAL ® treatment, especially when ascertained by direct questioning of patients.

This adverse event is dose-related, and in a study utilizing a checklist to detect adverse events, 41% of the high-dose patients (RISPERDAL ® 16 mg/day) reported somnolence compared to 16% of placebo patients.

Direct questioning is more sensitive for detecting adverse events than spontaneous reporting, by which 8% of RISPERDAL ® 16 mg/day patients and 1% of placebo patients reported somnolence as an adverse event.

Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely.

5.10 Seizures During premarketing testing in adult patients with schizophrenia, seizures occurred in 0.3% (9/2607) of RISPERDAL ® -treated patients, two in association with hyponatremia.

RISPERDAL ® should be used cautiously in patients with a history of seizures.

5.11 Dysphagia Esophageal dysmotility and aspiration have been associated with antipsychotic drug use.

Aspiration pneumonia is a common cause of morbidity and mortality in patients with advanced Alzheimer’s dementia.

RISPERDAL ® and other antipsychotic drugs should be used cautiously in patients at risk for aspiration pneumonia.

[See also Boxed Warning and Warnings and Precautions (5.1) ] 5.12 Priapism Rare cases of priapism have been reported.

While the relationship of the events to RISPERDAL ® use has not been established, other drugs with alpha-adrenergic blocking effects have been reported to induce priapism, and it is possible that RISPERDAL ® may share this capacity.

Severe priapism may require surgical intervention.

5.13 Thrombotic Thrombocytopenic Purpura (TTP) A single case of TTP was reported in a 28 year-old female patient receiving oral RISPERDAL ® in a large, open premarketing experience (approximately 1300 patients).

She experienced jaundice, fever, and bruising, but eventually recovered after receiving plasmapheresis.

The relationship to RISPERDAL ® therapy is unknown.

5.14 Body Temperature Regulation Disruption of body temperature regulation has been attributed to antipsychotic agents.

Both hyperthermia and hypothermia have been reported in association with oral RISPERDAL ® use.

Caution is advised when prescribing for patients who will be exposed to temperature extremes.

5.15 Antiemetic Effect Risperidone has an antiemetic effect in animals; this effect may also occur in humans, and may mask signs and symptoms of overdosage with certain drugs or of conditions such as intestinal obstruction, Reye’s syndrome, and brain tumor.

5.16 Suicide The possibility of a suicide attempt is inherent in patients with schizophrenia and bipolar mania, including children and adolescent patients, and close supervision of high-risk patients should accompany drug therapy.

Prescriptions for RISPERDAL ® should be written for the smallest quantity of tablets, consistent with good patient management, in order to reduce the risk of overdose.

5.17 Use in Patients with Concomitant Illness Clinical experience with RISPERDAL ® in patients with certain concomitant systemic illnesses is limited.

Patients with Parkinson’s Disease or Dementia with Lewy Bodies who receive antipsychotics, including RISPERDAL ® , are reported to have an increased sensitivity to antipsychotic medications.

Manifestations of this increased sensitivity have been reported to include confusion, obtundation, postural instability with frequent falls, extrapyramidal symptoms, and clinical features consistent with the neuroleptic malignant syndrome.

Caution is advisable in using RISPERDAL ® in patients with diseases or conditions that could affect metabolism or hemodynamic responses.

RISPERDAL ® has not been evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or unstable heart disease.

Patients with these diagnoses were excluded from clinical studies during the product’s premarket testing.

Increased plasma concentrations of risperidone and 9-hydroxyrisperidone occur in patients with severe renal impairment (creatinine clearance <30 mL/min/1.73 m 2 ), and an increase in the free fraction of risperidone is seen in patients with severe hepatic impairment.

A lower starting dose should be used in such patients [ see Dosage and Administration (2.4) ] .

5.18 Monitoring: Laboratory Tests No specific laboratory tests are recommended.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION Physicians are advised to discuss the following issues with patients for whom they prescribe RISPERDAL ® : 17.1 Orthostatic Hypotension Patients should be advised of the risk of orthostatic hypotension, especially during the period of initial dose titration [see Warnings and Precautions (5.7) ] .

17.2 Interference with Cognitive and Motor Performance Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely [see Warnings and Precautions (5.9) ] .

17.3 Pregnancy Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy [see Use in Specific Populations (8.1) ] .

17.4 Nursing Patients should be advised not to breast-feed an infant if they are taking RISPERDAL ® [see Use in Specific Populations (8.3) ] .

17.5 Concomitant Medication Patients should be advised to inform their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs, since there is a potential for interactions [see Drug Interactions (7) ] .

17.6 Alcohol Patients should be advised to avoid alcohol while taking RISPERDAL ® [see Drug Interactions (7.1) ] .

17.7 Phenylketonurics Phenylalanine is a component of aspartame.

Each 4 mg RISPERDAL ® M-TAB ® Orally Orally Disintegrating Tablet contains 0.14 mg phenylalanine.

DOSAGE AND ADMINISTRATION

2 Initial Dose Titration Target Dose Effective Dose Range Schizophrenia- adults ( 2.1 ) 2 mg/day 1–2 mg daily 4–8 mg daily 4–16 mg/day Schizophrenia – adolescents ( 2.1 ) 0.5mg/day 0.5– 1 mg daily 3mg/day 1–6 mg/day Bipolar mania – adults ( 2.2 ) 2–3 mg/day 1mg daily 1–6mg/day 1–6 mg/day Bipolar mania in children/adolescents ( 2.2 ) 0.5 mg/day 0.5–1mg daily 2.5mg/day 0.5–6 mg/day Irritability associated with autistic disorder ( 2.3 ) 0.25 mg/day (<20 kg) 0.5 mg/day (≥20 kg) 0.25–0.5 mg at ≥ 2 weeks 0.5 mg/day (<20 kg) 1 mg/day (≥20 kg) 0.5–3 mg/day 2.1 Schizophrenia Adults Usual Initial Dose RISPERDAL ® can be administered once or twice daily.

Initial dosing is generally 2 mg/day.

Dose increases should then occur at intervals not less than 24 hours, in increments of 1–2 mg/day, as tolerated, to a recommended dose of 4–8 mg/day.

In some patients, slower titration may be appropriate.

Efficacy has been demonstrated in a range of 4–16 mg/day [see Clinical Studies (14.1) ] .

However, doses above 6 mg/day for twice daily dosing were not demonstrated to be more efficacious than lower doses, were associated with more extrapyramidal symptoms and other adverse effects, and are generally not recommended.

In a single study supporting once-daily dosing, the efficacy results were generally stronger for 8 mg than for 4 mg.

The safety of doses above 16 mg/day has not been evaluated in clinical trials.

Maintenance Therapy While it is unknown how long a patient with schizophrenia should remain on RISPERDAL ® , the effectiveness of RISPERDAL ® 2 mg/day to 8 mg/day at delaying relapse was demonstrated in a controlled trial in patients who had been clinically stable for at least 4 weeks and were then followed for a period of 1 to 2 years [ see Clinical Studies (14.1) ] .

Patients should be periodically reassessed to determine the need for maintenance treatment with an appropriate dose.

Adolescents The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 3 mg/day.

Although efficacy has been demonstrated in studies of adolescent patients with schizophrenia at doses between 1 and 6 mg/day, no additional benefit was seen above 3 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

There are no controlled data to support the longer term use of RISPERDAL ® beyond 8 weeks in adolescents with schizophrenia.

The physician who elects to use RISPERDAL ® for extended periods in adolescents with schizophrenia should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

Reinitiation of Treatment in Patients Previously Discontinued Although there are no data to specifically address reinitiation of treatment, it is recommended that after an interval off RISPERDAL ® , the initial titration schedule should be followed.

Switching From Other Antipsychotics There are no systematically collected data to specifically address switching schizophrenic patients from other antipsychotics to RISPERDAL ® , or treating patients with concomitant antipsychotics.

While immediate discontinuation of the previous antipsychotic treatment may be acceptable for some schizophrenic patients, more gradual discontinuation may be most appropriate for others.

The period of overlapping antipsychotic administration should be minimized.

When switching schizophrenic patients from depot antipsychotics, initiate RISPERDAL ® therapy in place of the next scheduled injection.

The need for continuing existing EPS medication should be re-evaluated periodically.

2.2 Bipolar Mania Usual Dose Adults RISPERDAL ® should be administered on a once-daily schedule, starting with 2 mg to 3 mg per day.

Dosage adjustments, if indicated, should occur at intervals of not less than 24 hours and in dosage increments/decrements of 1 mg per day, as studied in the short-term, placebo-controlled trials.

In these trials, short-term (3 week) anti-manic efficacy was demonstrated in a flexible dosage range of 1–6 mg per day [see Clinical Studies (14.2 , 14.3) ] .

RISPERDAL ® doses higher than 6 mg per day were not studied.

Pediatrics The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 2.5 mg/day.

Although efficacy has been demonstrated in studies of pediatric patients with bipolar mania at doses between 0.5 and 6 mg/day, no additional benefit was seen above 2.5 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

Maintenance Therapy There is no body of evidence available from controlled trials to guide a clinician in the longer-term management of a patient who improves during treatment of an acute manic episode with RISPERDAL ® .

While it is generally agreed that pharmacological treatment beyond an acute response in mania is desirable, both for maintenance of the initial response and for prevention of new manic episodes, there are no systematically obtained data to support the use of RISPERDAL ® in such longer-term treatment (i.e., beyond 3 weeks).

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

2.3 Irritability Associated with Autistic Disorder – Pediatrics (Children and Adolescents) The safety and effectiveness of RISPERDAL ® in pediatric patients with autistic disorder less than 5 years of age have not been established.

The dosage of RISPERDAL ® should be individualized according to the response and tolerability of the patient.

The total daily dose of RISPERDAL ® can be administered once daily, or half the total daily dose can be administered twice daily.

Dosing should be initiated at 0.25 mg per day for patients < 20 kg and 0.5 mg per day for patients ≥ 20 kg.

After a minimum of four days from treatment initiation, the dose may be increased to the recommended dose of 0.5 mg per day for patients < 20 kg and 1 mg per day for patients ≥ 20 kg.

This dose should be maintained for a minimum of 14 days.

In patients not achieving sufficient clinical response, dose increases may be considered at ≥ 2-week intervals in increments of 0.25 mg per day for patients < 20 kg or 0.5 mg per day for patients ≥ 20 kg.

Caution should be exercised with dosage for smaller children who weigh less than 15 kg.

In clinical trials, 90% of patients who showed a response (based on at least 25% improvement on ABC-I, [see Clinical Studies (14.4) ] ) received doses of RISPERDAL ® between 0.5 mg and 2.5 mg per day.

The maximum daily dose of RISPERDAL ® in one of the pivotal trials, when the therapeutic effect reached plateau, was 1 mg in patients 45 kg.

No dosing data is available for children who weighed less than 15 kg.

Once sufficient clinical response has been achieved and maintained, consideration should be given to gradually lowering the dose to achieve the optimal balance of efficacy and safety.

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

Patients experiencing persistent somnolence may benefit from a once-daily dose administered at bedtime or administering half the daily dose twice daily, or a reduction of the dose.

2.4 Dosage in Special Populations The recommended initial dose is 0.5 mg twice daily in patients who are elderly or debilitated, patients with severe renal or hepatic impairment, and patients either predisposed to hypotension or for whom hypotension would pose a risk.

Dosage increases in these patients should be in increments of no more than 0.5 mg twice daily.

Increases to dosages above 1.5 mg twice daily should generally occur at intervals of at least 1 week.

In some patients, slower titration may be medically appropriate.

Elderly or debilitated patients, and patients with renal impairment, may have less ability to eliminate RISPERDAL ® than normal adults.

Patients with impaired hepatic function may have increases in the free fraction of risperidone, possibly resulting in an enhanced effect [see Clinical Pharmacology (12.3) ] .

Patients with a predisposition to hypotensive reactions or for whom such reactions would pose a particular risk likewise need to be titrated cautiously and carefully monitored [see Warnings and Precautions (5.2 , 5.7 , 5.17) ] .

If a once-daily dosing regimen in the elderly or debilitated patient is being considered, it is recommended that the patient be titrated on a twice-daily regimen for 2–3 days at the target dose.

Subsequent switches to a once-daily dosing regimen can be done thereafter.

2.5 Co-Administration of RISPERDAL ® with Certain Other Medications Co-administration of carbamazepine and other enzyme inducers (e.g., phenytoin, rifampin, phenobarbital) with RISPERDAL ® would be expected to cause decreases in the plasma concentrations of the sum of risperidone and 9-hydroxyrisperidone combined, which could lead to decreased efficacy of RISPERDAL ® treatment.

The dose of RISPERDAL ® needs to be titrated accordingly for patients receiving these enzyme inducers, especially during initiation or discontinuation of therapy with these inducers [see Drug Interactions (7.11) ] .

Fluoxetine and paroxetine have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

The dose of RISPERDAL ® needs to be titrated accordingly when fluoxetine or paroxetine is co-administered [see Drug Interactions (7.10) ] .

2.6 Administration of RISPERDAL ® Oral Solution RISPERDAL ® Oral Solution can be administered directly from the calibrated pipette, or can be mixed with a beverage prior to administration.

RISPERDAL ® Oral Solution is compatible in the following beverages: water, coffee, orange juice, and low-fat milk; it is NOT compatible with either cola or tea.

2.7 Directions for Use of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets Tablet Accessing RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg are supplied in blister packs of 4 tablets each.

Do not open the blister until ready to administer.

For single tablet removal, separate one of the four blister units by tearing apart at the perforations.

Bend the corner where indicated.

Peel back foil to expose the tablet.

DO NOT push the tablet through the foil because this could damage the tablet.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg are supplied in a child-resistant pouch containing a blister with 1 tablet each.

The child-resistant pouch should be torn open at the notch to access the blister.

Do not open the blister until ready to administer.

Peel back foil from the side to expose the tablet.

DO NOT push the tablet through the foil, because this could damage the tablet.

Tablet Administration Using dry hands, remove the tablet from the blister unit and immediately place the entire RISPERDAL ® M-TAB ® Orally Disintegrating Tablet on the tongue.

The RISPERDAL ® M-TAB ® Orally Disintegrating Tablet should be consumed immediately, as the tablet cannot be stored once removed from the blister unit.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets disintegrate in the mouth within seconds and can be swallowed subsequently with or without liquid.

Patients should not attempt to split or to chew the tablet.

Generic Name: MIRTAZAPINE
Brand Name: REMERON
  • Substance Name(s):
  • MIRTAZAPINE

DRUG INTERACTIONS

7 Table 5 includes clinically important drug interactions with REMERON/REMERONSolTab [see Clinical Pharmacology (12.3) ].

Table 5: Clinically Important Drug Interactions with REMERON/REMERONSolTab Monoamine Oxidase Inhibitors (MAOIs) Clinical Impact The concomitant use of serotonergic drugs, including REMERON/REMERONSolTab, and MAOIs increases the risk of serotonin syndrome.

Intervention REMERON/REMERONSolTab is contraindicated in patients taking MAOIs, including MAOIs such as linezolid or intravenous methylene blue [see Dosage and Administration (2.4) , Contraindications (4) , Warnings and Precautions (5.3) ].

Examples selegiline, tranylcypromine, isocarboxazid, phenelzine, linezolid, methylene blue Other Serotonergic Drugs Clinical Impact The concomitant use of serotonergic drugs with REMERON/REMERONSolTab increases the risk of serotonin syndrome.

Intervention Monitor patients for signs and symptoms of serotonin syndrome, particularly during treatment initiation and dosage increases.

If serotonin syndrome occurs, consider discontinuation of REMERON/REMERONSolTab and/or concomitant serotonergic drugs [see Warnings and Precautions (5.3) ].

Examples SSRIs, SNRIs, triptans, tricyclic antidepressants, fentanyl, lithium, amphetamines, St.

John’s Wort, tramadol, tryptophan, buspirone Strong CYP3A Inducers Clinical Impact The concomitant use of strong CYP3A inducers with REMERON/REMERONSolTab decreases the plasma concentration of mirtazapine [see Clinical Pharmacology (12.3) ] .

Intervention Increase the dose of REMERON/REMERONSolTab if needed with concomitant CYP3A inducer use.

Conversely, a decrease in dosage of REMERON/REMERONSolTab may be needed if the CYP3A inducer is discontinued [see Dosage and Administration (2.5) ].

Examples phenytoin, carbamazepine, rifampin Strong CYP3A Inhibitors Clinical Impact The concomitant use of strong CYP3A inhibitors with REMERON/REMERONSolTab may increase the plasma concentration of mirtazapine [see Clinical Pharmacology (12.3) ] .

Intervention Decrease the dose of REMERON/REMERONSolTab if needed with concomitant strong CYP3A inhibitor use.

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if the CYP3A inhibitor is discontinued [see Dosage and Administration (2.5) ].

Examples itraconazole, ritonavir, nefazodone Cimetidine Clinical Impact The concomitant use of cimetidine, a CYP1A2, CYP2D6, and CYP3A inhibitor, with REMERON/REMERONSolTab may increase the plasma concentration of mirtazapine [see Clinical Pharmacology (12.3) ].

Intervention Decrease the dose of REMERON/REMERONSolTab if needed with concomitant cimetidine use.

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if cimetidine is discontinued [see Dosage and Administration (2.5) ] .

Benzodiazepines and Alcohol Clinical Impact The concomitant use of benzodiazepines or alcohol with REMERON/REMERONSolTab increases the impairment of cognitive and motor skills produced by REMERON/REMERONSolTab alone.

Intervention Avoid concomitant use of benzodiazepines and alcohol with REMERON/REMERONSolTab [see Warnings and Precautions (5.7) , Clinical Pharmacology (12.3) ] ] .

Examples diazepam, alprazolam, alcohol Drugs that Prolong QTc Interval Clinical Impact The concomitant use of other drugs which prolong the QTc interval with REMERON/REMERONSolTab, increase the risk of QT prolongation and/or ventricular arrhythmias (e.g., Torsades de Pointes).

Intervention Use caution when using REMERON/REMERONSolTab concomitantly with drugs that prolong the QTc interval [see Warnings and Precautions (5.5) , Clinical Pharmacology (12.3) ].

Warfarin Clinical Impact The concomitant use of warfarin with REMERON/REMERONSolTab may result in an increase in INR [see Clinical Pharmacology (12.3) ] .

Intervention Monitor INR during concomitant use of warfarin with REMERON/REMERONSolTab.

Strong CYP3A inducers: Dosage increase may be needed for REMERON/REMERONSolTab with concomitant use of strong CYP3A inducers.

( 2.5 , 7 ) Strong CYP3A inhibitors : Dosage decrease may be needed when REMERON/REMERONSolTab is coadministered with strong CYP3A inhibitors.

( 2.5 , 7 ) Cimetidine: Dosage decrease may be needed when REMERON/REMERONSolTab is coadministered with cimetidine.

( 2.5 , 7 ) Warfarin : Monitor INR during concomitant use.

( 7 )

OVERDOSAGE

10 Human Experience In premarketing clinical studies, there were reports of REMERON overdose alone or in combination with other pharmacological agents.

Signs and symptoms reported in association with overdose included disorientation, drowsiness, impaired memory, and tachycardia.

Based on postmarketing reports, serious outcomes (including fatalities) may occur at dosages higher than the recommended doses, especially with mixed overdoses.

In these cases, QT prolongation and Torsades de Pointes have also been reported [see Warnings and Precautions (5.5) , Adverse Reactions (6.2) , and Drug Interactions (7) ].

Overdose Management No specific antidotes for mirtazapine are known.

Contact Poison Control (1-800-222-1222) for the latest recommendations.

DESCRIPTION

11 REMERON and REMERONSolTab contain mirtazapine.

Mirtazapine has a tetracyclic chemical structure and belongs to the piperazino-azepine group of compounds.

It is designated 1,2,3,4,10,14b-hexahydro-2-methylpyrazino [2,1-a] pyrido [2,3-c][2] benzazepine and has the empirical formula of C 17 H 19 N 3 .

Its molecular weight is 265.35.

The structural formula is the following and it is the racemic mixture: Mirtazapine is a white to creamy white crystalline powder which is practically insoluble in water.

REMERON is available for oral administration as scored film-coated tablets containing 15 or 30 mg of mirtazapine Each tablet contains the following inactive ingredients: colloidal silicon dioxide anhydrous, corn starch, ferric oxide (yellow), hydroxypropyl cellulose, hypromellose, magnesium stearate, lactose monohydrate, polyethylene glycol 8000, and titanium dioxide.

The 30 mg tablets also contain ferric oxide (red).

REMERONSolTab is available for oral administration as an orally disintegrating tablet containing 15, 30, or 45 mg of mirtazapine.

REMERONSolTab also contains the following inactive ingredients: aspartame, citric acid anhydrous fine granular, crospovidone, hypromellose, magnesium stearate, mannitol, granular mannitol 2080, microcrystalline cellulose, natural and artificial orange flavor, polymethacrylate (Eudragit E100), povidone, sodium bicarbonate, and sugar spheres (composed of starch and sucrose).

Chemical Structure

CLINICAL STUDIES

14 The efficacy of REMERON as a treatment for major depressive disorder was established in 4 placebo-controlled, 6-week trials in adult outpatients meeting DSM-III criteria for major depressive disorder.

Patients were titrated with REMERON from a dose range of 5 mg to 35 mg/day.

The mean mirtazapine dose for patients who completed these 4 studies ranged from 21 to 32 mg/day.

Overall, these studies demonstrated REMERON to be superior to placebo on at least 3 of the following 4 measures: 21-Item Hamilton Depression Rating Scale (HDRS) total score; HDRS Depressed Mood Item; CGI Severity score; and Montgomery and Asberg Depression Rating Scale (MADRS).

Superiority of REMERON over placebo was also found for certain factors of the HDRS, including anxiety/somatization factor and sleep disturbance factor.

Examination of age and gender subsets of the population did not reveal any differential responsiveness on the basis of these subgroupings.

In a longer-term study, patients meeting (DSM-IV) criteria for major depressive disorder who had responded during an initial 8 to 12 weeks of acute treatment on REMERON were randomized to continuation of REMERON or placebo for up to 40 weeks of observation for relapse.

Response during the open phase was defined as having achieved a HAM-D 17 total score of ≤8 and a CGI-Improvement score of 1 or 2 at 2 consecutive visits beginning with week 6 of the 8 to 12 weeks in the open-label phase of the study.

Relapse during the double-blind phase was determined by the individual investigators.

Patients receiving continued REMERON treatment experienced significantly lower relapse rates over the subsequent 40 weeks compared to those receiving placebo.

This pattern was demonstrated in both male and female patients.

HOW SUPPLIED

16 /STORAGE AND HANDLING REMERON tablets are supplied as: Tablet Strength Tablet Color/Shape Tablet Markings Package Configuration NDC Code 15 mg Yellow, oval tablet Scored with “Organon” debossed on one side and ” T 3 Z ” on other side, on both sides of score line Bottle / 30 count 0052-0105-30 15 mg Yellow, oval tablet Scored with “MSD” debossed on one side and ” T 3 Z ” on other side, on both sides of score line Bottle / 30 count 0052-4364-01 30 mg Red-brown, oval tablet Scored with “Organon” debossed on one side and ” T 5 Z ” on other side, on both sides of score line Bottle / 30 count 0052-0107-30 30 mg Red-brown, oval tablet Scored with “MSD” debossed on one side and ” T 5 Z ” on other side, on both sides of score line Bottle / 30 count 0052-4365-01 Storage Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].

Protect from light and moisture.

REMERONSolTab orally disintegrating tablets are supplied as: Tablet Strength Tablet Color/Shape Tablet Markings Package Configuration NDC Code 15 mg White, round tablet ” T 1 Z ” debossed on one side.

Box of 5 × 6-unit dose blister packs/ 30 count 0052-0106-30 30 mg White, round tablet ” T 2 Z ” debossed on one side.

Box of 5 × 6-unit dose blister packs/30 count 0052-0108-30 45 mg White, round tablet ” T 4 Z ” debossed on one side Box of 5 × 6-unit dose blister packs/30 count 0052-0110-30 Storage Store at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].

Protect from light and moisture.

Use immediately upon opening individual tablet blister.

GERIATRIC USE

8.5 Geriatric Use Approximately 190 patients ≥65 years of age participated in clinical studies with REMERON.

REMERON/REMERONSolTab is known to be substantially excreted by the kidney (75%), and the risk of decreased clearance of this drug is greater in patients with impaired renal function.

Pharmacokinetic studies revealed a decreased clearance of mirtazapine in the elderly [see Clinical Pharmacology (12.3) ] .

Sedating drugs, including REMERON/REMERONSolTab, may cause confusion and over-sedation in the elderly.

Elderly patients may be at greater risk of developing hyponatremia.

Caution is indicated when administering REMERON/REMERONSolTab to elderly patients [see Warnings and Precautions (5.11) , (5.14) and Clinical Pharmacology (12.3) ] .

In general, dose selection for an elderly patient should be conservative, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.

DOSAGE FORMS AND STRENGTHS

3 REMERON is supplied as: 15 mg tablets: Oval, scored, yellow, with “Organon” debossed on one side and ” T 3 Z ” on the other side, on both sides of the score line 15 mg tablets: Oval, scored, yellow, with “MSD” debossed on one side and ” T 3 Z ” on the other side, on both sides of the score line 30 mg tablets: Oval, scored, red-brown, with “Organon” debossed on one side and ” T 5 Z ” on the other side, on both sides of the score line 30 mg tablets: Oval, scored, red-brown, with “MSD” debossed on one side and ” T 5 Z ” on the other side, on both sides of the score line REMERONSolTab is supplied as: 15 mg orally disintegrating tablets: Round, white, with ” T 1 Z ” debossed on one side 30 mg orally disintegrating tablets: Round, white, with ” T 2 Z ” debossed on one side 45 mg orally disintegrating tablets: Round, white, with ” T 4 Z ” debossed on one side Tablets : 15 mg scored and 30 mg scored.

( 3 ) Orally disintegrating tablets : 15 mg, 30 mg, and 45 mg.

( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of action of mirtazapine for the treatment of major depressive disorder, is unclear.

However, its efficacy could be mediated through its activity as an antagonist at central presynaptic α 2 -adrenergic inhibitory autoreceptors and heteroreceptors and enhancing central noradrenergic and serotonergic activity.

INDICATIONS AND USAGE

1 REMERON/REMERONSolTab are indicated for the treatment of major depressive disorder (MDD) in adults [see Clinical Studies (14) ] .

REMERON/REMERONSolTab is indicated for the treatment of major depressive disorder (MDD) in adults.

( 1 )

PEDIATRIC USE

8.4 Pediatric Use The safety and effectiveness of REMERON/REMERONSolTab have not been established in pediatric patients with MDD.

Two placebo-controlled trials in 258 pediatric patients with MDD have been conducted with REMERON, and the data were insufficient to establish the safety and effectiveness of REMERON/REMERONSolTab in pediatric patients with MDD.

Antidepressants increased the risk of suicidal thoughts and behaviors in pediatric patients [see Boxed Warning and Warnings and Precautions (5.1) ] .

In an 8-week-long clinical trial in pediatric patients receiving doses between 15 to 45 mg per day, 49% of REMERON-treated patients had a weight gain of at least 7%, compared to 5.7% of placebo-treated patients.

The mean increase in weight was 4 kg (2 kg SD) for REMERON-treated patients versus 1 kg (2 kg SD) for placebo-treated patients [see Warnings and Precautions (5.6) ] .

PREGNANCY

8.1 Pregnancy Pregnancy Exposure Registry There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antidepressants during pregnancy.

Healthcare providers are encouraged to register patients by calling the National Pregnancy Registry for Antidepressants at 1-844-405-6185 or visiting online at https://womensmentalhealth.org/clinical-and-research-programs/pregnancyregistry/antidepressants/.

Risk Summary Prolonged experience with mirtazapine in pregnant women, based on published observational studies and postmarketing reports, has not reliably identified a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes.

There are risks associated with untreated depression in pregnancy (see Clinical Considerations ).

In animal reproduction studies, oral administration of mirtazapine to pregnant rats and rabbits during the period of organogenesis revealed no evidence of teratogenic effects up to 20 and 17 times the maximum recommended human dose (MRHD) of 45 mg, respectively, based on mg/m 2 body surface area.

However, in rats, there was an increase in postimplantation loss at 20 times the MRHD based on mg/m 2 body surface area.

Oral administration of mirtazapine to pregnant rats during pregnancy and lactation resulted in an increase in pup deaths and a decrease in pup birth weights at doses 20 times the MRHD based on mg/m 2 body surface area (see Data ).

The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

All pregnancies have a background risk of birth defect, loss, or other adverse outcomes.

In the U.S.

general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.

Clinical Considerations Disease-Associated Maternal and/or Embryo/Fetal Risk Women who discontinue antidepressants during pregnancy are more likely to experience a relapse of major depression than women who continue antidepressants.

This finding is from a prospective, longitudinal study that followed 201 pregnant women with a history of major depressive disorder who were euthymic and taking antidepressants at the beginning of pregnancy.

Consider the risk of untreated depression when discontinuing or changing treatment with antidepressant medication during pregnancy and postpartum.

Data Animal Data Mirtazapine was administered orally to pregnant rats and rabbits during the period of organogenesis at doses of 2.5, 15, and 100 mg/kg/day and 2.5, 10, and 40 mg/kg/day, respectively, which are up to 20 and 17 times the maximum recommended human dose (MRHD) of 45 mg based on mg/m 2 body surface area, respectively.

No evidence of teratogenic effects was observed.

However, in rats, there was an increase in postimplantation loss in dams treated with mirtazapine at 100 mg/kg/day which is 20 times the MRHD based on mg/m 2 body surface area.

Oral administration of mirtazapine at doses of 2.5, 15, and 100 mg/kg/day to pregnant rats during pregnancy and lactation resulted in an increase in pup deaths during the first 3 days of lactation and a decrease in pup birth weights at 20 times the MRHD based on mg/m 2 body surface area.

The cause of these deaths is not known.

The no effect dose level is 3 times the MRHD based on mg/m 2 body surface area.

BOXED WARNING

WARNING: SUICIDAL THOUGHTS AND BEHAVIORS Antidepressants increased the risk of suicidal thoughts and behaviors in pediatric and young adult patients in short-term studies.

Closely monitor all antidepressant-treated patients for clinical worsening, and for emergence of suicidal thoughts and behaviors [see Warnings and Precautions (5.1) ] .

REMERON/REMERONSolTab is not approved for use in pediatric patients [see Use in Specific Populations (8.4) ].

WARNING: SUICIDAL THOUGHTS AND BEHAVIORS See full prescribing information for complete boxed warning.

Increased risk of suicidal thoughts and behavior in pediatric and young adult patients taking antidepressants.

Closely monitor all antidepressant-treated patients for clinical worsening and emergence of suicidal thoughts and behaviors.

REMERON/REMERONSolTab is not approved for use in pediatric patients.

( 5.1 , 8.4 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Agranulocytosis : If sore throat, fever, stomatitis or signs of infection occur, along with a low white blood cell count, treatment with REMERON/REMERONSolTab should be discontinued and the patient should be closely monitored.

( 5.2 ) Serotonin Syndrome : Increased risk when co-administered with other serotonergic drugs (e.g., SSRI, SNRI, triptans), but also when taken alone.

If it occurs, discontinue REMERON/REMERONSolTab and initiate supportive treatment.

( 2.4 , 4 , 5.3 , 7 ) Angle-Closure Glaucoma : Angle closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressants.

( 5.4 ) QT Prolongation : Use REMERON/REMERONSolTab with caution in patients with risk factors for QT prolongation.

( 5.5 , 7 ) Increased Appetite/Weight Gain : REMERON/REMERONSolTab has been associated with increased appetite and weight gain.

( 5.6 ) Somnolence : May impair judgment, thinking and/or motor skills.

Use with caution when engaging in activities requiring alertness, such as driving or operating machinery.

( 5.7 , 7 ) Activation of Mania/Hypomania : Screen patients for bipolar disorder prior to initiating treatment.

( 2.3 , 5.8 ) Seizures : Use with caution in patients with a seizure disorder.

( 5.9 ) Elevated Cholesterol/Triglycerides : Has been reported with REMERON use.

( 5.10 ) Hyponatremia : May occur as a result of treatment with serotonergic antidepressants, including REMERON/REMERONSolTab.

( 5.11 ) Transaminase Elevations : Clinically significant elevations have occurred.

Use with caution in patients with impaired hepatic function.

( 5.12 ) 5.1 Suicidal Thoughts and Behaviors in Adolescents and Young Adults In pooled analyses of placebo-controlled trials of antidepressant drugs (SSRIs and other antidepressant classes) that included approximately 77,000 adult patients and 4,500 pediatric patients, the incidence of suicidal thoughts and behaviors in antidepressant-treated patients age 24 years and younger was greater than in placebo-treated patients.

There was considerable variation in risk of suicidal thoughts and behaviors among drugs, but there was an increased risk identified in young patients for most drugs studied.

There were differences in absolute risk of suicidal thoughts and behaviors across the different indications, with the highest incidence in patients with MDD.

The drug-placebo differences in the number of cases of suicidal thoughts and behaviors per 1000 patients treated are provided in Table 1.

Table 1: Risk Differences of the Number of Patients with Suicidal Thoughts and Behavior in the Pooled Placebo-Controlled Trials of Antidepressants in Pediatric and Adult Patients Age Range Drug-Placebo Difference in Number of Patients with Suicidal Thoughts or Behaviors per 1000 Patients Treated Increases Compared to Placebo <18 years old 14 additional patients 18–24 years old 5 additional patients Decreases Compared to Placebo 25–64 years old 1 fewer patient ≥65 years old 6 fewer patients It is unknown whether the risk of suicidal thoughts and behaviors in children, adolescents, and young adults extends to longer-term use, i.e., beyond four months.

However, there is substantial evidence from placebo-controlled maintenance trials in adults with MDD that antidepressants delay the recurrence of depression and that depression itself is a risk factor for suicidal thoughts and behaviors.

Monitor all antidepressant-treated patients for any indication of clinical worsening and emergence of suicidal thoughts and behaviors, especially during the initial few months of drug therapy, and at times of dosage changes.

Counsel family members or caregivers of patients to monitor for changes in behavior and to alert the healthcare provider.

Consider changing the therapeutic regimen, including possibly discontinuing REMERON/REMERONSolTab, in patients whose depression is persistently worse, or who are experiencing emergent suicidal thoughts or behaviors.

5.2 Agranulocytosis In premarketing clinical trials, 2 (1 with Sjögren’s Syndrome) out of 2796 patients treated with REMERON developed agranulocytosis [absolute neutrophil count (ANC) <500/mm 3 with associated signs and symptoms, e.g., fever, infection, etc.] and a third patient developed severe neutropenia (ANC <500/mm 3 without any associated symptoms).

For these 3 patients, onset of severe neutropenia was detected on days 61, 9, and 14 of treatment, respectively.

All 3 patients recovered after REMERON was stopped.

If a patient develops a sore throat, fever, stomatitis, or other signs of infection, along with a low white blood cell (WBC) count, treatment with REMERON/REMERONSolTab should be discontinued and the patient should be closely monitored.

5.3 Serotonin Syndrome Serotonergic antidepressants, including REMERON/REMERONSolTab, can precipitate serotonin syndrome, a potentially life-threatening condition.

The risk is increased with concomitant use of other serotonergic drugs (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, amphetamines, and St.

John’s Wort) and with drugs that impair metabolism of serotonin, i.e., MAOIs [see Contraindications (4) , Drug Interactions (7) ] .

Serotonin syndrome can also occur when these drugs are used alone.

Serotonin syndrome signs and symptoms may include mental status changes (e.g., agitation, hallucinations, delirium, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, dizziness, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea).

The concomitant use of REMERON/REMERONSolTab with MAOIs is contraindicated.

In addition, do not initiate REMERON/REMERONSolTab in a patient being treated with MAOIs such as linezolid or intravenous methylene blue.

No reports involved the administration of methylene blue by other routes (such as oral tablets or local tissue injection).

If it is necessary to initiate treatment with an MAOI such as linezolid or intravenous methylene blue in a patient taking REMERON/REMERONSolTab, discontinue REMERON/REMERONSolTab before initiating treatment with the MAOI [see Contraindications (4) , Drug Interactions (7) ] .

Monitor all patients taking REMERON/REMERONSolTab for the emergence of serotonin syndrome.

Discontinue treatment with REMERON/REMERONSolTab and any concomitant serotonergic agents immediately if the above symptoms occur, and initiate supportive symptomatic treatment.

If concomitant use of REMERON/REMERONSolTab with other serotonergic drugs is clinically warranted, inform patients of the increased risk for serotonin syndrome and monitor for symptoms.

5.4 Angle-Closure Glaucoma The pupillary dilation that occurs following use of many antidepressant drugs, including REMERON/REMERONSolTab, may trigger an angle-closure attack in a patient with anatomically narrow angles who does not have a patent iridectomy.

5.5 QT Prolongation and Torsades de Pointes The effect of REMERON (mirtazapine) on QTc interval was assessed in a clinical randomized trial with placebo and positive (moxifloxacin) controls involving 54 healthy volunteers using exposure response analysis.

This trial showed a positive relationship between mirtazapine concentrations and prolongation of the QTc interval.

However, the degree of QT prolongation observed with both 45 mg and 75 mg (1.67 times the maximum recommended daily dose) doses of mirtazapine was not at a level generally considered to be clinically meaningful.

During postmarketing use of mirtazapine, cases of QT prolongation, Torsades de Pointes, ventricular tachycardia, and sudden death, have been reported [see Adverse Reactions (6.1 , 6.2) ] .

The majority of reports occurred in association with overdose or in patients with other risk factors for QT prolongation, including concomitant use of QTc-prolonging medicines [see Drug Interactions (7) and Overdosage (10) ] .

Exercise caution when REMERON/REMERONSolTab is prescribed in patients with known cardiovascular disease or family history of QT prolongation, and in concomitant use with other drugs thought to prolong the QTc interval.

5.6 Increased Appetite and Weight Gain In U.S.

controlled clinical studies, appetite increase was reported in 17% of patients treated with REMERON, compared to 2% for placebo.

In these same trials, weight gain of ≥7% of body weight was reported in 7.5% of patients treated with mirtazapine, compared to 0% for placebo.

In a pool of premarketing U.S.

clinical studies, including many patients for long-term, open-label treatment, 8% of patients receiving REMERON discontinued for weight gain.

In an 8-week-long pediatric clinical trial of doses between 15 to 45 mg/day, 49% of REMERON-treated pediatric patients had a weight gain of at least 7%, compared to 5.7% of placebo-treated patients.

The safety and effectiveness of REMERON/REMERONSolTab in pediatric patients with MDD have not been established [see Use in Specific Populations (8.4) ] .

5.7 Somnolence In U.S.

controlled studies, somnolence was reported in 54% of patients treated with REMERON, compared to 18% for placebo.

In these studies, somnolence resulted in discontinuation for 10.4% of REMERON-treated patients, compared to 2.2% for placebo.

It is unclear whether tolerance develops to the somnolent effects of REMERON/REMERONSolTab.

Because of the potentially significant effects of REMERON/REMERONSolTab on impairment of performance, caution patients about engaging in activities that require alertness, including operating hazardous machinery and motor vehicles, until they are reasonably certain that REMERON/REMERONSolTab does not affect them adversely.

The concomitant use of benzodiazepines and alcohol with REMERON/REMERONSolTab should be avoided [see Drug Interactions (7) ] .

5.8 Activation of Mania or Hypomania In patients with bipolar disorder, treating a depressive episode with REMERON/REMERONSolTab or another antidepressant may precipitate a mixed/manic episode.

In controlled clinical trials, patients with bipolar disorder were generally excluded; however, symptoms of mania or hypomania were reported in 0.2% of patients treated with REMERON.

Prior to initiating treatment with REMERON/REMERONSolTab, screen patients for any personal or family history of bipolar disorder, mania, or hypomania.

5.9 Seizures REMERON/REMERONSolTab has not been systematically evaluated in patients with seizure disorders.

In premarketing clinical trials, 1 seizure was reported among the 2796 U.S.

and non-U.S.

patients treated with REMERON.

REMERON/REMERONSolTab should be prescribed with caution in patients with a seizure disorder.

5.10 Elevated Cholesterol and Triglycerides In U.S.

controlled studies, nonfasting cholesterol increases to ≥20% above the upper limits of normal were observed in 15% of patients treated with REMERON, compared to 7% for placebo.

In these same studies, nonfasting triglyceride increases to ≥500 mg/dL were observed in 6% of patients treated with REMERON, compared to 3% for placebo.

5.11 Hyponatremia Hyponatremia may occur as a result of treatment with serotonergic antidepressants, including REMERON/REMERONSolTab.

Cases with serum sodium lower than 110 mmol/L have been reported.

Signs and symptoms of hyponatremia include headache, difficulty concentrating, memory impairment, confusion, weakness, and unsteadiness, which may lead to falls.

Signs and symptoms associated with more severe or acute cases have included hallucination, syncope, seizure, coma, respiratory arrest, and death.

In many cases, this hyponatremia appears to be the result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

In patients with symptomatic hyponatremia, discontinue REMERON/REMERONSolTab and institute appropriate medical intervention.

Elderly patients, patients taking diuretics, and those who are volume-depleted may be at greater risk of developing hyponatremia [see Use in Specific Populations (8.5) ] .

5.12 Transaminase Elevations Clinically significant ALT (SGPT) elevations (≥3 times the upper limit of the normal range) were observed in 2.0% (8/424) of patients treated with REMERON in a pool of short-term, U.S.

controlled trials, compared to 0.3% (1/328) of placebo patients.

While some patients were discontinued for the ALT increases, in other cases, the enzyme levels returned to normal despite continued REMERON treatment.

REMERON/REMERONSolTab should be used with caution in patients with impaired hepatic function [see Use in Specific Populations (8.6) , Clinical Pharmacology (12.3) ] .

5.13 Discontinuation Syndrome There have been reports of adverse reactions upon the discontinuation of REMERON/REMERONSolTab (particularly when abrupt), including but not limited to the following: dizziness, abnormal dreams, sensory disturbances (including paresthesia and electric shock sensations), agitation, anxiety, fatigue, confusion, headache, tremor, nausea, vomiting, and sweating, or other symptoms which may be of clinical significance.

A gradual reduction in the dosage, rather than an abrupt cessation, is recommended [see Dosage and Administration (2.6) ].

5.14 Use in Patients with Concomitant Illness REMERON/REMERONSolTab has not been systematically evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or other significant heart disease.

REMERON was associated with significant orthostatic hypotension in early clinical pharmacology trials with normal volunteers.

Orthostatic hypotension was infrequently observed in clinical trials with depressed patients [see Adverse Reactions (6.1) ] .

REMERON/REMERONSolTab should be used with caution in patients with known cardiovascular or cerebrovascular disease that could be exacerbated by hypotension (history of myocardial infarction, angina, or ischemic stroke) and conditions that would predispose patients to hypotension (dehydration, hypovolemia, and treatment with antihypertensive medication).

5.15 Risks in Patients with Phenylketonuria Phenylalanine can be harmful to patients with phenylketonuria (PKU).

REMERONSolTab contains phenylalanine, a component of aspartame.

REMERONSolTab contains the following amount of phenylalanine: 2.6 mg in 15 mg orally disintegrating tablet, 5.2 mg in 30 mg orally disintegrating tablet, and 7.8 mg in 45 mg orally disintegrating tablet.

Before prescribing REMERONSolTab to a patient with PKU, consider the combined daily amount of phenylalanine from all sources, including REMERONSolTab.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION Advise the patient to read the FDA-approved patient labeling (Medication Guide).

Suicidal Thoughts and Behaviors Advise patients and caregivers to look for the emergence of suicidality, especially early during treatment and when the dosage is adjusted up or down, and instruct them to report such symptoms to the healthcare provider [see Boxed Warning and Warnings and Precautions (5.1) ].

Agranulocytosis Advise patients to contact their physician if they experience fever, chills, sore throat, mucous membrane ulceration, flu-like complaints, or other symptoms that might suggest infection [see Warnings and Precautions (5.2) ].

Serotonin Syndrome Caution patients about the risk of serotonin syndrome, particularly with the concomitant use of REMERON/REMERONSolTab with other serotonergic drugs including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, amphetamines, St.

John’s Wort, and with drugs that impair metabolism of serotonin (in particular, MAOIs, both those intended to treat psychiatric disorders and also others, such as linezolid).

Advise patients to contact their healthcare provider or report to the emergency room if they experience signs or symptoms of serotonin syndrome [see Dosage and Administration (2.4) , Contraindications (4) , Warnings and Precautions (5.3) , Drug Interactions (7) ].

QT Prolongation and Torsades de Pointes Inform patients to consult their physician immediately if they feel faint, lose consciousness, or have heart palpitations [see Warnings and Precautions (5.5) , Drug Interactions (7) , Overdosage (10) ].

Advise patients to inform physicians that they are taking REMERON/REMERONSolTab before any new drug is taken.

Somnolence Advise patients that REMERON/REMERONSolTab may impair judgment, thinking, and particularly, motor skills, because of its prominent sedative effect.

Caution patients about performing activities requiring mental alertness, such as operating hazardous machinery or operating a motor vehicle, until they are reasonably certain that REMERON/REMERONSolTab therapy does not adversely affect their ability to engage in such activities.

[see Warnings and Precautions (5.7) ].

Alcohol Advise patients to avoid alcohol while taking REMERON/REMERONSolTab [see Warnings and Precautions (5.7) , Drug Interactions (7) ].

Activation of Mania/Hypomania Advise patients and their caregivers to observe for signs of activation of mania/hypomania and instruct them to report such symptoms to the healthcare provider [see Warnings and Precautions (5.8) ] .

Discontinuation Syndrome Advise patients not to abruptly discontinue REMERON/REMERONSolTab and to discuss any tapering regimen with their healthcare provider.

Adverse reactions can occur when REMERON/REMERONSolTab is discontinued [see Dosage and Administration (2.6) , Warnings and Precautions (5.13) ].

Allergic Reactions Advise patients to notify their healthcare provider if they develop an allergic reaction such as rash, hives, swelling, or difficulty breathing [see Contraindications (4) , Adverse Reactions (6.2) ] .

Pregnancy Advise patients to notify their physician if they become pregnant or intend to become pregnant during REMERON/REMERONSolTab therapy.

Advise patients that there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to REMERON/REMERONSolTab during pregnancy [see Use in Specific Populations (8.1) ] .

Lactation Advise patients to notify their physician if they are breastfeeding an infant [see Use in Specific Populations (8.2) ].

Angle-Closure Glaucoma Patients should be advised that taking REMERON can cause mild pupillary dilation, which in susceptible individuals, can lead to an episode of angle-closure glaucoma.

Pre-existing glaucoma is almost always open-angle glaucoma because angle-closure glaucoma, when diagnosed, can be treated definitively with iridectomy.

Open-angle glaucoma is not a risk factor for angle-closure glaucoma.

Patients may wish to be examined to determine whether they are susceptible to angle-closure, and have a prophylactic procedure (e.g., iridectomy), if they are susceptible [see Warnings and Precautions (5.4) .] Patients with Phenylketonuria Inform patients with phenylketonuria that REMERONSolTab contains phenylalanine [see Warnings and Precautions (5.15) ].

DOSAGE AND ADMINISTRATION

2 Starting dose: 15-mg once daily; may increase up to maximum recommended dose of 45 mg once daily.

( 2.1 ) Administer orally once daily, preferably in the evening prior to sleep.

( 2.1 ) Administer REMERONSolTab immediately after removal from blister pack.

( 2.2 ) Reduce dose gradually when discontinuing REMERON/REMERONSolTab.

( 2.6 , 5.13 ) 2.1 Recommended Dosage The recommended starting dose of REMERON/REMERONSolTab is 15 mg once daily, administered orally, preferably in the evening prior to sleep.

If patients do not have an adequate response to the initial 15 mg dose, increase the dose up to a maximum of 45 mg per day.

Dose changes should not be made in intervals of less than 1 to 2 weeks to allow sufficient time for evaluation of response to a given dose [see Clinical Pharmacology (12.3) ] .

2.2 Administration of REMERONSolTab The tablet should remain in the blister pack until the patient is ready to take it.

The patient or caregiver should use dry hands to open the blister.

As soon as the blister is opened, the tablet should be removed and placed on the patient’s tongue.

Use REMERONSolTab immediately after removal from its blister; once removed, it cannot be stored.

The whole tablet should be placed on the tongue and allowed to disintegrate without chewing or crushing.

Do not attempt to split the tablet.

The tablet will disintegrate in saliva so that it can be swallowed.

2.3 Screen for Bipolar Disorder Prior to Starting REMERON/REMERONSolTab Prior to initiating treatment with REMERON/REMERONSolTab or another antidepressant, screen patients for a personal or family history of bipolar disorder, mania, or hypomania [see Warnings and Precautions (5.8) ].

2.4 Switching Patients to or from a Monoamine Oxidase Inhibitor Antidepressant At least 14 days must elapse between discontinuation of a monoamine oxidase inhibitor (MAOI) antidepressant and initiation of REMERON/REMERONSolTab.

In addition, at least 14 days must elapse after stopping REMERON/REMERONSolTab before starting an MAOI antidepressant [see Contraindications (4) and Warnings and Precautions (5.3) ] .

2.5 Dosage Modifications Due to Drug Interactions Strong CYP3A Inducers An increase in dosage of REMERON/REMERONSolTab may be needed with concomitant strong CYP3A inducer (e.g., carbamazepine, phenytoin, rifampin) use.

Conversely, a decrease in dosage of REMERON/REMERONSolTab may be needed if the CYP3A inducer is discontinued [see Drug Interactions (7) ].

Strong CYP3A Inhibitors A decrease in dosage of REMERON/REMERONSolTab may be needed with concomitant use of strong CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin).

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if the CYP3A4 inhibitor is discontinued [see Drug Interactions (7) ].

Cimetidine A decrease in dosage of REMERON/REMERONSolTab may be needed with concomitant use of cimetidine.

Conversely, an increase in dosage of REMERON/REMERONSolTab may be needed if cimetidine is discontinued [see Drug Interactions (7) ].

2.6 Discontinuation of REMERON/REMERONSolTab Treatment Adverse reactions may occur upon discontinuation or dose reduction of REMERON/REMERONSolTab [see Warnings and Precautions (5.13) ] .

Gradually reduce the dosage of REMERON/REMERONSolTab rather than stopping abruptly whenever possible.

DRUG INTERACTIONS

Drug Interactions Section Concomitant use of strong CYP3A4 inhibitors: Reduce quetiapine dose to one sixth when coadministered with strong CYP3A4 inhibitors (e.g., ketoconazole, ritonavir) ( 2.5, 7.1 , 12.3 ) Concomitant use of strong CYP3A4 inducers: Increase quetiapine dose up to 5 fold when used in combination with a chronic treatment (more than 7 to 14 days) of potent CYP3A4 inducers (e.g., phenytoin, rifampin, St.

John’s wort) ( 2.6 , 7.1 , 12.3 ) Discontinuation of strong CYP3A4 inducers: Reduce quetiapine dose by 5 fold within 7 to 14 days of discontinuation of CYP3A4 inducers ( 2.6 , 7.1 , 12.3 ) The risks of using quetiapine in combination with other drugs have not been extensively evaluated in systematic studies.

Given the primary CNS effects of quetiapine, caution should be used when it is taken in combination with other centrally acting drugs.

Quetiapine potentiated the cognitive and motor effects of alcohol in a clinical trial in subjects with selected psychotic disorders, and alcoholic beverages should be limited while taking quetiapine.

Quetiapine exposure is increased by the prototype CYP3A4 inhibitors (e.g., ketoconazole, itraconazole, indinavir, ritonavir, nefazodone, etc.)and decreased by the prototype CYP3A4 inducers (e.g., phenytoin, carbamazepine, rifampin, avasimibe, St.

John’s wort etc.).

Dose adjustment of quetiapine will be necessary if it is coadministered with potent CYP3A4 inducers or inhibitors.

CYP3A4 inhibitors: Coadministration of ketoconazole, a potent inhibitor of cytochrome CYP3A4, resulted in significant increase in quetiapine exposure.

The dose of quetiapine should be reduced to one sixth of the original dose if coadministered with a strong CYP3A4 inhibitor [see Dosage and Administration ( 2.5 ) and Clinical Pharmacology (12.3)] .

CYP3A4 inducers: Coadministration of quetiapine and phenytoin, a CYP3A4 inducer increased the mean oral clearance of quetiapine by 5-fold.

Increased doses of quetiapine up to 5 fold may be required to maintain control of symptoms of schizophrenia in patients receiving quetiapine and phenytoin, or other known potent CYP3A4 inducers [see Dosage and Administration ( 2.6 ) and Clinical Pharmacology (12.3)] .

When the CYP3A4 inducer is discontinued, the dose of quetiapine should be reduced to the original level within 7 to 14 days [see Dosage and Administration ( 2.6 )] .

The potential effects of several concomitant medications on quetiapine pharmacokinetics were studied [see Clinical Pharmacology (12.3)].

Because of its potential for inducing hypotension, quetiapine may enhance the effects of certain antihypertensive agents.

Quetiapine may antagonize the effects of levodopa and dopamine agonists.

There are no clinically relevant pharmacokinetic interactions of quetiapine on other drugs based on the CYP pathway.

Quetiapine and its metabolites are non-inhibitors of major metabolizing CYP’s (1A2, 2C9, 2C19, 2D6 and 3A4).

OVERDOSAGE

Overdosage Section In clinical trials, survival has been reported in acute overdoses of up to 30 grams of quetiapine.

Most patients who overdosed experienced no adverse reactions or recovered fully from the reported reactions.

Death has been reported in a clinical trial following an overdose of 13.6 grams of quetiapine alone.

In general, reported signs and symptoms were those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness and sedation, tachycardia and hypotension.

Patients with preexisting severe cardiovascular disease may be at an increased risk of the effects of overdose [s ee Warnings and Precautions (5.11)].

One case, involving an estimated overdose of 9600 mg, was associated with hypokalemia and first degree heart block.

In postmarketing experience, there were cases reported of QT prolongation with overdose.

There were also very rare reports of overdose of quetiapine alone resulting in death or coma.

In case of acute overdosage, establish and maintain an airway and ensure adequate oxygenation and ventilation.

Gastric lavage (after intubation, if patient is unconscious) and administration of activated charcoal together with a laxative should be considered.

The possibility of obtundation, seizure or dystonic reaction of the head and neck following overdose may create a risk of aspiration with induced emesis.

Cardiovascular monitoring should commence immediately and should include continuous electrocardiographic monitoring to detect possible arrhythmias.

If antiarrhythmic therapy is administered, disopyramide, procainamide and quinidine carry a theoretical hazard of additive QT-prolonging effects when administered in patients with acute overdosage of quetiapine.

Similarly it is reasonable to expect that the alpha-adrenergic-blocking properties of bretylium might be additive to those of quetiapine, resulting in problematic hypotension.

There is no specific antidote to quetiapine.

Therefore, appropriate supportive measures should be instituted.

The possibility of multiple drug involvement should be considered.

Hypotension and circulatory collapse should be treated with appropriate measures such as intravenous fluids and/or sympathomimetic agents (epinephrine and dopamine should not be used, since beta stimulation may worsen hypotension in the setting of quetiapine-induced alpha blockade).

In cases of severe extrapyramidal symptoms, anticholinergic medication should be administered.

Close medical supervision and monitoring should continue until the patient recovers.

DESCRIPTION

Description Section Quetiapine fumarate is a psychotropic agent belonging to a chemical class, the dibenzothiazepine derivatives.

The chemical designation is 2-[2-(4-dibenzo [b,f ] [1,4]thiazepin-11-yl-1-piperazinyl)ethoxy]-ethanol fumarate (2:1) (salt).

It is present in tablets as the fumarate salt.

All doses and tablet strengths are expressed as milligrams of base, not as fumarate salt.

Its molecular formula is C 42 H 50 N 6 O 4 S 2 •C 4 H 4 O 4 and it has a molecular weight of 883.10 (fumarate salt).

The structural formula is: Quetiapine fumarate is a white to off-white powder which is insoluble in water.

Quetiapine fumarate tablets are supplied for oral administration as 25 mg (round, peach), 50 mg (round, white), 100 mg (round, yellow), 200 mg (round, white), 300 mg (capsule-shaped, white), and 400 mg (capsule-shaped, yellow) tablets.

Inactive ingredients are microcrystalline cellulose, colloidal silicon dioxide, silicon dioxide, crospovidone, anhydrous citric acid, polysorbate 80, magnesium stearate, lactose monohydrate, hypromellose, polyethylene glycol and titanium dioxide.

The 25 mg tablets contain red ferric oxide and yellow ferric oxide and the 100 mg and 400 mg tablets contain only yellow ferric oxide.

CLINICAL STUDIES

Clinical Studies Section Short-term Trials – Adults The efficacy of quetiapine in the treatment of schizophrenia was established in 3 short-term (6-­week) controlled trials of inpatients with schizophrenia who met DSM III-R criteria for schizophrenia.

Although a single fixed dose haloperidol arm was included as a comparative treatment in one of the three trials, this single haloperidol dose group was inadequate to provide a reliable and valid comparison of quetiapine and haloperidol.

Several instruments were used for assessing psychiatric signs and symptoms in these studies, among them the Brief Psychiatric Rating Scale (BPRS), a multi-item inventory of general psychopathology traditionally used to evaluate the effects of drug treatment in schizophrenia.

The BPRS psychosis cluster (conceptual disorganization, hallucinatory behavior, suspiciousness, and unusual thought content) is considered a particularly useful subset for assessing actively psychotic schizophrenic patients.

A second traditional assessment, the Clinical Global Impression (CGI), reflects the impression of a skilled observer, fully familiar with the manifestations of schizophrenia, about the overall clinical state of the patient.

The results of the trials follow: In a 6-week, placebo-controlled trial (n=361) (study 1) involving 5 fixed doses of quetiapine (75 mg/day, 150 mg/day, 300 mg/day, 600 mg/day and 750 mg/day given in divided doses three times per day), the 4 highest doses of quetiapine were generally superior to placebo on the BPRS total score, the BPRS psychosis cluster and the CGI severity score, with the maximal effect seen at 300 mg/day, and the effects of doses of 150 mg/day to 750 mg/day were generally indistinguishable.

In a 6-week, placebo-controlled trial (n=286) (study 2) involving titration of quetiapine in high (up to 750 mg/day given in divided doses three times per day) and low (up to 250 mg/day given in divided doses three times per day) doses, only the high dose quetiapine group (mean dose, 500 mg/day) was superior to placebo on the BPRS total score, the BPRS psychosis cluster, and the CGI severity score.

In a 6-week dose and dose regimen comparison trial (n=618) (study 3) involving two fixed doses of quetiapine (450 mg/day given in divided doses both twice daily and three times daily and 50 mg/day given in divided doses twice daily), only the 450 mg/day (225 mg given twice daily) dose group was superior to the 50 mg/day (25 mg given twice daily) quetiapine dose group on the BPRS total score, the BPRS psychosis cluster, and the CGI severity score.

The primary efficacy results of these three studies in the treatment of schizophrenia in adults is presented in Table 19.

Examination of population subsets (race, gender, and age) did not reveal any differential responsiveness on the basis of race or gender, with an apparently greater effect in patients under the age of 40 years compared to those older than 40.

The clinical significance of this finding is unknown.

Adolescents (ages 13 to 17) The efficacy of quetiapine in the treatment of schizophrenia in adolescents (13 to 17 years of age) was demonstrated in a 6-week, double-blind, placebo-controlled trial (study 4).

Patients who met DSM-IV diagnostic criteria for schizophrenia were randomized into one of three treatment groups: quetiapine 400 mg/day (n = 73), quetiapine 800 mg/day (n = 74), or placebo (n = 75).

Study medication was initiated at 50 mg/day and on day 2 increased to 100 mg/per day (divided and given two or three times per day).

Subsequently, the dose was titrated to the target dose of 400 mg/day or 800 mg/day using increments of 100 mg/day, divided and given two or three times daily.

The primary efficacy variable was the mean change from baseline in total Positive and Negative Syndrome Scale (PANSS).

Quetiapine at 400 mg/day and 800 mg/day was superior to placebo in the reduction of PANSS total score.

The primary efficacy results of this study in the treatment of schizophrenia in adolescents is presented in Table 19.

Table 19: Schizophrenia Short-Term Trials Study Number Treatment Group Primary Efficacy Endpoint: BPRS Total Mean Baseline Score (SD) LS Mean Change from Baseline (SE) Placebo-subtracted Difference * (95% CI) Study 1 Quetiapine(75 mg/day) 45.7 (10.9) -2.2 (2) -4 (-11.2, 3.3) Quetiapine(150 mg/day) † 47.2 (10.1) -8.7 (2.1) -10.4 (-17.8, -3) Quetiapine(300 mg/day) 45.3 (10.9) -8.6 (2.1) -10.3 (-17.6, -3) Quetiapine(600 mg/day) 43.5 (11.3) -7.7 (2.1) -9.4 (-16.7, -2.1) Quetiapine(750 mg/day) 45.7 (11) -6.3 (2) -8 (-15.2, -0.8) Placebo 45.3 (9.2) 1.7 (2.1) — Study 2 Quetiapine(250 mg/day) 38.9 (9.8) -4.2 (1.6) -3.2 (-7.6, 1.2) Quetiapine(750 mg/day) 41 (9.6) -8.7 (1.6) -7.8 (-12.2, -3.4) Placebo 38.4 (9.7) -1 (1.6) — Study 3 Quetiapine(450 mg/day BID) 42.1 (10.7) -10 (1.3) -4.6 (-7.8, -1.4) Quetiapine(450 mg/day TID) 42.7 (10.4) -8.6 (1.3) -3.2 (-6.4, 0) Quetiapine (50 mg BID) 41.7 (10) -5.4 (1.3) — Primary Efficacy Endpoint: PANSS Total Mean Baseline Score (SD) LS Mean Change from Baseline (SE) Placebo-subtracted Difference (95% CI) Study 4 Quetiapine(400 mg/day) 96.2 (17.7) -27.3 (2.6) -8.2 (-16.1, -0.3) Quetiapine(800 mg/day) 96.9 (15.3) -28.4 (1.8) -9.3 (-16.2, -2.4) Placebo 96.2 (17.7) -19.2 (3) — SD: standard deviation; SE: standard error; LS Mean: least-squares mean; CI: unadjusted confidence interval.

# Doses that are statistically significant superior to quetiapine 50 mg BID.

Difference (drug minus placebo) in least-squares mean change from baseline.

Doses that are statistically significant superior to placebo.

Bipolar I disorder, manic or mixed episodes Adults The efficacy of quetiapine in the acute treatment of manic episodes was established in 3 placebo-controlled trials in patients who met DSM-IV criteria for bipolar I disorder with manic episodes.

These trials included patients with or without psychotic features and excluded patients with rapid cycling and mixed episodes.

Of these trials, 2 were monotherapy (12 weeks) and 1 was adjunct therapy (3 weeks) to either lithium or divalproex.

Key outcomes in these trials were change from baseline in the Young Mania Rating Scale (YMRS) score at 3 and 12 weeks for monotherapy and at 3 weeks for adjunct therapy.

Adjunct therapy is defined as the simultaneous initiation or subsequent administration of quetiapine with lithium or divalproex.

The primary rating instrument used for assessing manic symptoms in these trials was YMRS, an 11-­item clinician-rated scale traditionally used to assess the degree of manic symptomatology (irritability, disruptive/aggressive behavior, sleep, elevated mood, speech, increased activity, sexual interest, language/thought disorder, thought content, appearance, and insight) in a range from 0 (no manic features) to 60 (maximum score).

The results of the trials follow: Monotherapy The efficacy of quetiapine in the acute treatment of bipolar mania was established in 2 placebo-controlled trials.

In two 12-week trials (n=300, n=299) comparing quetiapine to placebo, quetiapine was superior to placebo in the reduction of the YMRS total score at weeks 3 and 12.

The majority of patients in these trials taking quetiapine were dosed in a range between 400 mg/day and 800 mg per day (studies 1 and 2 in Table 20).

Adjunct Therapy In this 3-week placebo-controlled trial, 170 patients with bipolar mania (YMRS ≥ 20) were randomized to receive quetiapine or placebo as adjunct treatment to lithium or divalproex.

Patients may or may not have received an adequate treatment course of lithium or divalproex prior to randomization.

Quetiapine was superior to placebo when added to lithium or divalproex alone in the reduction of YMRS total score.

(study 3 in Table 20).

The majority of patients in this trial taking quetiapine were dosed in a range between 400 mg/day and 800 mg per day.

In a similarly designed trial (n=200), quetiapine was associated with an improvement in YMRS scores but did not demonstrate superiority to placebo, possibly due to a higher placebo effect.

The primary efficacy results of these studies in the treatment of mania in adults is presented in Table 20.

Children and Adolescents (ages 10 to 17) The efficacy of quetiapine in the acute treatment of manic episodes associated with bipolar I disorder in children and adolescents (10 to 17 years of age) was demonstrated in a 3-week, double-blind, placebo-controlled, multicenter trial (study 4 in Table 20).

Patients who met DSM-IV diagnostic criteria for a manic episode were randomized into one of three treatment groups: quetiapine 400 mg/day (n = 95), quetiapine 600 mg/day (n = 98), or placebo (n = 91).

Study medication was initiated at 50 mg/day and on day 2 increased to 100 mg/day (divided doses given two or three times daily).

Subsequently, the dose was titrated to a target dose of 400 mg/day or 600 mg/day using increments of 100 mg/day, given in divided doses two or three times daily.

The primary efficacy variable was the mean change from baseline in total YMRS score.

Quetiapine 400 mg/day and 600 mg/day were superior to placebo in the reduction of YMRS total score (Table 20).

Table 20: Mania Trials Study Number Treatment Group Primary Efficacy Measure: YMRS Total Mean Baseline Score (SD) * LS Mean Change from Baseline (SE) Placebo-subtracted Difference † (95% CI) Study 1 Quetiapine(200 to 800 mg/day) ‡ § 34 (6.1) -12.3 (1.3) -4 (-7, -1) Haloperidol 32.3 (6) -15.7 (1.3) -7.4 (-10.4, -4.4) Placebo 33.1 (6.6) -8.3 (1.3) — Study 2 Quetiapine(200 to 800 mg/day) 32.7 (6.5) -14.6 (1.5) -7.9 (-10.9, -5) Lithium 33.3 (7.1) -15.2 (1.6) -8.5 (-11.5, -5.5) Placebo 34 (6.9) -6.7 (1.6) — Study 3 Quetiapine(200 to 800 mg/day) + mood stabilizer 31.5 (5.8) -13.8 (1.6) -3.8 (-7.1, -0.6) Placebo + mood stabilizer 31.1 (5.5) -10 (1.5) — Study 4 Quetiapine(400 mg/day) 29.4 (5.9) -14.3 (0.96) -5.2 (-8.1, -2.3) Quetiapine(600 mg/day) 29.6 (6.4) -15.6 (0.97) -6.6 (-9.5, -3.7) Placebo 30.7 (5.9) -9 (1.1) — Mood stabilizer: lithium or divalproex; SD: standard deviation; SE: standard error; LS Mean: least-squares mean; CI: unadjusted confidence interval.

Adult data mean baseline score is based on patients included in the primary analysis; pediatric mean baseline score is based on all patients in the ITT population Difference (drug minus placebo) in least-squares mean change from baseline.

Doses that are statistically significantly superior to placebo.

Included in the trial as an active comparator Bipolar Disorder, Depressive Episodes Adults The efficacy of quetiapine for the acute treatment of depressive episodes associated with bipolar disorder was established in 2 identically designed 8-week, randomized, double-blind, placebo-controlled studies (N=1045) (studies 5 and 6 in Table 21).

These studies included patients with either bipolar I or II disorder and those with or without a rapid cycling course.

Patients randomized to quetiapine were administered fixed doses of either 300 mg or 600 mg once daily.

The primary rating instrument used to assess depressive symptoms in these studies was the Montgomery-Asberg Depression Rating Scale (MADRS), a 10-item clinician-rated scale with scores ranging from 0 to 60.

The primary endpoint in both studies was the change from baseline in MADRS score at week 8.

In both studies, quetiapine was superior to placebo in reduction of MADRS score.

Improvement in symptoms, as measured by change in MADRS score relative to placebo, was seen in both studies at Day 8 (week 1) and onwards.

In these studies, no additional benefit was seen with the 600 mg dose.

For the 300 mg dose group, statistically significant improvements over placebo were seen in overall quality of life and satisfaction related to various areas of functioning, as measured using the Q-LES-Q(SF).

The primary efficacy results of these studies in the acute treatment of depressive episodes associated with bipolar disorder in adults is presented in Table 21.

Table 21: Depressive Episodes Associated with Bipolar Disorder Study Number Treatment Group Primary Efficacy Measure: MADRS Total Mean Baseline Score (SD) LS Mean Change from Baseline (SE) Placebo-subtracted Difference * (95% CI) Study 5 Quetiapine (300 mg/day) † 30.3 (5) -16.4 (0.9) -6.1 (-8.3, -3.9) Quetiapine (600 mg/day) 30.3 (5.3) -16.7 (0.9) -6.5 (-8.7, -4.3) Placebo 30.6 (5.3) -10.3 (0.9) — Study 6 Quetiapine (300 mg/day) 31.1 (5.7) -16.9 (1) -5 (-7.3, -2.7) Quetiapine (600 mg/day) 29.9 (5.6) -16 (1) -4.1 (-6.4, -1.8) Placebo 29.6 (5.4) -11.9 (1) — SD: standard deviation; SE: standard error; LS Mean: least-squares mean; CI: unadjusted confidence interval.

Difference (drug minus placebo) in least-squares mean change from baseline.

Doses that are statistically significantly superior to placebo.

Maintenance Treatment as an Adjunct to Lithium or Divalproex The efficacy of quetiapine in the maintenance treatment of bipolar I disorder was established in 2 placebo-controlled trials in patients (n=1326) who met DSM-IV criteria for bipolar I disorder (studies 7 and 8 in Figures 1 and 2).

The trials included patients whose most recent episode was manic, depressed, or mixed, with or without psychotic features.

In the open-label phase, patients were required to be stable on quetiapine plus lithium or divalproex for at least 12 weeks in order to be randomized.

On average, patients were stabilized for 15 weeks.

In the randomization phase, patients continued treatment with lithium or divalproex and were randomized to receive either quetiapine (administered twice daily totaling 400 mg/day to 800 mg/day) or placebo.

Approximately 50% of the patients had discontinued from the quetiapine group by day 280 and 50% of the placebo group had discontinued by day 117 of double-blind treatment.

The primary endpoint in these studies was time to recurrence of a mood event (manic, mixed or depressed episode).

A mood event was defined as medication initiation or hospitalization for a mood episode; YMRS score ≥ 20 or MADRS score ≥ 20 at 2 consecutive assessments; or study discontinuation due to a mood event.

(Figure 1 and Figure 2) In both studies, quetiapine was superior to placebo in increasing the time to recurrence of any mood event.

The treatment effect was present for increasing time to recurrence of both manic and depressed episodes.

The effect of quetiapine was independent of any specific subgroup (assigned mood stabilizer, sex, age, race, most recent bipolar episode, or rapid cycling course).

HOW SUPPLIED

How Supplied Section 25 mg tablets are peach, round, biconvex, film-coated tablets, debossed with ‘25’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-902-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-902-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-902-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-902-61 50 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘50’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-903-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-903-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-903-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-903-61 100 mg tablets are yellow, round, biconvex, film-coated tablets, debossed with ‘904’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-904-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-904-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-904-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-904-61 200 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘905’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-905-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-905-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-905-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-905-61 300 mg tablets are white, capsule-shaped, biconvex, film-coated tablets, debossed with ‘906’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-906-83 Bottles of 60’s with Child Resistant Cap ……………… NDC 47335-906-86 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-906-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-906-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-906-61 400 mg tablets are yellow, capsule-shaped, biconvex, film-coated tablets, debossed with ‘907’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-907-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-907-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-907-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-907-61 Store at 20° to 25°C (68° to 77°F); excursions permitted between 15° and 30°C (59° and 86°F) [see USP Controlled Room Temperature].

RECENT MAJOR CHANGES

Recent Major Changes Section Warnings and Precautions, Cerebrovascular Adverse Reactions, Including Stroke, in Elderly Patients with Dementia-Related Psychosis (5.3 ) ———————4/2013

DOSAGE FORMS AND STRENGTHS

Dosage Forms & Strengths Section 25 mg tablets are peach, round, biconvex, film-coated tablets, debossed with ‘25’ on one side and plain on the other side 50 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘50’ on one side and plain on the other side 100 mg tablets are yellow, round, biconvex, film-coated tablets, debossed with ‘904’ on one side and plain on the other side 200 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘905’ on one side and plain on the other side 300 mg tablets are white, capsule-shaped, biconvex, film-coated tablets, debossed with ‘906’ on one side and plain on the other side 400 mg tablets are yellow, capsule-shaped, biconvex, film-coated tablets, debossed with ‘907’ on one side and plain on the other side

INDICATIONS AND USAGE

Indications & Usage Section Quetiapine fumarate tablets are atypical antipsychotic indicated for the treatment of: Schizophrenia ( 1.1 ) Bipolar I disorder manic episodes ( 1.2 ) Bipolar disorder, depressive episodes ( 1.2 ) Quetiapine fumarate tablets are indicated for the treatment of schizophrenia.

The efficacy of quetiapine fumarate tablets in schizophrenia was established in three 6-week trials in adults and one 6-week trial in adolescents (13 to ¬17 years).

The effectiveness of quetiapine fumarate tablets for the maintenance treatment of schizophrenia has not been systematically evaluated in controlled clinical trials [ see Clinical Studies ( 14.1 ) ].

Quetiapine fumarate tablets are indicated for the acute treatment of manic episodes associated with bipolar I disorder, both as monotherapy and as an adjunct to lithium or divalproex.

Efficacy was established in two 12-week monotherapy trials in adults, in one 3-week adjunctive trial in adults, and in one 3-week monotherapy trial in pediatric patients (10 to 17 years) [ see Clinical Studies ( 14.2 ) ].

Quetiapine fumarate tablets are indicated as monotherapy for the acute treatment of depressive episodes associated with bipolar disorder.

Efficacy was established in two 8-week monotherapy trials in adult patients with bipolar I and bipolar II disorder [ see Clinical Studies ( 14.2 ) ].

Quetiapine fumarate tablets are indicated for the maintenance treatment of bipolar I disorder, as an adjunct to lithium or divalproex.

Efficacy was established in two maintenance trials in adults.

The effectiveness of quetiapine fumarate tablets as monotherapy for the maintenance treatment of bipolar disorder has not been systematically evaluated in controlled clinical trials [ see Clinical Studies ( 14.2 ) ].

Pediatric schizophrenia and bipolar I disorder are serious mental disorders, however, diagnosis can be challenging.

For pediatric schizophrenia, symptom profiles can be variable, and for bipolar I disorder, patients may have variable patterns of periodicity of manic or mixed symptoms.

It is recommended that medication therapy for pediatric schizophrenia and bipolar I disorder be initiated only after a thorough diagnostic evaluation has been performed and careful consideration given to the risks associated with medication treatment.

Medication treatment for both pediatric schizophrenia and bipolar I disorder is indicated as part of a total treatment program that often includes psychological, educational and social interventions.

BOXED WARNING

Boxed Warning Section Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death [see Warnings and Precautions (5.1)] .

Quetiapine is not approved for the treatment of patients with dementia-related psychosis [see Warnings and Precautions (5.1)] .

Suicidal Thoughts and Behaviors Antidepressants increased the risk of suicidal thoughts and behavior in children, adolescents, and young adults in short-term studies.

These studies did not show an increase in the risk of suicidal thoughts and behavior with antidepressant use in patients over age 24; there was a reduction in risk with antidepressant use in patients aged 65 and older [see Warnings and Precautions (5.2)] .

In patients of all ages who are started on antidepressant therapy, monitor closely for worsening, and for emergence of suicidal thoughts and behaviors.

Advise families and caregivers of the need for close observation and communication with the prescriber [see Warnings and Precautions (5.2)] .

Quetiapine is not approved for use in pediatric patients under ten years of age [see Use in Specific Populations (8.4)] .

WARNING AND CAUTIONS

Warnings And Precautions Section Cerebrovascular Adverse Reactions: Increased incidence of cerebrovascular adverse events (e.g., stroke, transient ischemic attack) has been seen in elderly patients with dementia-related psychoses treated with atypical antipsychotic drugs ( 5.3 ) Neuroleptic Malignant Syndrome (NMS): Manage with immediate discontinuation and close monitoring ( 5.4 ) Metabolic Changes: Atypical antipsychotics have been associated with metabolic changes.

These metabolic changes include hyperglycemia, dyslipidemia, and weight gain ( 5.5 ) Hyperglycemia and Diabetes Mellitus: Monitor patients for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Monitor glucose regularly in patients with diabetes or at risk for diabetes Dyslipidemia: Undesirable alterations have been observed in patients treated with atypical antipsychotics.

Appropriate clinical monitoring is recommended, including fasting blood lipid testing at the beginning of, and periodically, during treatment Weight Gain: Gain in body weight has been observed; clinical monitoring of weight is recommended Tardive Dyskinesia: Discontinue if clinically appropriate ( 5.6 ) Hypotension: Use with caution in patients with known cardiovascular or cerebrovascular disease ( 5.7 ) Increased Blood Pressure in Children and Adolescents: Monitor blood pressure at the beginning of, and periodically during treatment in children and adolescents ( 5.8 ) Leukopenia, Neutropenia and Agranulocytosis: Monitor complete blood count frequently during the first few months of treatment in patients with a preexisting low white cell count or a history of leukopenia/neutropenia and discontinue quetiapine at the first sign of a decline in WBC in absence of other causative factors ( 5.9 ) Cataracts: Lens changes have been observed in patients during long-term quetiapine treatment.

Lens examination is recommended when starting treatment and at 6-month intervals during chronic treatment ( 5.10 ) Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

Analysis of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients.

Over the course of a typical 10-­week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature.

Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.

The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear.

Quetiapine fumarate tablets are not approved for the treatment of patients with dementia-related psychosis [ see Boxed Warning ] .

Patients with major depressive disorder (MDD), both adult and pediatric, may experience worsening of their depression and/or the emergence of suicidal ideation and behavior (suicidality) or unusual changes in behavior, whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs.

Suicide is a known risk of depression and certain other psychiatric disorders, and these disorders themselves are the strongest predictors of suicide.

There has been a long-standing concern, however, that antidepressants may have a role in inducing worsening of depression and the emergence of suicidality in certain patients during the early phases of treatment.

Pooled analyses of short-term placebo-controlled trials of antidepressant drugs (SSRIs and others) showed that these drugs increase the risk of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults (ages 18 to 24) with major depressive disorder (MDD) and other psychiatric disorders.

Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction with antidepressants compared to placebo in adults aged 65 and older.

The pooled analyses of placebo-controlled trials in children and adolescents with MDD, obsessive compulsive disorder (OCD), or other psychiatric disorders included a total of 24 short-term trials of 9 antidepressant drugs in over 4400 patients.

The pooled analyses of placebo-controlled trials in adults with MDD or other psychiatric disorders included a total of 295 short-term trials (median duration of 2 months) of 11 antidepressant drugs in over 77,000 patients.

There was considerable variation in risk of suicidality among drugs, but a tendency toward an increase in the younger patients for almost all drugs studied.

There were differences in absolute risk of suicidality across the different indications, with the highest incidence in MDD.

The risk differences (drug vs.

placebo), however, were relatively stable within age strata and across indications.

These risk differences (drug-placebo difference in the number of cases of suicidality per 1000 patients treated) are provided in Table 2.

Table 2 Drug-Placebo Difference in Number of Cases of Suicidality per 1000 Patients Treated Age Range Drug-Placebo Difference in Number of Cases of Suicidality per 1000 Patients Treated Increases Compared to Placebo <18 14 additional cases 18 to 24 5 additional cases Decreases Compared to Placebo 25 to 64 1 fewer case ≥65 6 fewer cases No suicides occurred in any of the pediatric trials.

There were suicides in the adult trials, but the number was not sufficient to reach any conclusion about drug effect on suicide.

It is unknown whether the suicidality risk extends to longer-term use, i.e., beyond several months.

However, there is substantial evidence from placebo-controlled maintenance trials in adults with depression that the use of antidepressants can delay the recurrence of depression.

All patients being treated with antidepressants for any indication should be monitored appropriately and observed closely for clinical worsening, suicidality, and unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases.

The following symptoms, anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric.

Although a causal link between the emergence of such symptoms and either the worsening of depression and/or the emergence of suicidal impulses has not been established, there is concern that such symptoms may represent precursors to emerging suicidality.

Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse, or who are experiencing emergent suicidality or symptoms that might be precursors to worsening depression or suicidality, especially if these symptoms are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Families and caregivers of patients being treated with antidepressants for major depressive disorder or other indications, both psychiatric and nonpsychiatric, should be alerted about the need to monitor patients for the emergence of agitation, irritability, unusual changes in behavior, and the other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to healthcare providers.

Such monitoring should include daily observation by families and caregivers.

Prescriptions for quetiapine fumarate tablets should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

Screening Patients for Bipolar Disorder: A major depressive episode may be the initial presentation of bipolar disorder.

It is generally believed (though not established in controlled trials) that treating such an episode with an antidepressant alone may increase the likelihood of precipitation of a mixed/manic episode in patients at risk for bipolar disorder.

Whether any of the symptoms described above represent such a conversion is unknown.

However, prior to initiating treatment with an antidepressant, including quetiapine, patients with depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression In placebo-controlled trials with risperidone, aripiprazole, and olanzapine in elderly subjects with dementia, there was a higher incidence of cerebrovascular adverse reactions (cerebrovascular accidents and transient ischemic attacks) including fatalities compared to placebo-treated subjects.

Quetiapine is not approved for the treatment of patients with dementia-related psychosis [see also Boxed Warning and Warnings and Precautions (5.1)].

A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with administration of antipsychotic drugs, including quetiapine fumarate tablets.

Rare cases of NMS have been reported with quetiapine fumarate tablets.

Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).

Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis) and acute renal failure.

The diagnostic evaluation of patients with this syndrome is complicated.

In arriving at a diagnosis, it is important to exclude cases where the clinical presentation includes both serious medical illness (e.g., pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and symptoms (EPS).

Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever and primary central nervous system (CNS) pathology.

The management of NMS should include: 1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; 2) intensive symptomatic treatment and medical monitoring; and 3) treatment of any concomitant serious medical problems for which specific treatments are available.

There is no general agreement about specific pharmacological treatment regimens for NMS.

If a patient requires antipsychotic drug treatment after recovery from NMS, the potential reintroduction of drug therapy should be carefully considered.

The patient should be carefully monitored since recurrences of NMS have been reported.

Atypical antipsychotic drugs have been associated with metabolic changes that include hyperglycemia/diabetes mellitus, dyslipidemia, and body weight gain.

While all of the drugs in the class have been shown to produce some metabolic changes, each drug has its own specific risk profile.

In some patients, a worsening of more than one of the metabolic parameters of weight, blood glucose, and lipids was observed in clinical studies.

Changes in these metabolic profiles should be managed as clinically appropriate.

Hyperglycemia and Diabetes Mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics, including quetiapine.

Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population.

Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse reactions is not completely understood.

However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse reactions in patients treated with the atypical antipsychotics.

Precise risk estimates for hyperglycemia-related adverse reactions in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics should be monitored regularly for worsening of glucose control.

Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment.

Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should undergo fasting blood glucose testing.

In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of the suspect drug.

Adults : Table 3: Fasting Glucose—Proportion of Patients Shifting to ≥ 126 mg/dL in Short-Term (≤ 12 weeks) Placebo-Controlled Studies * Laboratory Analyte Category Change (At Least Once) from Baseline Treatment Arm N Patients n(%) Fasting Glucose Normal to High (<100 mg/dL to ≥ 126 mg/dL) Quetiapine 2907 71 (2.4%) Placebo 1346 19 (1.4%) Borderline to High (≥ 100 mg/dL and <126 mg/dL to ≥ 126 mg/dL) Quetiapine 572 67 (11.7%) Placebo 279 33 (11.8%) Includes quetiapine fumarate tablets and quetiapine fumarate extended-release tablets data.

In a 24-week trial (active-controlled, 115 patients treated with quetiapine) designed to evaluate glycemic status with oral glucose tolerance testing of all patients, at week 24 the incidence of a treatment-emergent post-glucose challenge glucose level ≥ 200 mg/dL was 1.7% and the incidence of a fasting treatment-emergent blood glucose level ≥ 126 mg/dL was 2.6%.

The mean change in fasting glucose from baseline was 3.2 mg/dL and mean change in 2 hour glucose from baseline was -1.8 mg/dL for quetiapine.

In 2 long-term placebo-controlled randomized withdrawal clinical trials for bipolar I disorder maintenance, mean exposure of 213 days for quetiapine (646 patients) and 152 days for placebo (680 patients), the mean change in glucose from baseline was +5 mg/dL for quetiapine and –0.05 mg/dL for placebo.

The exposure-adjusted rate of any increased blood glucose level (≥ 126 mg/dL) for patients more than 8 hours since a meal (however, some patients may not have been precluded from calorie intake from fluids during fasting period) was 18 per 100 patient years for quetiapine (10.7% of patients; n=556) and 9.5 for placebo per 100 patient years (4.6% of patients; n=581).

Children and Adolescents : In a placebo-controlled quetiapine monotherapy study of adolescent patients (13 to 17 years of age) with schizophrenia (6 weeks duration), the mean change in fasting glucose levels for quetiapine (n=138) compared to placebo (n=67) was –0.75 mg/dL versus –1.7 mg/dL.

In a placebo-controlled quetiapine monotherapy study of children and adolescent patients (10 to 17 years of age) with bipolar mania (3 weeks duration), the mean change in fasting glucose level for quetiapine (n=170) compared to placebo (n=81) was 3.62 mg/dL versus –1.17 mg/dL.

No patient in either study with a baseline normal fasting glucose level (<100 mg/dL) or a baseline borderline fasting glucose level (≥100 mg/dL and <126 mg/dL) had a treatment-emergent blood glucose level of ≥126 mg/dL.

In a placebo-controlled quetiapine fumarate extended-release tablets monotherapy study (8 weeks duration) of children and adolescent patients (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the mean change in fasting glucose levels for quetiapine fumarate extended-release tablets (n = 60) compared to placebo (n = 62) was 1.8 mg/dL versus 1.6 mg/dL.

In this study, there were no patients in the quetiapine fumarate extended-release tablets or placebo-treated groups with a baseline normal fasting glucose level ( 126 mg/dL.

There was one patient in the quetiapine fumarate extended-release tablets group with a baseline borderline fasting glucose level ( > 100 mg/dL) and ( 126 mg/dL compared to zero patients in the placebo group.

Dyslipidemia Adults : Table 4 shows the percentage of adult patients with changes in total cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol from baseline by indication in clinical trials with quetiapine.

Table 4: Percentage of Adult Patients with Shifts in Total Cholesterol, Triglycerides, LDL-Cholesterol and HDL-Cholesterol from Baseline to Clinically Significant Levels by Indication Laboratory Analyte Indication Treatment Arm N Patients n (%) Total Cholesterol ≥240 mg/dL Schizophrenia * Quetiapine 137 24 (18%) Placebo 92 6 (7%) Bipolar Depression † Quetiapine 463 41 (9%) Placebo 250 15 (6%) Triglycerides ≥200 mg/dL Schizophrenia Quetiapine 120 26 (22%) Placebo 70 11 (16%) Bipolar Depression Quetiapine 436 59 (14%) Placebo 232 20 (9%) LDL-Cholesterol ≥ 160 mg/dL Schizophrenia Quetiapine na ‡ na Placebo na na Bipolar Depression Quetiapine 465 29 (6%) Placebo 256 12 (5%) HDL-Cholesterol ≤ 40 mg/dL Schizophrenia Quetiapine na na Placebo na na Bipolar Depression Quetiapine 393 56 (14%) Placebo 214 29 (14%) 6 weeks duration 8 weeks duration Parameters not measured in the quetiapine registration studies for schizophrenia.

Lipid parameters also were not measured in the bipolar mania registration studies.

Children and Adolescents : Table 5 shows the percentage of children and adolescents with changes in total cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol from baseline in clinical trials with quetiapine.

Table 5: Percentage of Children and Adolescents with Shifts in Total Cholesterol, Triglycerides, LDL-Cholesterol and HDL-Cholesterol from Baseline to Clinically Significant Levels Laboratory Analyte Indication Treatment Arm N Patients n (%) Total Cholesterol ≥200 mg/dL Schizophrenia * Quetiapine 107 13 (12%) Placebo 56 1 (2%) Bipolar Mania † Quetiapine 159 16 (10%) Placebo 66 2 (3%) Triglycerides ≥150 mg/dL Schizophrenia Quetiapine 103 17 (17%) Placebo 51 4 (8%) Bipolar Mania Quetiapine 149 32 (22%) Placebo 60 8 (13%) LDL-Cholesterol ≥ 130 mg/dL Schizophrenia Quetiapine 112 4 (4%) Placebo 60 1 (2%) Bipolar Mania Quetiapine 169 13 (8%) Placebo 74 4 (5%) HDL-Cholesterol ≤ 40 mg/dL Schizophrenia Quetiapine 104 16 (15%) Placebo 54 10 (19%) Bipolar Mania Quetiapine 154 16 (10%) Placebo 61 4 (7%) 13 to 17 years, 6 weeks duration 10 to 17 years, 3 weeks duration In a placebo-controlled quetiapine fumarate extended-release tablets monotherapy study (8 weeks duration) of children and adolescent patients (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the percentage of children and adolescents with shifts in total cholesterol (≥200 mg/dL), triglycerides (≥150 mg/dL), LDL-cholesterol (≥ 130 mg/dL) and HDL-cholesterol (≤40 mg/dL) from baseline to clinically significant levels were: total cholesterol 8% (7/83) for quetiapine fumarate extended-release tablets vs.

6% (5/84) for placebo; triglycerides 28% (22/80) for quetiapine fumarate extended-release tablets vs.

9% (7/82) for placebo; LDL-cholesterol 2% (2/86) for quetiapine fumarate extended-release tablets vs.

4% (3/85) for placebo and HDL-cholesterol 20% (13/65) for quetiapine fumarate extended-release tablets vs.

15% (11/74) for placebo.

Weight Gain Increases in weight have been observed in clinical trials.

Patients receiving quetiapine should receive regular monitoring of weight.

Adults : In clinical trials with quetiapine the following increases in weight have been reported.

Table 6: Proportion of Patients with Weight Gain ≥7% of Body Weight (Adults) Vital Sign Indication Treatment Arm N Patients n (%) Weight Gain ≥ 7% of Body Weight Schizophrenia * Quetiapine 391 89 (23%) Placebo 206 11 (6%) Bipolar Mania (monotherapy) † Quetiapine 209 44 (21%) Placebo 198 13 (7%) Bipolar Mania (adjunct therapy) ‡ Quetiapine 196 25 (13%) Placebo 203 8 (4%) Bipolar Depression § Quetiapine 554 47 (8%) Placebo 295 7 (2%) up to 6 weeks duration up to 12 weeks duration up to 3 weeks duration up to 8 weeks duration Children and Adolescents : In two clinical trials with quetiapine, one in bipolar mania and one in schizophrenia, reported increases in weight are included in table 7.

Table 7: Proportion of Patients with Weight Gain ≥7% of Body Weight (Children and Adolescents) Vital Sign Indication Treatment Arm N Patients n (%) Weight Gain ≥ 7% of Body Weight Schizophrenia * Quetiapine 111 23 (21%) Placebo 44 3 (7%) Bipolar Mania † Quetiapine 157 18 (12%) Placebo 68 0 (0%) 6 weeks duration 3 weeks duration The mean change in body weight in the schizophrenia trial was 2 kg in the quetiapine group and -0.4 kg in the placebo group and in the bipolar mania trial it was 1.7 kg in the quetiapine group and 0.4 kg in the placebo group.

In an open-label study that enrolled patients from the above two pediatric trials, 63% of patients (241/380) completed 26 weeks of therapy with quetiapine.

After 26 weeks of treatment, the mean increase in body weight was 4.4 kg.

Forty-five percent of the patients gained ≥ 7% of their body weight, not adjusted for normal growth.

In order to adjust for normal growth over 26 weeks an increase of at least 0.5 standard deviation from baseline in BMI was used as a measure of a clinically significant change; 18.3% of patients on quetiapine met this criterion after 26 weeks of treatment.

In a clinical trial for quetiapine fumarate extended-release tablets in children and adolescents (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the percentage of patients with weight gain ≥7% of body weight at any time was 15% (14/92) for quetiapine fumarate extended-release tablets vs.

10% (10/100) for placebo.

The mean change in body weight was 1.4 kg in the quetiapine fumarate extended-release tablets group vs.

0.6 kg in the placebo group.

When treating pediatric patients with quetiapine fumarate tablets for any indication, weight gain should be assessed against that expected for normal growth.

A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs, including quetiapine.

Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.

Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.

The risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase.

However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses or may even arise after discontinuation of treatment.

There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.

Antipsychotic treatment, itself, however, may suppress (or partially suppress) the signs and symptoms of the syndrome and thereby may possibly mask the underlying process.

The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown.

Given these considerations, quetiapine should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.

Chronic antipsychotic treatment should generally be reserved for patients who appear to suffer from a chronic illness that (1) is known to respond to antipsychotic drugs, and (2) for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.

In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

The need for continued treatment should be reassessed periodically.

If signs and symptoms of tardive dyskinesia appear in a patient on quetiapine, drug discontinuation should be considered.

However, some patients may require treatment with quetiapine despite the presence of the syndrome.

Quetiapine may induce orthostatic hypotension associated with dizziness, tachycardia and, in some patients, syncope, especially during the initial dose-titration period, probably reflecting its α 1 ­-adrenergic antagonist properties.

Syncope was reported in 1% (28/3265) of the patients treated with quetiapine, compared with 0.2% (2/954) on placebo and about 0.4% (2/527) on active control drugs.

Orthostatic hypotension, dizziness, and syncope may lead to falls.

Quetiapine should be used with particular caution in patients with known cardiovascular disease (history of myocardial infarction or ischemic heart disease, heart failure or conduction abnormalities), cerebrovascular disease or conditions which would predispose patients to hypotension (dehydration, hypovolemia and treatment with antihypertensive medications).

The risk of orthostatic hypotension and syncope may be minimized by limiting the initial dose to 25 mg twice daily [ s ee Dosage and Administration ( 2.2 )] .

If hypotension occurs during titration to the target dose, a return to the previous dose in the titration schedule is appropriate.

In placebo-controlled trials in children and adolescents with schizophrenia (6-week duration) or bipolar mania (3-week duration), the incidence of increases at any time in systolic blood pressure (≥20 mmHg) was 15.2% (51/335) for quetiapine and 5.5% (9/163) for placebo; the incidence of increases at any time in diastolic blood pressure (≥10 mmHg) was 40.6% (136/335) for quetiapine and 24.5% (40/163) for placebo.

In the 26-week open-label clinical trial, one child with a reported history of hypertension experienced a hypertensive crisis.

Blood pressure in children and adolescents should be measured at the beginning of, and periodically during treatment.

In a placebo-controlled quetiapine fumarate extended-release tablets clinical trial (8 weeks duration) in children and adolescents (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the incidence of increases at any time in systolic blood pressure (≥20 mmHg) was 6.5% (6/92) for quetiapine fumarate extended-release tablets and 6% (6/100) for placebo; the incidence of increases at any time in diastolic blood pressure (≥10 mmHg) was 46.7% (43/92) for quetiapine fumarate extended-release tablets and 36% (36/100) for placebo.

In clinical trial and postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to atypical antipsychotic agents, including quetiapine.

Agranulocytosis (including fatal cases) has also been reported.

Possible risk factors for leukopenia/neutropenia include preexisting low white cell count (WBC) and history of drug induced leukopenia/neutropenia.

Patients with a preexisting low WBC or a history of drug induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and should discontinue quetiapine at the first sign of a decline in WBC in absence of other causative factors.

Patients with neutropenia should be carefully monitored for fever or other symptoms or signs of infection and treated promptly if such symptoms or signs occur.

Patients with severe neutropenia (absolute neutrophil count <1000/mm 3 ) should discontinue quetiapine and have their WBC followed until recovery.

The development of cataracts was observed in association with quetiapine treatment in chronic dog studies [ see Nonclinical Toxicology ( 13.2 )].

Lens changes have also been observed in adults, children and adolescents during long-term quetiapine treatment, but a causal relationship to quetiapine use has not been established.

Nevertheless, the possibility of lenticular changes cannot be excluded at this time.

Therefore, examination of the lens by methods adequate to detect cataract formation, such as slit lamp exam or other appropriately sensitive methods, is recommended at initiation of treatment or shortly thereafter, and at 6-month intervals during chronic treatment.

In clinical trials quetiapine was not associated with a persistent increase in QT intervals.

However, the QT effect was not systematically evaluated in a thorough QT study.

In post marketing experience, there were cases reported of QT prolongation in patients who overdosed on quetiapine [see Overdosage (10.1)] , in patients with concomitant illness, and in patients taking medicines known to cause electrolyte imbalance or increase QT interval [see Drug Interactions (7.1)] .

The use of quetiapine should be avoided in combination with other drugs that are known to prolong QTc including Class 1A antiarrythmics (e.g., quinidine, procainamide) or Class III antiarrythmics (e.g., amiodarone, sotalol), antipsychotic medications (e.g., ziprasidone, chlorpromazine, thioridazine), antibiotics (e.g., gatifloxacin, moxifloxacin), or any other class of medications known to prolong the QTc interval (e.g., pentamidine, levomethadyl acetate, methadone).

Quetiapine should also be avoided in circumstances that may increase the risk of occurrence of torsade de pointes and/or sudden death including (1) a history of cardiac arrhythmias such as bradycardia; (2) hypokalemia or hypomagnesemia; (3) concomitant use of other drugs that prolong the QTc interval; and (4) presence of congenital prolongation of the QT interval.

Caution should also be exercised when quetiapine is prescribed in patients with increased risk of QT prolongation (e.g.

cardiovascular disease, family history of QT prolongation, the elderly, congestive heart failure and heart hypertrophy).

During clinical trials, seizures occurred in 0.5% (20/3490) of patients treated with quetiapine compared to 0.2% (2/954) on placebo and 0.7% (4/527) on active control drugs.

As with other antipsychotics, quetiapine should be used cautiously in patients with a history of seizures or with conditions that potentially lower the seizure threshold, e.g., Alzheimer’s dementia.

Conditions that lower the seizure threshold may be more prevalent in a population of 65 years or older.

Adults: Clinical trials with quetiapine demonstrated dose-related decreases in thyroid hormone levels.

The reduction in total and free thyroxine (T4) of approximately 20% at the higher end of the therapeutic dose range was maximal in the first six weeks of treatment and maintained without adaptation or progression during more chronic therapy.

In nearly all cases, cessation of quetiapine treatment was associated with a reversal of the effects on total and free T4, irrespective of the duration of treatment.

The mechanism by which quetiapine effects the thyroid axis is unclear.

If there is an effect on the hypothalamic-pituitary axis, measurement of TSH alone may not accurately reflect a patient’s thyroid status.

Therefore, both TSH and free T4, in addition to clinical assessment, should be measured at baseline and at follow-up.

In the mania adjunct studies, where quetiapine was added to lithium or divalproex, 12% (24/196) of quetiapine treated patients compared to 7% (15/203) of placebo-treated patients had elevated TSH levels.

Of the quetiapine treated patients with elevated TSH levels, 3 had simultaneous low free T4 levels (free T4 <0.8 LLN).

About 0.7% (26/3489) of quetiapine patients did experience TSH increases in monotherapy studies.

Some patients with TSH increases needed replacement thyroid treatment.

In all quetiapine trials, the incidence of significant shifts in thyroid hormones and TSH were*: decrease in free T4 (free T4 <0.8 LLN), 2% (357/17513); decrease in total T4, 4% (75/1861); decrease in free T3, 0.4% (53/13766); decrease in total T3, 2% (26/1312), and increase in TSH, 4.9% (956/19412).

In eight patients, where TBG was measured, levels of TBG were unchanged.

Table 8 shows the incidence of these shifts in short-term placebo-controlled clinical trials.

Table 8: Incidence of shifts in thyroid hormone levels and TSH in short-term placebo-controlled clinical trials * , † Total T4 Free T4 Total T3 Free T3 TSH Quetiapine Placebo Quetiapine Placebo Quetiapine Placebo Quetiapine Placebo Quetiapine Placebo 3.4 % (37/1097) 0.6% (4/651) 0.7% (52/7218) 0.1% (4/3668) 0.5% (2/369) 0% (0/113) 0.2% (11/5673) 0% (1/2679) 3.2% (240/7587) 2.7% (105/3912) Based on shifts from normal baseline to potentially clinically important value at anytime post-baseline.

Shifts in total T Includes quetiapine fumarate tablets and quetiapine fumarate extended-release tablets data.

In short-term placebo-controlled monotherapy trials, the incidence of reciprocal, shifts in T 3 and TSH was 0 % for both quetiapine (1/4800) and placebo (0/2190) and for T 4 and TSH the shifts were 0.1% (7/6154) for quetiapine versus 0% (1/3007) for placebo.

Children and Adolescents : In acute placebo-controlled trials in children and adolescent patients with schizophrenia (6-week duration) or bipolar mania (3-week duration), the incidence of shifts for thyroid function values at any time for quetiapine treated patients and placebo-treated patients for elevated TSH was 2.9% (8/280) vs.

0.7% (1/138), respectively and for decreased total thyroxine was 2.8% (8/289) vs.

0% (0/145, respectively).

Of the quetiapine treated patients with elevated TSH levels, 1 had simultaneous low free T4 level at end of treatment.

Adults : During clinical trials with quetiapine, the incidence of shifts in prolactin levels to a clinically significant value occurred in 3.6% (158/4416) of patients treated with quetiapine compared to 2.6% (51/1968) on placebo.

Children and Adolescents : In acute placebo-controlled trials in children and adolescent patients with bipolar mania (3-week duration) or schizophrenia (6-week duration), the incidence of shifts in prolactin levels to a value (>20 mcg/L males; > 26 mcg/L females at any time) was 13.4% (18/134) for quetiapine compared to 4% (3/75) for placebo in males and 8.7% (9/104) for quetiapine compared to 0% (0/39) for placebo in females.

Like other drugs that antagonize dopamine D 2 receptors, quetiapine elevates prolactin levels in some patients and the elevation may persist during chronic administration.

Hyperprolactinemia, regardless of etiology, may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotrophin secretion.

This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is considered in a patient with previously detected breast cancer.

As is common with compounds which increase prolactin release, mammary gland, and pancreatic islet cell neoplasia (mammary adenocarcinomas, pituitary and pancreatic adenomas) was observed in carcinogenicity studies conducted in mice and rats.

Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans, but the available evidence is too limited to be conclusive [see Nonclinical Toxicology (13.1)] .

Somnolence was a commonly reported adverse event reported in patients treated with quetiapine especially during the 3 to 5 day period of initial dose-titration.

In schizophrenia trials, somnolence was reported in 18% (89/510) of patients on quetiapine compared to 11% (22/206) of placebo patients.

In acute bipolar mania trials using quetiapine as monotherapy, somnolence was reported in 16% (34/209) of patients on quetiapine compared to 4% of placebo patients.

In acute bipolar mania trials using quetiapine as adjunct therapy, somnolence was reported in 34% (66/196) of patients on quetiapine compared to 9% (19/203) of placebo patients.

In bipolar depression trials, somnolence was reported in 57% (398/698) of patients on quetiapine compared to 15% (51/347) of placebo patients.

Since quetiapine has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about performing activities requiring mental alertness, such as operating a motor vehicle (including automobiles) or operating hazardous machinery until they are reasonably certain that quetiapine therapy does not affect them adversely.

Somnolence may lead to falls.

Although not reported with quetiapine, disruption of the body’s ability to reduce core body temperature has been attributed to antipsychotic agents.

Appropriate care is advised when prescribing quetiapine for patients who will be experiencing conditions which may contribute to an elevation in core body temperature, e.g., exercising strenuously, exposure to extreme heat, receiving concomitant medication with anticholinergic activity, or being subject to dehydration.

Esophageal dysmotility and aspiration have been associated with antipsychotic drug use.

Aspiration pneumonia is a common cause of morbidity and mortality in elderly patients, in particular those with advanced Alzheimer’s dementia.

Quetiapine and other antipsychotic drugs should be used cautiously in patients at risk for aspiration pneumonia.

Acute withdrawal symptoms, such as insomnia, nausea, and vomiting have been described after abrupt cessation of atypical antipsychotic drugs, including quetiapine.

In short-term placebo-controlled, monotherapy clinical trials with quetiapine fumarate extended-release tablets that included a discontinuation phase which evaluated discontinuation symptoms, the aggregated incidence of patients experiencing one or more discontinuation symptoms after abrupt cessation was 12.1% (241/1993) for quetiapine fumarate extended-release tablets and 6.7% (71/1065) for placebo.

The incidence of the individual adverse events (i.e., insomnia, nausea, headache, diarrhea, vomiting, dizziness and irritability) did not exceed 5.3% in any treatment group and usually resolved after 1 week post-discontinuation.

Gradual withdrawal is advised.

INFORMATION FOR PATIENTS

Information For Patients Section See FDA-approved patient labeling (Medication Guide) Prescribers or other health professionals should inform patients, their families, and their caregivers about the benefits and risks associated with treatment with quetiapine fumarate tablets and should counsel them in its appropriate use.

A patient Medication Guide about “Antidepressant Medicines, Depression and other Serious Mental Illness, and Suicidal Thoughts or Actions” is available for quetiapine fumarate tablets.

The prescriber or health professional should instruct patients, their families, and their caregivers to read the Medication Guide and should assist them in understanding its contents.

Patients should be given the opportunity to discuss the contents of the Medication Guide and to obtain answers to any questions they may have.

The complete text of the Medication Guide is reprinted at the end of this document.

Patients should be advised of the following issues and asked to alert their prescriber if these occur while taking quetiapine fumarate tablets.

Increased Mortality in Elderly Patients with Dementia-Related Psychosis Patients and caregivers should be advised that elderly patients with dementia-related psychosis treated with atypical antipsychotic drugs are at increased risk of death compared with placebo.

Quetiapine is not approved for elderly patients with dementia-related psychosis [see Warnings and Precautions (5.1)] .

Suicidal Thoughts and Behaviors Patients, their families, and their caregivers should be encouraged to be alert to the emergence of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, mania, other unusual changes in behavior, worsening of depression, and suicidal ideation, especially early during antidepressant treatment and when the dose is adjusted up or down.

Families and caregivers of patients should be advised to look for the emergence of such symptoms on a day-to-day basis, since changes may be abrupt.

Such symptoms should be reported to the patient’s prescriber or health professional, especially if they are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Symptoms such as these may be associated with an increased risk for suicidal thinking and behavior and indicate a need for very close monitoring and possibly changes in the medication [ s ee Warnings and Precautions (5.2)] .

Neuroleptic Malignant Syndrome (NMS) Patients should be advised to report to their physician any signs or symptoms that may be related to NMS.

These may include muscle stiffness and high fever [ s ee Warnings and Precautions (5.4)] .

Hyperglycemia and Diabetes Mellitus Patients should be aware of the symptoms of hyperglycemia (high blood sugar) and diabetes mellitus.

Patients who are diagnosed with diabetes, those with risk factors for diabetes, or those that develop these symptoms during treatment should have their blood glucose monitored at the beginning of and periodically during treatment [ s ee Warnings and Precautions (5.5)] .

Hyperlipidemia Patients should be advised that elevations in total cholesterol, LDL-cholesterol and triglycerides and decreases in HDL-cholesterol may occur.

Patients should have their lipid profile monitored at the beginning of and periodically during treatment [ s ee Warnings and Precautions (5.5)].

Weight Gain Patients should be advised that they may experience weight gain.

Patients should have their weight monitored regularly [ s ee Warnings and Precautions (5.5)].

Orthostatic Hypotension Patients should be advised of the risk of orthostatic hypotension (symptoms include feeling dizzy or lightheaded upon standing, which may lead to falls), especially during the period of initial dose titration, and also at times of re-initiating treatment or increases in dose [ s ee Warnings and Precautions (5.7)].

Increased Blood Pressure in Children and Adolescents Children and adolescent patients should have their blood pressure measured at the beginning of, and periodically during, treatment [ s ee Warnings and Precautions (5.8)] .

Leukopenia/Neutropenia Patients with a preexisting low WBC or a history of drug induced leukopenia/neutropenia should be advised that they should have their CBC monitored while taking quetiapine fumarate tablets [ s ee Warnings and Precautions (5.9)].

Interference with Cognitive and Motor Performance Patients should be advised of the risk of somnolence or sedation (which may lead to falls), especially during the period of initial dose titration.

Patients should be cautioned about performing any activity requiring mental alertness, such as operating a motor vehicle (including automobiles) or operating machinery, until they are reasonably certain quetiapine therapy does not affect them adversely.

[ s ee Warnings and Precautions (5.15)].

Heat Exposure and Dehydration Patients should be advised regarding appropriate care in avoiding overheating and dehydration [ s ee Warnings and Precautions (5.16)].

Concomitant Medication As with other medications, patients should be advised to notify their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs .

[ s ee Drug Interactions (7.1)] .

Pregnancy and Nursing Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy with quetiapine fumarate tablets.

[see Use in Specific Populations (8.1) and (8.3)].

Need for Comprehensive Treatment Program Quetiapine fumarate tablets are indicated as an integral part of a total treatment program for adolescents with schizophrenia and pediatric bipolar disorder that may include other measures (psychological, educational, and social).

Effectiveness and safety of quetiapine fumarate tablets have not been established in pediatric patients less than 13 years of age for schizophrenia or less than 10 years of age for bipolar mania.

Appropriate educational placement is essential and psychosocial intervention is often helpful.

The decision to prescribe atypical antipsychotic medication will depend upon the physician’s assessment of the chronicity and severity of the patient’s symptoms [see Indications and Usage (1.3)] .

DOSAGE AND ADMINISTRATION

Dosage & Administration Section Quetiapine fumarate tablets can be taken with or without food ( 2.1 ) Indication Initial Dose Recommended Dose Maximum Dose Schizophrenia-Aults ( 2.2 ) 25 mg twice daily 150 to 750 mg/day 750 mg/day Schizophrenia-Adolescents (13 to 17 years) ( 2.2 ) 25 mg twice daily 400 to 800 mg/day 800 mg/day Bipolar Mania- Adults Monotherapy or as an adjunct to lithium or divalproex ( 2.2 ) 50 mg twice daily 400 to 800 mg/day 800 mg/day Bipolar Mania- Children and Adolescents (10 to 17 years), Monotherapy ( 2.2 ) 25 mg twice daily 400 to 600 mg/day 600 mg/day Bipolar Depression-Adults ( 2.2 ) 50 mg once daily at bedtime 300 mg/day 300 mg/day Geriatric Use: Consider a lower starting dose (50 mg/day), slower titration and careful monitoring during the initial dosing period in the elderly ( 2.3 , 8.5 ) Hepatic Impairment: Lower starting dose (25 mg/day) and slower titration may be needed ( 2.4 , 8.7 , 12.3 ) Quetiapine fumarate tablets can be taken with or without food.

The recommended initial dose, titration, dose range and maximum quetiapine fumarate tablets dose for each approved indication is displayed in Table 1.

After initial dosing, adjustments can be made upwards or downwards, if necessary, depending upon the clinical response and tolerability of the patient [see Clinical Studies (14.1 and 14.2)].

Table 1: Recommended Dosing for Quetiapine Fumarate Tablets Indication Initial Dose and Titration Recommended Dose Maximum Dose Schizophrenia-Adults Day 1: 25 mg twice daily.

Increase in increments of 25 mg to 50 mg divided two or three times on Days 2 and 3 to range of 300 to 400 mg by Day 4.

Further adjustments can be made in increments of 25 to 50 mg twice a day, in intervals of not less than 2 days.

150 to 750 mg/day 750 mg/day Schizophrenia- Adolescents (13 to 17 years) Day 1: 25 mg twice daily.

Day 2: Twice daily dosing totaling 100 mg.

Day 3: Twice daily dosing totaling 200 mg.

Day 4: Twice daily dosing totaling 300 mg.

Day 5: Twice daily dosing totaling 400 mg.

Further adjustments should be in increments no greater than 100 mg/day within the recommended dose range of 400 to 800 mg/day.

Based on response and tolerability, may be administered three times daily.

400 to 800 mg/day 800 mg/day Schizophrenia-Maintenance N/A * 400 to 800 mg/day 800 mg/day Bipolar Mania- Adults Monotherapy or as an adjunct to lithium or divalproex Day 1: Twice daily dosing totaling 100 mg.

Day 2: Twice daily dosing totaling 200 mg.

Day 3: Twice daily dosing totaling 300 mg.

Day 4: Twice daily dosing totaling 400 mg.

Further dosage adjustments up to 800 mg/day by Day 6 should be in increments of no greater than 200 mg/day.

400 to 800 mg/day 800 mg/day Bipolar Mania-Children and Adolescents (10 to 17 years), Monotherapy Day 1: 25 mg twice daily.

Day 2: Twice daily dosing totaling 100 mg.

Day 3: Twice daily dosing totaling 200 mg.

Day 4: Twice daily dosing totaling 300 mg.

Day 5: Twice daily dosing totaling 400 mg.

Further adjustments should be in increments no greater than 100 mg/day within the recommended dose range of 400 to 600 mg/day.

Based on response and tolerability, may be administered three times daily.

400 to 600 mg/day 600 mg/day Bipolar Depression- Adults Administer once daily at bedtime.

Day 1: 50 mg Day 2: 100 mg Day 3: 200 mg Day 4: 300 mg 300 mg/day 300 mg/day Bipolar I Disorder Maintenance Therapy- Adults Administer twice daily totaling 400 to 800 mg/day as adjunct to lithium or divalproex.

Generally, in the maintenance phase, patients continued on the same dose on which they were stabilized.

400 to 800 mg/day 800 mg/day N/A Not applicable Maintenance Treatment for Schizophrenia and Bipolar I Disorder Maintenance Treatment —Patients should be periodically reassessed to determine the need for maintenance treatment and the appropriate dose for such treatment [see Clinical Studies (14.2)].

Consideration should be given to a slower rate of dose titration and a lower target dose in the elderly and in patients who are debilitated or who have a predisposition to hypotensive reactions [see Clinical Pharmacology (12.3)] .

When indicated, dose escalation should be performed with caution in these patients.

Elderly patients should be started on quetiapine fumarate tablets 50 mg/day and the dose can be increased in increments of 50 mg/day depending on the clinical response and tolerability of the individual patient .

Patients with hepatic impairment should be started on 25 mg/day.

The dose should be increased daily in increments of 25 mg/day to 50 mg/day to an effective dose, depending on the clinical response and tolerability of the patient.

Quetiapine fumarate tablets dose should be reduced to one sixth of original dose when co-medicated with a potent CYP3A4 inhibitor (e.g., ketoconazole, itraconazole, indinavir, ritonavir, nefazodone, etc.).

When the CYP3A4 inhibitor is discontinued, the dose of quetiapine fumarate tablets should be increased by 6 fold [see Clinical Pharmacology (12.3) and Drug Interactions (7.1)] .

Quetiapine fumarate tablets dose should be increased up to 5 fold of the original dose when used in combination with a chronic treatment (e.g., greater than 7 to 14 days) of a potent CYP3A4 inducer (e.g., phenytoin, carbamazepine, rifampin, avasimibe, St.

John’s wort etc.).

The dose should be titrated based on the clinical response and tolerability of the individual patient.

When the CYP3A4 inducer is discontinued, the dose of quetiapine fumarate tablets should be reduced to the original level within 7 to 14 days [see Clinical Pharmacology (12.3) and Drug Interactions (7.1)] .

Although there are no data to specifically address re-initiation of treatment, it is recommended that when restarting therapy of patients who have been off quetiapine fumarate tablets for more than one week, the initial dosing schedule should be followed.

When restarting patients who have been off quetiapine fumarate tablets for less than one week, gradual dose escalation may not be required and the maintenance dose may be reinitiated.

There are no systematically collected data to specifically address switching patients with schizophrenia from antipsychotics to quetiapine fumarate tablets, or concerning concomitant administration with antipsychotics.

While immediate discontinuation of the previous antipsychotic treatment may be acceptable for some patients with schizophrenia, more gradual discontinuation may be most appropriate for others.

In all cases, the period of overlapping antipsychotic administration should be minimized.

When switching patients with schizophrenia from depot antipsychotics, if medically appropriate, initiate quetiapine fumarate tablets therapy in place of the next scheduled injection.

The need for continuing existing EPS medication should be re-evaluated periodically.

DRUG INTERACTIONS

7 Due to CNS effects, use caution when administering with other centrally-acting drugs.

Avoid alcohol.

( 7.1 ) Due to hypotensive effects, hypotensive effects of other drugs with this potential may be enhanced.

( 7.2 ) Effects of levodopa and dopamine agonists may be antagonized.

( 7.3 ) Cimetidine and ranitidine increase the bioavailability of risperidone.

( 7.5 ) Clozapine may decrease clearance of risperidone.

( 7.6 ) Fluoxetine and paroxetine increase plasma concentrations of risperidone.

( 7.10 ) Carbamazepine and other enzyme inducers decrease plasma concentrations of risperidone.

( 7.11 ) 7.1 Centrally-Acting Drugs and Alcohol Given the primary CNS effects of risperidone, caution should be used when RISPERDAL ® is taken in combination with other centrally-acting drugs and alcohol.

7.2 Drugs with Hypotensive Effects Because of its potential for inducing hypotension, RISPERDAL ® may enhance the hypotensive effects of other therapeutic agents with this potential.

7.3 Levodopa and Dopamine Agonists RISPERDAL ® may antagonize the effects of levodopa and dopamine agonists.

7.4 Amitriptyline Amitriptyline did not affect the pharmacokinetics of risperidone or risperidone and 9-hydroxyrisperidone combined.

7.5 Cimetidine and Ranitidine Cimetidine and ranitidine increased the bioavailability of risperidone by 64% and 26%, respectively.

However, cimetidine did not affect the AUC of risperidone and 9-hydroxyrisperidone combined, whereas ranitidine increased the AUC of risperidone and 9-hydroxyrisperidone combined by 20%.

7.6 Clozapine Chronic administration of clozapine with RISPERDAL ® may decrease the clearance of risperidone.

7.7 Lithium Repeated oral doses of RISPERDAL ® (3 mg twice daily) did not affect the exposure (AUC) or peak plasma concentrations (C max ) of lithium (n=13).

7.8 Valproate Repeated oral doses of RISPERDAL ® (4 mg once daily) did not affect the pre-dose or average plasma concentrations and exposure (AUC) of valproate (1000 mg/day in three divided doses) compared to placebo (n=21).

However, there was a 20% increase in valproate peak plasma concentration (C max ) after concomitant administration of RISPERDAL ® .

7.9 Digoxin RISPERDAL ® (0.25 mg twice daily) did not show a clinically relevant effect on the pharmacokinetics of digoxin.

7.10 Drugs That Inhibit CYP 2D6 and Other CYP Isozymes Risperidone is metabolized to 9-hydroxyrisperidone by CYP 2D6, an enzyme that is polymorphic in the population and that can be inhibited by a variety of psychotropic and other drugs [see Clinical Pharmacology (12.3) ] .

Drug interactions that reduce the metabolism of risperidone to 9-hydroxyrisperidone would increase the plasma concentrations of risperidone and lower the concentrations of 9-hydroxyrisperidone.

Analysis of clinical studies involving a modest number of poor metabolizers (n≅70) does not suggest that poor and extensive metabolizers have different rates of adverse effects.

No comparison of effectiveness in the two groups has been made.

In vitro studies showed that drugs metabolized by other CYP isozymes, including 1A1, 1A2, 2C9, 2C19, and 3A4, are only weak inhibitors of risperidone metabolism.

Fluoxetine and Paroxetine Fluoxetine (20 mg once daily) and paroxetine (20 mg once daily) have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

When either concomitant fluoxetine or paroxetine is initiated or discontinued, the physician should re-evaluate the dosing of RISPERDAL ® .

The effects of discontinuation of concomitant fluoxetine or paroxetine therapy on the pharmacokinetics of risperidone and 9-hydroxyrisperidone have not been studied.

Erythromycin There were no significant interactions between RISPERDAL ® and erythromycin.

7.11 Carbamazepine and Other Enzyme Inducers Carbamazepine co-administration decreased the steady-state plasma concentrations of risperidone and 9-hydroxyrisperidone by about 50%.

Plasma concentrations of carbamazepine did not appear to be affected.

The dose of RISPERDAL ® may need to be titrated accordingly for patients receiving carbamazepine, particularly during initiation or discontinuation of carbamazepine therapy.

Co-administration of other known enzyme inducers (e.g., phenytoin, rifampin, and phenobarbital) with RISPERDAL ® may cause similar decreases in the combined plasma concentrations of risperidone and 9-hydroxyrisperidone, which could lead to decreased efficacy of RISPERDAL ® treatment.

7.12 Drugs Metabolized by CYP 2D6 In vitro studies indicate that risperidone is a relatively weak inhibitor of CYP 2D6.

Therefore, RISPERDAL ® is not expected to substantially inhibit the clearance of drugs that are metabolized by this enzymatic pathway.

In drug interaction studies, RISPERDAL ® did not significantly affect the pharmacokinetics of donepezil and galantamine, which are metabolized by CYP 2D6.

OVERDOSAGE

10 10.1 Human Experience Premarketing experience included eight reports of acute RISPERDAL ® overdosage with estimated doses ranging from 20 to 300 mg and no fatalities.

In general, reported signs and symptoms were those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness and sedation, tachycardia and hypotension, and extrapyramidal symptoms.

One case, involving an estimated overdose of 240 mg, was associated with hyponatremia, hypokalemia, prolonged QT, and widened QRS.

Another case, involving an estimated overdose of 36 mg, was associated with a seizure.

Postmarketing experience includes reports of acute RISPERDAL ® overdosage, with estimated doses of up to 360 mg.

In general, the most frequently reported signs and symptoms are those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness, sedation, tachycardia, hypotension, and extrapyramidal symptoms.

Other adverse reactions reported since market introduction related to RISPERDAL ® overdose include prolonged QT interval and convulsions.

Torsade de pointes has been reported in association with combined overdose of RISPERDAL ® and paroxetine.

10.2 Management of Overdosage In case of acute overdosage, establish and maintain an airway and ensure adequate oxygenation and ventilation.

Gastric lavage (after intubation, if patient is unconscious) and administration of activated charcoal together with a laxative should be considered.

Because of the rapid disintegration of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets, pill fragments may not appear in gastric contents obtained with lavage.

The possibility of obtundation, seizures, or dystonic reaction of the head and neck following overdose may create a risk of aspiration with induced emesis.

Cardiovascular monitoring should commence immediately and should include continuous electrocardiographic monitoring to detect possible arrhythmias.

If antiarrhythmic therapy is administered, disopyramide, procainamide, and quinidine carry a theoretical hazard of QT-prolonging effects that might be additive to those of risperidone.

Similarly, it is reasonable to expect that the alpha-blocking properties of bretylium might be additive to those of risperidone, resulting in problematic hypotension.

There is no specific antidote to RISPERDAL ® .

Therefore, appropriate supportive measures should be instituted.

The possibility of multiple drug involvement should be considered.

Hypotension and circulatory collapse should be treated with appropriate measures, such as intravenous fluids and/or sympathomimetic agents (epinephrine and dopamine should not be used, since beta stimulation may worsen hypotension in the setting of risperidone-induced alpha blockade).

In cases of severe extrapyramidal symptoms, anticholinergic medication should be administered.

Close medical supervision and monitoring should continue until the patient recovers.

DESCRIPTION

11 RISPERDAL ® contains risperidone, a psychotropic agent belonging to the chemical class of benzisoxazole derivatives.

The chemical designation is 3-[2-[4-(6-fluoro-1,2-benzisoxazol-3-yl)-1-piperidinyl]ethyl]-6,7,8,9-tetrahydro-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one.

Its molecular formula is C 23 H 27 FN 4 O 2 and its molecular weight is 410.49.

The structural formula is: Risperidone is a white to slightly beige powder.

It is practically insoluble in water, freely soluble in methylene chloride, and soluble in methanol and 0.1 N HCl.

RISPERDAL ® Tablets are available in 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green) strengths.

RISPERDAL ® tablets contain the following inactive ingredients: colloidal silicon dioxide, hypromellose, lactose, magnesium stearate, microcrystalline cellulose, propylene glycol, sodium lauryl sulfate, and starch (corn).

The 0.25 mg, 0.5 mg, 2 mg, 3 mg, and 4 mg tablets also contain talc and titanium dioxide.

The 0.25 mg tablets contain yellow iron oxide; the 0.5 mg tablets contain red iron oxide; the 2 mg tablets contain FD&C Yellow No.

6 Aluminum Lake; the 3 mg and 4 mg tablets contain D&C Yellow No.

10; the 4 mg tablets contain FD&C Blue No.

2 Aluminum Lake.

RISPERDAL ® is also available as a 1 mg/mL oral solution.

RISPERDAL ® Oral Solution contains the following inactive ingredients: tartaric acid, benzoic acid, sodium hydroxide, and purified water.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in 0.5 mg (light coral), 1 mg (light coral), 2 mg (coral), 3 mg (coral), and 4 mg (coral) strengths.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain the following inactive ingredients: Amberlite ® resin, gelatin, mannitol, glycine, simethicone, carbomer, sodium hydroxide, aspartame, red ferric oxide, and peppermint oil.

In addition, the 2 mg, 3 mg, and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain xanthan gum.

Chemical Structure

CLINICAL STUDIES

14 14.1 Schizophrenia Adults Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of schizophrenia was established in four short-term (4- to 8-week) controlled trials of psychotic inpatients who met DSM-III-R criteria for schizophrenia.

Several instruments were used for assessing psychiatric signs and symptoms in these studies, among them the Brief Psychiatric Rating Scale (BPRS), a multi-item inventory of general psychopathology traditionally used to evaluate the effects of drug treatment in schizophrenia.

The BPRS psychosis cluster (conceptual disorganization, hallucinatory behavior, suspiciousness, and unusual thought content) is considered a particularly useful subset for assessing actively psychotic schizophrenic patients.

A second traditional assessment, the Clinical Global Impression (CGI), reflects the impression of a skilled observer, fully familiar with the manifestations of schizophrenia, about the overall clinical state of the patient.

In addition, the Positive and Negative Syndrome Scale (PANSS) and the Scale for Assessing Negative Symptoms (SANS) were employed.

The results of the trials follow: (1)In a 6-week, placebo-controlled trial (n=160) involving titration of RISPERDAL ® in doses up to 10 mg/day (twice-daily schedule), RISPERDAL ® was generally superior to placebo on the BPRS total score, on the BPRS psychosis cluster, and marginally superior to placebo on the SANS.

(2)In an 8-week, placebo-controlled trial (n=513) involving 4 fixed doses of RISPERDAL ® (2 mg/day, 6 mg/day, 10 mg/day, and 16 mg/day, on a twice-daily schedule), all 4 RISPERDAL ® groups were generally superior to placebo on the BPRS total score, BPRS psychosis cluster, and CGI severity score; the 3 highest RISPERDAL ® dose groups were generally superior to placebo on the PANSS negative subscale.

The most consistently positive responses on all measures were seen for the 6 mg dose group, and there was no suggestion of increased benefit from larger doses.

(3)In an 8-week, dose comparison trial (n=1356) involving 5 fixed doses of RISPERDAL ® (1 mg/day, 4 mg/day, 8 mg/day, 12 mg/day, and 16 mg/day, on a twice-daily schedule), the four highest RISPERDAL ® dose groups were generally superior to the 1 mg RISPERDAL ® dose group on BPRS total score, BPRS psychosis cluster, and CGI severity score.

None of the dose groups were superior to the 1 mg group on the PANSS negative subscale.

The most consistently positive responses were seen for the 4 mg dose group.

(4)In a 4-week, placebo-controlled dose comparison trial (n=246) involving 2 fixed doses of RISPERDAL ® (4 and 8 mg/day on a once-daily schedule), both RISPERDAL ® dose groups were generally superior to placebo on several PANSS measures, including a response measure (>20% reduction in PANSS total score), PANSS total score, and the BPRS psychosis cluster (derived from PANSS).

The results were generally stronger for the 8 mg than for the 4 mg dose group.

Long-Term Efficacy In a longer-term trial, 365 adult outpatients predominantly meeting DSM-IV criteria for schizophrenia and who had been clinically stable for at least 4 weeks on an antipsychotic medication were randomized to RISPERDAL ® (2–8 mg/day) or to an active comparator, for 1 to 2 years of observation for relapse.

Patients receiving RISPERDAL ® experienced a significantly longer time to relapse over this time period compared to those receiving the active comparator.

Pediatrics The efficacy of RISPERDAL ® in the treatment of schizophrenia in adolescents aged 13–17 years was demonstrated in two short-term (6 and 8 weeks), double-blind controlled trials.

All patients met DSM-IV diagnostic criteria for schizophrenia and were experiencing an acute episode at time of enrollment.

In the first trial (study #1), patients were randomized into one of three treatment groups: RISPERDAL ® 1–3 mg/day (n = 55, mean modal dose = 2.6 mg), RISPERDAL ® 4–6 mg/day (n = 51, mean modal dose = 5.3 mg), or placebo (n = 54).

In the second trial (study #2), patients were randomized to either RISPERDAL ® 0.15–0.6 mg/day (n = 132, mean modal dose = 0.5 mg) or RISPERDAL ® 1.5–6 mg/day (n = 125, mean modal dose = 4 mg).

In all cases, study medication was initiated at 0.5 mg/day (with the exception of the 0.15–0.6 mg/day group in study #2, where the initial dose was 0.05 mg/day) and titrated to the target dosage range by approximately Day 7.

Subsequently, dosage was increased to the maximum tolerated dose within the target dose range by Day 14.

The primary efficacy variable in all studies was the mean change from baseline in total PANSS score.

Results of the studies demonstrated efficacy of RISPERDAL ® in all dose groups from 1–6 mg/day compared to placebo, as measured by significant reduction of total PANSS score.

The efficacy on the primary parameter in the 1–3 mg/day group was comparable to the 4–6 mg/day group in study #1, and similar to the efficacy demonstrated in the 1.5–6 mg/day group in study #2.

In study #2, the efficacy in the 1.5–6 mg/day group was statistically significantly greater than that in the 0.15–0.6 mg/day group.

Doses higher than 3 mg/day did not reveal any trend towards greater efficacy.

14.2 Bipolar Mania – Monotherapy Adults The efficacy of RISPERDAL ® in the treatment of acute manic or mixed episodes was established in two short-term (3-week) placebo-controlled trials in patients who met the DSM-IV criteria for Bipolar I Disorder with manic or mixed episodes.

These trials included patients with or without psychotic features.

The primary rating instrument used for assessing manic symptoms in these trials was the Young Mania Rating Scale (YMRS), an 11-item clinician-rated scale traditionally used to assess the degree of manic symptomatology (irritability, disruptive/aggressive behavior, sleep, elevated mood, speech, increased activity, sexual interest, language/thought disorder, thought content, appearance, and insight) in a range from 0 (no manic features) to 60 (maximum score).

The primary outcome in these trials was change from baseline in the YMRS total score.

The results of the trials follow: (1)In one 3-week placebo-controlled trial (n=246), limited to patients with manic episodes, which involved a dose range of RISPERDAL ® 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 4.1 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

(2)In another 3-week placebo-controlled trial (n=286), which involved a dose range of 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 5.6 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

Pediatrics The efficacy of RISPERDAL ® in the treatment of mania in children or adolescents with Bipolar I disorder was demonstrated in a 3-week, randomized, double-blind, placebo-controlled, multicenter trial including patients ranging in ages from 10 to 17 years who were experiencing a manic or mixed episode of bipolar I disorder.

Patients were randomized into one of three treatment groups: RISPERDAL ® 0.5–2.5 mg/day (n = 50, mean modal dose = 1.9 mg), RISPERDAL ® 3–6 mg/day (n = 61, mean modal dose = 4.7 mg), or placebo (n = 58).

In all cases, study medication was initiated at 0.5 mg/day and titrated to the target dosage range by Day 7, with further increases in dosage to the maximum tolerated dose within the targeted dose range by Day 10.

The primary rating instrument used for assessing efficacy in this study was the mean change from baseline in the total YMRS score.

Results of this study demonstrated efficacy of RISPERDAL ® in both dose groups compared with placebo, as measured by significant reduction of total YMRS score.

The efficacy on the primary parameter in the 3–6 mg/day dose group was comparable to the 0.5–2.5 mg/day dose group.

Doses higher than 2.5 mg/day did not reveal any trend towards greater efficacy.

14.3 Bipolar Mania – Combination Therapy The efficacy of RISPERDAL ® with concomitant lithium or valproate in the treatment of acute manic or mixed episodes was established in one controlled trial in adult patients who met the DSM-IV criteria for Bipolar I Disorder.

This trial included patients with or without psychotic features and with or without a rapid-cycling course.

(1)In this 3-week placebo-controlled combination trial, 148 in- or outpatients on lithium or valproate therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® , placebo, or an active comparator, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.8 mg/day), combined with lithium or valproate (in a therapeutic range of 0.6 mEq/L to 1.4 mEq/L or 50 mcg/mL to 120 mcg/mL, respectively) was superior to lithium or valproate alone in the reduction of YMRS total score.

(2)In a second 3-week placebo-controlled combination trial, 142 in- or outpatients on lithium, valproate, or carbamazepine therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® or placebo, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.7 mg/day), combined with lithium, valproate, or carbamazepine (in therapeutic ranges of 0.6 mEq/L to 1.4 mEq/L for lithium, 50 mcg/mL to 125 mcg/mL for valproate, or 4–12 mcg/mL for carbamazepine, respectively) was not superior to lithium, valproate, or carbamazepine alone in the reduction of YMRS total score.

A possible explanation for the failure of this trial was induction of risperidone and 9-hydroxyrisperidone clearance by carbamazepine, leading to subtherapeutic levels of risperidone and 9-hydroxyrisperidone.

14.4 Irritability Associated with Autistic Disorder Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of irritability associated with autistic disorder was established in two 8-week, placebo-controlled trials in children and adolescents (aged 5 to 16 years) who met the DSM-IV criteria for autistic disorder.

Over 90% of these subjects were under 12 years of age and most weighed over 20 kg (16–104.3 kg).

Efficacy was evaluated using two assessment scales: the Aberrant Behavior Checklist (ABC) and the Clinical Global Impression – Change (CGI-C) scale.

The primary outcome measure in both trials was the change from baseline to endpoint in the Irritability subscale of the ABC (ABC-I).

The ABC-I subscale measured the emotional and behavioral symptoms of autism, including aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods.

The CGI-C rating at endpoint was a co-primary outcome measure in one of the studies.

The results of these trials are as follows: (1)In one of the 8-week, placebo-controlled trials, children and adolescents with autistic disorder (n=101), aged 5 to 16 years, received twice daily doses of placebo or RISPERDAL ® 0.5–3.5 mg/day on a weight-adjusted basis.

RISPERDAL ® , starting at 0.25 mg/day or 0.5 mg/day depending on baseline weight (< 20 kg and ≥ 20 kg, respectively) and titrated to clinical response (mean modal dose of 1.9 mg/day, equivalent to 0.06 mg/kg/day), significantly improved scores on the ABC-I subscale and on the CGI-C scale compared with placebo.

(2)In the other 8-week, placebo-controlled trial in children with autistic disorder (n=55), aged 5 to 12 years, RISPERDAL ® 0.02 to 0.06 mg/kg/day given once or twice daily, starting at 0.01 mg/kg/day and titrated to clinical response (mean modal dose of 0.05 mg/kg/day, equivalent to 1.4 mg/day), significantly improved scores on the ABC-I subscale compared with placebo.

Long-Term Efficacy Following completion of the first 8-week double-blind study, 63 patients entered an open-label study extension where they were treated with RISPERDAL ® for 4 or 6 months (depending on whether they received RISPERDAL ® or placebo in the double-blind study).

During this open-label treatment period, patients were maintained on a mean modal dose of RISPERDAL ® of 1.8–2.1 mg/day (equivalent to 0.05 – 0.07 mg/kg/day).

Patients who maintained their positive response to RISPERDAL ® (response was defined as ≥ 25% improvement on the ABC-I subscale and a CGI-C rating of ‘much improved’ or ‘very much improved’) during the 4–6 month open-label treatment phase for about 140 days, on average, were randomized to receive RISPERDAL ® or placebo during an 8-week, double-blind withdrawal study (n=39 of the 63 patients).

A pre-planned interim analysis of data from patients who completed the withdrawal study (n=32), undertaken by an independent Data Safety Monitoring Board, demonstrated a significantly lower relapse rate in the RISPERDAL ® group compared with the placebo group.

Based on the interim analysis results, the study was terminated due to demonstration of a statistically significant effect on relapse prevention.

Relapse was defined as ≥ 25% worsening on the most recent assessment of the ABC-I subscale (in relation to baseline of the randomized withdrawal phase).

HOW SUPPLIED

16 /STORAGE AND HANDLING RISPERDAL ® (risperidone) Tablets RISPERDAL ® (risperidone) Tablets are imprinted ” JANSSEN ” on one side and either “R1”, or “R3” according to their respective strengths.

1 mg white, capsule-shaped tablets: bottles of 15 NDC 21695-113-15 3 mg yellow, capsule-shaped tablets: bottles of 30 NDC 21695-115-30 and bottles of 60 NDC 21695-113-60.

Storage and Handling RISPERDAL ® Tablets should be stored at controlled room temperature 15°–25°C (59°–77°F).

Protect from light and moisture.

Keep out of reach of children.

RECENT MAJOR CHANGES

Warnings and Precautions, Leukopenia, Neutropenia, and Agranulocytosis ( 5.8 ) 07/2009

GERIATRIC USE

8.5 Geriatric Use Clinical studies of RISPERDAL ® in the treatment of schizophrenia did not include sufficient numbers of patients aged 65 and over to determine whether or not they respond differently than younger patients.

Other reported clinical experience has not identified differences in responses between elderly and younger patients.

In general, a lower starting dose is recommended for an elderly patient, reflecting a decreased pharmacokinetic clearance in the elderly, as well as a greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy [see Clinical Pharmacology (12.3) and Dosage and Administration (2.4 , 2.5) ] .

While elderly patients exhibit a greater tendency to orthostatic hypotension, its risk in the elderly may be minimized by limiting the initial dose to 0.5 mg twice daily followed by careful titration [see Warnings and Precautions (5.7) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

This drug is substantially excreted by the kidneys, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.

Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see Dosage and Administration (2.4) ] .

Concomitant use with Furosemide in Elderly Patients with Dementia-Related Psychosis In two of four placebo-controlled trials in elderly patients with dementia-related psychosis, a higher incidence of mortality was observed in patients treated with furosemide plus RISPERDAL ® when compared to patients treated with RISPERDAL ® alone or with placebo plus furosemide.

No pathological mechanism has been identified to explain this finding, and no consistent pattern for cause of death was observed.

An increase of mortality in elderly patients with dementia-related psychosis was seen with the use of RISPERDAL ® regardless of concomitant use with furosemide.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See Boxed Warning and Warnings and Precautions (5.1) ]

DOSAGE FORMS AND STRENGTHS

3 RISPERDAL ® Tablets are available in the following strengths and colors: 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green).

All are capsule shaped, and imprinted with “JANSSEN” on one side and either “Ris 0.25”, “Ris 0.5”, “R1”, “R2”, “R3”, or “R4” on the other side according to their respective strengths.

RISPERDAL ® Oral Solution is available in a 1 mg/mL strength.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in the following strengths, colors, and shapes: 0.5 mg (light coral, round), 1 mg (light coral, square), 2 mg (coral, square), 3 mg (coral, round), and 4 mg (coral, round).

All are biconvex and etched on one side with “R0.5”, “R1”, “R2”, “R3”, or “R4” according to their respective strengths.

Tablets: 0.25 mg, 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 ) Oral solution: 1 mg/mL ( 3 ) Orally disintegrating tablets: 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of action of RISPERDAL ® , as with other drugs used to treat schizophrenia, is unknown.

However, it has been proposed that the drug’s therapeutic activity in schizophrenia is mediated through a combination of dopamine Type 2 (D 2 ) and serotonin Type 2 (5HT 2 ) receptor antagonism.

RISPERDAL ® is a selective monoaminergic antagonist with high affinity (Ki of 0.12 to 7.3 nM) for the serotonin Type 2 (5HT 2 ), dopamine Type 2 (D 2 ), α 1 and α 2 adrenergic, and H 1 histaminergic receptors.

RISPERDAL ® acts as an antagonist at other receptors, but with lower potency.

RISPERDAL ® has low to moderate affinity (Ki of 47 to 253 nM) for the serotonin 5HT 1C , 5HT 1D , and 5HT 1A receptors, weak affinity (Ki of 620 to 800 nM) for the dopamine D 1 and haloperidol-sensitive sigma site, and no affinity (when tested at concentrations >10 -5 M) for cholinergic muscarinic or β 1 and β 2 adrenergic receptors.

INDICATIONS AND USAGE

1 RISPERDAL® is an atypical antipsychotic agent indicated for: Treatment of schizophrenia in adults and adolescents aged 13–17 years ( 1.1 ) Alone, or in combination with lithium or valproate, for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults, and alone in children and adolescents aged 10–17 years ( 1.2 ) Treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years ( 1.3 ) 1.1 Schizophrenia Adults RISPERDAL ® (risperidone) is indicated for the acute and maintenance treatment of schizophrenia [see Clinical Studies (14.1) ] .

Adolescents RISPERDAL ® is indicated for the treatment of schizophrenia in adolescents aged 13–17 years [see Clinical Studies (14.1) ] .

1.2 Bipolar Mania Monotherapy – Adults and Pediatrics RISPERDAL ® is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults and in children and adolescents aged 10–17 years [see Clinical Studies (14.2) ] .

Combination Therapy – Adults The combination of RISPERDAL ® with lithium or valproate is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder [ see Clinical Studies (14.3) ] .

1.3 Irritability Associated with Autistic Disorder Pediatrics RISPERDAL ® is indicated for the treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years, including symptoms of aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods [see Clinical Studies (14.4) ] .

PEDIATRIC USE

8.4 Pediatric Use The efficacy and safety of RISPERDAL ® in the treatment of schizophrenia were demonstrated in 417 adolescents, aged 13 – 17 years, in two short-term (6 and 8 weeks, respectively) double-blind controlled trials [see Indications and Usage (1.1) , Adverse Reactions (6.1) , and Clinical Studies (14.1) ].

Additional safety and efficacy information was also assessed in one long-term (6-month) open-label extension study in 284 of these adolescent patients with schizophrenia.

Safety and effectiveness of RISPERDAL ® in children less than 13 years of age with schizophrenia have not been established.

The efficacy and safety of RISPERDAL ® in the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in 169 children and adolescent patients, aged 10 – 17 years, were demonstrated in one double-blind, placebo-controlled, 3-week trial [see Indications and Usage (1.2) , Adverse Reactions (6.2) , and Clinical Studies (14.2) ] .

Safety and effectiveness of RISPERDAL ® in children less than 10 years of age with bipolar disorder have not been established.

The efficacy and safety of RISPERDAL ® in the treatment of irritability associated with autistic disorder were established in two 8-week, double-blind, placebo-controlled trials in 156 children and adolescent patients, aged 5 to 16 years [see Indications and Usage (1.3) , Adverse Reactions (6.3) and Clinical Studies (14.4) ] .

Additional safety information was also assessed in a long-term study in patients with autistic disorder, or in short- and long-term studies in more than 1200 pediatric patients with psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania who were of similar age and weight, and who received similar dosages of RISPERDAL ® as patients treated for irritability associated with autistic disorder.

The safety and effectiveness of RISPERDAL ® in pediatric patients less than 5 years of age with autistic disorder have not been established.

Tardive Dyskinesia In clinical trials in 1885 children and adolescents treated with RISPERDAL ® , 2 (0.1%) patients were reported to have tardive dyskinesia, which resolved on discontinuation of RISPERDAL ® treatment [see also Warnings and Precautions (5.4) ] .

Weight Gain In a long-term, open-label extension study in adolescent patients with schizophrenia, weight increase was reported as a treatment-emergent adverse event in 14% of patients.

In 103 adolescent patients with schizophrenia, a mean increase of 9.0 kg was observed after 8 months of RISPERDAL ® treatment.

The majority of that increase was observed within the first 6 months.

The average percentiles at baseline and 8 months, respectively, were 56 and 72 for weight, 55 and 58 for height, and 51 and 71 for body mass index.

In long-term, open-label trials (studies in patients with autistic disorder or other psychiatric disorders), a mean increase of 7.5 kg after 12 months of RISPERDAL ® treatment was observed, which was higher than the expected normal weight gain (approximately 3 to 3.5 kg per year adjusted for age, based on Centers for Disease Control and Prevention normative data).

The majority of that increase occurred within the first 6 months of exposure to RISPERDAL ® .

The average percentiles at baseline and 12 months, respectively, were 49 and 60 for weight, 48 and 53 for height, and 50 and 62 for body mass index.

In one 3-week, placebo-controlled trial in children and adolescent patients with acute manic or mixed episodes of bipolar I disorder, increases in body weight were higher in the RISPERDAL ® groups than the placebo group, but not dose related (1.90 kg in the RISPERDAL ® 0.5–2.5 mg group, 1.44 kg in the RISPERDAL ® 3–6 mg group, and 0.65 kg in the placebo group).

A similar trend was observed in the mean change from baseline in body mass index.

When treating pediatric patients with RISPERDAL ® for any indication, weight gain should be assessed against that expected with normal growth.

[See also Adverse Reactions (6.7) ] Somnolence Somnolence was frequently observed in placebo-controlled clinical trials of pediatric patients with autistic disorder.

Most cases were mild or moderate in severity.

These events were most often of early onset with peak incidence occurring during the first two weeks of treatment, and transient with a median duration of 16 days.

Somnolence was the most commonly observed adverse event in the clinical trial of bipolar disorder in children and adolescents, as well as in the schizophrenia trials in adolescents.

As was seen in the autistic disorder trials, these events were most often of early onset and transient in duration.

[See also Adverse Reactions (6.1 , 6.2 , 6.3) ] Patients experiencing persistent somnolence may benefit from a change in dosing regimen [ see Dosage and Administration (2.1 , 2.2 , 2.3) ] .

Hyperprolactinemia, Growth, and Sexual Maturation RISPERDAL ® has been shown to elevate prolactin levels in children and adolescents as well as in adults [se e Warnings and Precautions (5.6) ] .

In double-blind, placebo-controlled studies of up to 8 weeks duration in children and adolescents (aged 5 to 17 years) with autistic disorder or psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania, 49% of patients who received RISPERDAL ® had elevated prolactin levels compared to 2% of patients who received placebo.

Similarly, in placebo-controlled trials in children and adolescents (aged 10 to 17 years) with bipolar disorder, or adolescents (aged 13 to 17 years) with schizophrenia, 82–87% of patients who received RISPERDAL ® had elevated levels of prolactin compared to 3–7% of patients on placebo.

Increases were dose-dependent and generally greater in females than in males across indications.

In clinical trials in 1885 children and adolescents, galactorrhea was reported in 0.8% of RISPERDAL ® -treated patients and gynecomastia was reported in 2.3% of RISPERDAL ® -treated patients.

The long-term effects of RISPERDAL ® on growth and sexual maturation have not been fully evaluated.

PREGNANCY

8.1 Pregnancy Pregnancy Category C.

The teratogenic potential of risperidone was studied in three Segment II studies in Sprague-Dawley and Wistar rats (0.63–10 mg/kg or 0.4 to 6 times the maximum recommended human dose [MRHD] on a mg/m 2 basis) and in one Segment II study in New Zealand rabbits (0.31–5 mg/kg or 0.4 to 6 times the MRHD on a mg/m 2 basis).

The incidence of malformations was not increased compared to control in offspring of rats or rabbits given 0.4 to 6 times the MRHD on a mg/m 2 basis.

In three reproductive studies in rats (two Segment III and a multigenerational study), there was an increase in pup deaths during the first 4 days of lactation at doses of 0.16–5 mg/kg or 0.1 to 3 times the MRHD on a mg/m 2 basis.

It is not known whether these deaths were due to a direct effect on the fetuses or pups or to effects on the dams.

There was no no-effect dose for increased rat pup mortality.

In one Segment III study, there was an increase in stillborn rat pups at a dose of 2.5 mg/kg or 1.5 times the MRHD on a mg/m 2 basis.

In a cross-fostering study in Wistar rats, toxic effects on the fetus or pups, as evidenced by a decrease in the number of live pups and an increase in the number of dead pups at birth (Day 0), and a decrease in birth weight in pups of drug-treated dams were observed.

In addition, there was an increase in deaths by Day 1 among pups of drug-treated dams, regardless of whether or not the pups were cross-fostered.

Risperidone also appeared to impair maternal behavior in that pup body weight gain and survival (from Day 1 to 4 of lactation) were reduced in pups born to control but reared by drug-treated dams.

These effects were all noted at the one dose of risperidone tested, i.e., 5 mg/kg or 3 times the MRHD on a mg/m 2 basis.

Placental transfer of risperidone occurs in rat pups.

There are no adequate and well-controlled studies in pregnant women.

However, there was one report of a case of agenesis of the corpus callosum in an infant exposed to risperidone in utero .

The causal relationship to RISPERDAL ® therapy is unknown.

Reversible extrapyramidal symptoms in the neonate were observed following postmarketing use of RISPERDAL ® during the last trimester of pregnancy.

RISPERDAL ® should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

NUSRING MOTHERS

8.3 Nursing Mothers In animal studies, risperidone and 9-hydroxyrisperidone are excreted in milk.

Risperidone and 9-hydroxyrisperidone are also excreted in human breast milk.

Therefore, women receiving RISPERDAL ® should not breast-feed.

BOXED WARNING

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

Analyses of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients.

Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature.

Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.

The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear.

RISPERDAL ® (risperidone) is not approved for the treatment of patients with dementia-related psychosis.

[See Warnings and Precautions (5.1) ] WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS See full prescribing information for complete boxed warning.

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis.

( 5.1 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Cerebrovascular events, including stroke, in elderly patients with dementia-related psychosis.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis ( 5.2 ) Neuroleptic Malignant Syndrome ( 5.3 ) Tardive dyskinesia ( 5.4 ) Hyperglycemia and diabetes mellitus ( 5.5 ) Hyperprolactinemia ( 5.6 ) Orthostatic hypotension ( 5.7 ) Leukopenia, Neutropenia, and Agranulocytosis: has been reported with antipsychotics, including risperidone.

Patients with a history of a clinically significant low white blood cell count (WBC) or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

( 5.8 ) Potential for cognitive and motor impairment ( 5.9 ) Seizures ( 5.10 ) Dysphagia ( 5.11 ) Priapism ( 5.12 ) Thrombotic Thrombocytopenic Purpura (TTP) ( 5.13 ) Disruption of body temperature regulation ( 5.14 ) Antiemetic Effect ( 5.15 ) Suicide ( 5.16 ) Increased sensitivity in patients with Parkinson’s disease or those with dementia with Lewy bodies ( 5.17 ) Diseases or conditions that could affect metabolism or hemodynamic responses ( 5.17 ) 5.1 Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® (risperidone) is not approved for the treatment of dementia-related psychosis [see Boxed Warning ] .

5.2 Cerebrovascular Adverse Events, Including Stroke, in Elderly Patients with Dementia-Related Psychosis Cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, were reported in patients (mean age 85 years; range 73–97) in trials of risperidone in elderly patients with dementia-related psychosis.

In placebo-controlled trials, there was a significantly higher incidence of cerebrovascular adverse events in patients treated with risperidone compared to patients treated with placebo.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See also Boxed Warnings and Warnings and Precautions (5.1) ] 5.3 Neuroleptic Malignant Syndrome (NMS) A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with antipsychotic drugs.

Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).

Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis), and acute renal failure.

The diagnostic evaluation of patients with this syndrome is complicated.

In arriving at a diagnosis, it is important to identify cases in which the clinical presentation includes both serious medical illness (e.g., pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and symptoms (EPS).

Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever, and primary central nervous system pathology.

The management of NMS should include: (1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; (2) intensive symptomatic treatment and medical monitoring; and (3) treatment of any concomitant serious medical problems for which specific treatments are available.

There is no general agreement about specific pharmacological treatment regimens for uncomplicated NMS.

If a patient requires antipsychotic drug treatment after recovery from NMS, the potential reintroduction of drug therapy should be carefully considered.

The patient should be carefully monitored, since recurrences of NMS have been reported.

5.4 Tardive Dyskinesia A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs.

Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.

Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.

The risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase.

However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses.

There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.

Antipsychotic treatment, itself, however, may suppress (or partially suppress) the signs and symptoms of the syndrome and thereby may possibly mask the underlying process.

The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown.

Given these considerations, RISPERDAL ® should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.

Chronic antipsychotic treatment should generally be reserved for patients who suffer from a chronic illness that: (1) is known to respond to antipsychotic drugs, and (2) for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.

In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

The need for continued treatment should be reassessed periodically.

If signs and symptoms of tardive dyskinesia appear in a patient treated with RISPERDAL ® , drug discontinuation should be considered.

However, some patients may require treatment with RISPERDAL ® despite the presence of the syndrome.

5.5 Hyperglycemia and Diabetes Mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics including RISPERDAL ® .

Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population.

Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse events is not completely understood.

However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse events in patients treated with the atypical antipsychotics.

Precise risk estimates for hyperglycemia-related adverse events in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics should be monitored regularly for worsening of glucose control.

Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment.

Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should undergo fasting blood glucose testing.

In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of the suspect drug.

5.6 Hyperprolactinemia As with other drugs that antagonize dopamine D 2 receptors, RISPERDAL ® elevates prolactin levels and the elevation persists during chronic administration.

RISPERDAL ® is associated with higher levels of prolactin elevation than other antipsychotic agents.

Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion.

This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is contemplated in a patient with previously detected breast cancer.

An increase in pituitary gland, mammary gland, and pancreatic islet cell neoplasia (mammary adenocarcinomas, pituitary and pancreatic adenomas) was observed in the risperidone carcinogenicity studies conducted in mice and rats [see Non-Clinical Toxicology (13.1) ] .

Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans; the available evidence is considered too limited to be conclusive at this time.

5.7 Orthostatic Hypotension RISPERDAL ® may induce orthostatic hypotension associated with dizziness, tachycardia, and in some patients, syncope, especially during the initial dose-titration period, probably reflecting its alpha-adrenergic antagonistic properties.

Syncope was reported in 0.2% (6/2607) of RISPERDAL ® -treated patients in Phase 2 and 3 studies in adults with schizophrenia.

The risk of orthostatic hypotension and syncope may be minimized by limiting the initial dose to 2 mg total (either once daily or 1 mg twice daily) in normal adults and 0.5 mg twice daily in the elderly and patients with renal or hepatic impairment [see Dosage and Administration (2.1 , 2.4) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

A dose reduction should be considered if hypotension occurs.

RISPERDAL ® should be used with particular caution in patients with known cardiovascular disease (history of myocardial infarction or ischemia, heart failure, or conduction abnormalities), cerebrovascular disease, and conditions which would predispose patients to hypotension, e.g., dehydration and hypovolemia.

Clinically significant hypotension has been observed with concomitant use of RISPERDAL ® and antihypertensive medication.

5.8 Leukopenia, Neutropenia, and Agranulocytosis Class Effect: In clinical trial and/or postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to antipsychotic agents, including RISPERDAL ® .

Agranulocytosis has also been reported.

Possible risk factors for leukopenia/neutropenia include pre-existing low white blood cell count (WBC) and history of drug-induced leukopenia/neutropenia.

Patients with a history of a clinically significant low WBC or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

Patients with clinically significant neutropenia should be carefully monitored for fever or other symptoms or signs of infection and treated promptly if such symptoms or signs occur.

Patients with severe neutropenia (absolute neutrophil count <1000/mm 3 ) should discontinue RISPERDAL ® and have their WBC followed until recovery.

5.9 Potential for Cognitive and Motor Impairment Somnolence was a commonly reported adverse event associated with RISPERDAL ® treatment, especially when ascertained by direct questioning of patients.

This adverse event is dose-related, and in a study utilizing a checklist to detect adverse events, 41% of the high-dose patients (RISPERDAL ® 16 mg/day) reported somnolence compared to 16% of placebo patients.

Direct questioning is more sensitive for detecting adverse events than spontaneous reporting, by which 8% of RISPERDAL ® 16 mg/day patients and 1% of placebo patients reported somnolence as an adverse event.

Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely.

5.10 Seizures During premarketing testing in adult patients with schizophrenia, seizures occurred in 0.3% (9/2607) of RISPERDAL ® -treated patients, two in association with hyponatremia.

RISPERDAL ® should be used cautiously in patients with a history of seizures.

5.11 Dysphagia Esophageal dysmotility and aspiration have been associated with antipsychotic drug use.

Aspiration pneumonia is a common cause of morbidity and mortality in patients with advanced Alzheimer’s dementia.

RISPERDAL ® and other antipsychotic drugs should be used cautiously in patients at risk for aspiration pneumonia.

[See also Boxed Warning and Warnings and Precautions (5.1) ] 5.12 Priapism Rare cases of priapism have been reported.

While the relationship of the events to RISPERDAL ® use has not been established, other drugs with alpha-adrenergic blocking effects have been reported to induce priapism, and it is possible that RISPERDAL ® may share this capacity.

Severe priapism may require surgical intervention.

5.13 Thrombotic Thrombocytopenic Purpura (TTP) A single case of TTP was reported in a 28 year-old female patient receiving oral RISPERDAL ® in a large, open premarketing experience (approximately 1300 patients).

She experienced jaundice, fever, and bruising, but eventually recovered after receiving plasmapheresis.

The relationship to RISPERDAL ® therapy is unknown.

5.14 Body Temperature Regulation Disruption of body temperature regulation has been attributed to antipsychotic agents.

Both hyperthermia and hypothermia have been reported in association with oral RISPERDAL ® use.

Caution is advised when prescribing for patients who will be exposed to temperature extremes.

5.15 Antiemetic Effect Risperidone has an antiemetic effect in animals; this effect may also occur in humans, and may mask signs and symptoms of overdosage with certain drugs or of conditions such as intestinal obstruction, Reye’s syndrome, and brain tumor.

5.16 Suicide The possibility of a suicide attempt is inherent in patients with schizophrenia and bipolar mania, including children and adolescent patients, and close supervision of high-risk patients should accompany drug therapy.

Prescriptions for RISPERDAL ® should be written for the smallest quantity of tablets, consistent with good patient management, in order to reduce the risk of overdose.

5.17 Use in Patients with Concomitant Illness Clinical experience with RISPERDAL ® in patients with certain concomitant systemic illnesses is limited.

Patients with Parkinson’s Disease or Dementia with Lewy Bodies who receive antipsychotics, including RISPERDAL ® , are reported to have an increased sensitivity to antipsychotic medications.

Manifestations of this increased sensitivity have been reported to include confusion, obtundation, postural instability with frequent falls, extrapyramidal symptoms, and clinical features consistent with the neuroleptic malignant syndrome.

Caution is advisable in using RISPERDAL ® in patients with diseases or conditions that could affect metabolism or hemodynamic responses.

RISPERDAL ® has not been evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or unstable heart disease.

Patients with these diagnoses were excluded from clinical studies during the product’s premarket testing.

Increased plasma concentrations of risperidone and 9-hydroxyrisperidone occur in patients with severe renal impairment (creatinine clearance <30 mL/min/1.73 m 2 ), and an increase in the free fraction of risperidone is seen in patients with severe hepatic impairment.

A lower starting dose should be used in such patients [ see Dosage and Administration (2.4) ] .

5.18 Monitoring: Laboratory Tests No specific laboratory tests are recommended.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION Physicians are advised to discuss the following issues with patients for whom they prescribe RISPERDAL ® : 17.1 Orthostatic Hypotension Patients should be advised of the risk of orthostatic hypotension, especially during the period of initial dose titration [see Warnings and Precautions (5.7) ] .

17.2 Interference with Cognitive and Motor Performance Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely [see Warnings and Precautions (5.9) ] .

17.3 Pregnancy Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy [see Use in Specific Populations (8.1) ] .

17.4 Nursing Patients should be advised not to breast-feed an infant if they are taking RISPERDAL ® [see Use in Specific Populations (8.3) ] .

17.5 Concomitant Medication Patients should be advised to inform their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs, since there is a potential for interactions [see Drug Interactions (7) ] .

17.6 Alcohol Patients should be advised to avoid alcohol while taking RISPERDAL ® [see Drug Interactions (7.1) ] .

17.7 Phenylketonurics Phenylalanine is a component of aspartame.

Each 4 mg RISPERDAL ® M-TAB ® Orally Orally Disintegrating Tablet contains 0.14 mg phenylalanine.

DOSAGE AND ADMINISTRATION

2 Initial Dose Titration Target Dose Effective Dose Range Schizophrenia- adults ( 2.1 ) 2 mg/day 1–2 mg daily 4–8 mg daily 4–16 mg/day Schizophrenia – adolescents ( 2.1 ) 0.5mg/day 0.5– 1 mg daily 3mg/day 1–6 mg/day Bipolar mania – adults ( 2.2 ) 2–3 mg/day 1mg daily 1–6mg/day 1–6 mg/day Bipolar mania in children/adolescents ( 2.2 ) 0.5 mg/day 0.5–1mg daily 2.5mg/day 0.5–6 mg/day Irritability associated with autistic disorder ( 2.3 ) 0.25 mg/day (<20 kg) 0.5 mg/day (≥20 kg) 0.25–0.5 mg at ≥ 2 weeks 0.5 mg/day (<20 kg) 1 mg/day (≥20 kg) 0.5–3 mg/day 2.1 Schizophrenia Adults Usual Initial Dose RISPERDAL ® can be administered once or twice daily.

Initial dosing is generally 2 mg/day.

Dose increases should then occur at intervals not less than 24 hours, in increments of 1–2 mg/day, as tolerated, to a recommended dose of 4–8 mg/day.

In some patients, slower titration may be appropriate.

Efficacy has been demonstrated in a range of 4–16 mg/day [see Clinical Studies (14.1) ] .

However, doses above 6 mg/day for twice daily dosing were not demonstrated to be more efficacious than lower doses, were associated with more extrapyramidal symptoms and other adverse effects, and are generally not recommended.

In a single study supporting once-daily dosing, the efficacy results were generally stronger for 8 mg than for 4 mg.

The safety of doses above 16 mg/day has not been evaluated in clinical trials.

Maintenance Therapy While it is unknown how long a patient with schizophrenia should remain on RISPERDAL ® , the effectiveness of RISPERDAL ® 2 mg/day to 8 mg/day at delaying relapse was demonstrated in a controlled trial in patients who had been clinically stable for at least 4 weeks and were then followed for a period of 1 to 2 years [ see Clinical Studies (14.1) ] .

Patients should be periodically reassessed to determine the need for maintenance treatment with an appropriate dose.

Adolescents The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 3 mg/day.

Although efficacy has been demonstrated in studies of adolescent patients with schizophrenia at doses between 1 and 6 mg/day, no additional benefit was seen above 3 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

There are no controlled data to support the longer term use of RISPERDAL ® beyond 8 weeks in adolescents with schizophrenia.

The physician who elects to use RISPERDAL ® for extended periods in adolescents with schizophrenia should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

Reinitiation of Treatment in Patients Previously Discontinued Although there are no data to specifically address reinitiation of treatment, it is recommended that after an interval off RISPERDAL ® , the initial titration schedule should be followed.

Switching From Other Antipsychotics There are no systematically collected data to specifically address switching schizophrenic patients from other antipsychotics to RISPERDAL ® , or treating patients with concomitant antipsychotics.

While immediate discontinuation of the previous antipsychotic treatment may be acceptable for some schizophrenic patients, more gradual discontinuation may be most appropriate for others.

The period of overlapping antipsychotic administration should be minimized.

When switching schizophrenic patients from depot antipsychotics, initiate RISPERDAL ® therapy in place of the next scheduled injection.

The need for continuing existing EPS medication should be re-evaluated periodically.

2.2 Bipolar Mania Usual Dose Adults RISPERDAL ® should be administered on a once-daily schedule, starting with 2 mg to 3 mg per day.

Dosage adjustments, if indicated, should occur at intervals of not less than 24 hours and in dosage increments/decrements of 1 mg per day, as studied in the short-term, placebo-controlled trials.

In these trials, short-term (3 week) anti-manic efficacy was demonstrated in a flexible dosage range of 1–6 mg per day [see Clinical Studies (14.2 , 14.3) ] .

RISPERDAL ® doses higher than 6 mg per day were not studied.

Pediatrics The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 2.5 mg/day.

Although efficacy has been demonstrated in studies of pediatric patients with bipolar mania at doses between 0.5 and 6 mg/day, no additional benefit was seen above 2.5 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

Maintenance Therapy There is no body of evidence available from controlled trials to guide a clinician in the longer-term management of a patient who improves during treatment of an acute manic episode with RISPERDAL ® .

While it is generally agreed that pharmacological treatment beyond an acute response in mania is desirable, both for maintenance of the initial response and for prevention of new manic episodes, there are no systematically obtained data to support the use of RISPERDAL ® in such longer-term treatment (i.e., beyond 3 weeks).

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

2.3 Irritability Associated with Autistic Disorder – Pediatrics (Children and Adolescents) The safety and effectiveness of RISPERDAL ® in pediatric patients with autistic disorder less than 5 years of age have not been established.

The dosage of RISPERDAL ® should be individualized according to the response and tolerability of the patient.

The total daily dose of RISPERDAL ® can be administered once daily, or half the total daily dose can be administered twice daily.

Dosing should be initiated at 0.25 mg per day for patients < 20 kg and 0.5 mg per day for patients ≥ 20 kg.

After a minimum of four days from treatment initiation, the dose may be increased to the recommended dose of 0.5 mg per day for patients < 20 kg and 1 mg per day for patients ≥ 20 kg.

This dose should be maintained for a minimum of 14 days.

In patients not achieving sufficient clinical response, dose increases may be considered at ≥ 2-week intervals in increments of 0.25 mg per day for patients < 20 kg or 0.5 mg per day for patients ≥ 20 kg.

Caution should be exercised with dosage for smaller children who weigh less than 15 kg.

In clinical trials, 90% of patients who showed a response (based on at least 25% improvement on ABC-I, [see Clinical Studies (14.4) ] ) received doses of RISPERDAL ® between 0.5 mg and 2.5 mg per day.

The maximum daily dose of RISPERDAL ® in one of the pivotal trials, when the therapeutic effect reached plateau, was 1 mg in patients 45 kg.

No dosing data is available for children who weighed less than 15 kg.

Once sufficient clinical response has been achieved and maintained, consideration should be given to gradually lowering the dose to achieve the optimal balance of efficacy and safety.

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

Patients experiencing persistent somnolence may benefit from a once-daily dose administered at bedtime or administering half the daily dose twice daily, or a reduction of the dose.

2.4 Dosage in Special Populations The recommended initial dose is 0.5 mg twice daily in patients who are elderly or debilitated, patients with severe renal or hepatic impairment, and patients either predisposed to hypotension or for whom hypotension would pose a risk.

Dosage increases in these patients should be in increments of no more than 0.5 mg twice daily.

Increases to dosages above 1.5 mg twice daily should generally occur at intervals of at least 1 week.

In some patients, slower titration may be medically appropriate.

Elderly or debilitated patients, and patients with renal impairment, may have less ability to eliminate RISPERDAL ® than normal adults.

Patients with impaired hepatic function may have increases in the free fraction of risperidone, possibly resulting in an enhanced effect [see Clinical Pharmacology (12.3) ] .

Patients with a predisposition to hypotensive reactions or for whom such reactions would pose a particular risk likewise need to be titrated cautiously and carefully monitored [see Warnings and Precautions (5.2 , 5.7 , 5.17) ] .

If a once-daily dosing regimen in the elderly or debilitated patient is being considered, it is recommended that the patient be titrated on a twice-daily regimen for 2–3 days at the target dose.

Subsequent switches to a once-daily dosing regimen can be done thereafter.

2.5 Co-Administration of RISPERDAL ® with Certain Other Medications Co-administration of carbamazepine and other enzyme inducers (e.g., phenytoin, rifampin, phenobarbital) with RISPERDAL ® would be expected to cause decreases in the plasma concentrations of the sum of risperidone and 9-hydroxyrisperidone combined, which could lead to decreased efficacy of RISPERDAL ® treatment.

The dose of RISPERDAL ® needs to be titrated accordingly for patients receiving these enzyme inducers, especially during initiation or discontinuation of therapy with these inducers [see Drug Interactions (7.11) ] .

Fluoxetine and paroxetine have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

The dose of RISPERDAL ® needs to be titrated accordingly when fluoxetine or paroxetine is co-administered [see Drug Interactions (7.10) ] .

2.6 Administration of RISPERDAL ® Oral Solution RISPERDAL ® Oral Solution can be administered directly from the calibrated pipette, or can be mixed with a beverage prior to administration.

RISPERDAL ® Oral Solution is compatible in the following beverages: water, coffee, orange juice, and low-fat milk; it is NOT compatible with either cola or tea.

2.7 Directions for Use of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets Tablet Accessing RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg are supplied in blister packs of 4 tablets each.

Do not open the blister until ready to administer.

For single tablet removal, separate one of the four blister units by tearing apart at the perforations.

Bend the corner where indicated.

Peel back foil to expose the tablet.

DO NOT push the tablet through the foil because this could damage the tablet.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg are supplied in a child-resistant pouch containing a blister with 1 tablet each.

The child-resistant pouch should be torn open at the notch to access the blister.

Do not open the blister until ready to administer.

Peel back foil from the side to expose the tablet.

DO NOT push the tablet through the foil, because this could damage the tablet.

Tablet Administration Using dry hands, remove the tablet from the blister unit and immediately place the entire RISPERDAL ® M-TAB ® Orally Disintegrating Tablet on the tongue.

The RISPERDAL ® M-TAB ® Orally Disintegrating Tablet should be consumed immediately, as the tablet cannot be stored once removed from the blister unit.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets disintegrate in the mouth within seconds and can be swallowed subsequently with or without liquid.

Patients should not attempt to split or to chew the tablet.

DRUG INTERACTIONS

Drug Interactions Section Concomitant use of strong CYP3A4 inhibitors: Reduce quetiapine dose to one sixth when coadministered with strong CYP3A4 inhibitors (e.g., ketoconazole, ritonavir) ( 2.5, 7.1 , 12.3 ) Concomitant use of strong CYP3A4 inducers: Increase quetiapine dose up to 5 fold when used in combination with a chronic treatment (more than 7 to 14 days) of potent CYP3A4 inducers (e.g., phenytoin, rifampin, St.

John’s wort) ( 2.6 , 7.1 , 12.3 ) Discontinuation of strong CYP3A4 inducers: Reduce quetiapine dose by 5 fold within 7 to 14 days of discontinuation of CYP3A4 inducers ( 2.6 , 7.1 , 12.3 ) The risks of using quetiapine in combination with other drugs have not been extensively evaluated in systematic studies.

Given the primary CNS effects of quetiapine, caution should be used when it is taken in combination with other centrally acting drugs.

Quetiapine potentiated the cognitive and motor effects of alcohol in a clinical trial in subjects with selected psychotic disorders, and alcoholic beverages should be limited while taking quetiapine.

Quetiapine exposure is increased by the prototype CYP3A4 inhibitors (e.g., ketoconazole, itraconazole, indinavir, ritonavir, nefazodone, etc.)and decreased by the prototype CYP3A4 inducers (e.g., phenytoin, carbamazepine, rifampin, avasimibe, St.

John’s wort etc.).

Dose adjustment of quetiapine will be necessary if it is coadministered with potent CYP3A4 inducers or inhibitors.

CYP3A4 inhibitors: Coadministration of ketoconazole, a potent inhibitor of cytochrome CYP3A4, resulted in significant increase in quetiapine exposure.

The dose of quetiapine should be reduced to one sixth of the original dose if coadministered with a strong CYP3A4 inhibitor [see Dosage and Administration ( 2.5 ) and Clinical Pharmacology (12.3)] .

CYP3A4 inducers: Coadministration of quetiapine and phenytoin, a CYP3A4 inducer increased the mean oral clearance of quetiapine by 5-fold.

Increased doses of quetiapine up to 5 fold may be required to maintain control of symptoms of schizophrenia in patients receiving quetiapine and phenytoin, or other known potent CYP3A4 inducers [see Dosage and Administration ( 2.6 ) and Clinical Pharmacology (12.3)] .

When the CYP3A4 inducer is discontinued, the dose of quetiapine should be reduced to the original level within 7 to 14 days [see Dosage and Administration ( 2.6 )] .

The potential effects of several concomitant medications on quetiapine pharmacokinetics were studied [see Clinical Pharmacology (12.3)].

Because of its potential for inducing hypotension, quetiapine may enhance the effects of certain antihypertensive agents.

Quetiapine may antagonize the effects of levodopa and dopamine agonists.

There are no clinically relevant pharmacokinetic interactions of quetiapine on other drugs based on the CYP pathway.

Quetiapine and its metabolites are non-inhibitors of major metabolizing CYP’s (1A2, 2C9, 2C19, 2D6 and 3A4).

OVERDOSAGE

Overdosage Section In clinical trials, survival has been reported in acute overdoses of up to 30 grams of quetiapine.

Most patients who overdosed experienced no adverse reactions or recovered fully from the reported reactions.

Death has been reported in a clinical trial following an overdose of 13.6 grams of quetiapine alone.

In general, reported signs and symptoms were those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness and sedation, tachycardia and hypotension.

Patients with preexisting severe cardiovascular disease may be at an increased risk of the effects of overdose [s ee Warnings and Precautions (5.11)].

One case, involving an estimated overdose of 9600 mg, was associated with hypokalemia and first degree heart block.

In postmarketing experience, there were cases reported of QT prolongation with overdose.

There were also very rare reports of overdose of quetiapine alone resulting in death or coma.

In case of acute overdosage, establish and maintain an airway and ensure adequate oxygenation and ventilation.

Gastric lavage (after intubation, if patient is unconscious) and administration of activated charcoal together with a laxative should be considered.

The possibility of obtundation, seizure or dystonic reaction of the head and neck following overdose may create a risk of aspiration with induced emesis.

Cardiovascular monitoring should commence immediately and should include continuous electrocardiographic monitoring to detect possible arrhythmias.

If antiarrhythmic therapy is administered, disopyramide, procainamide and quinidine carry a theoretical hazard of additive QT-prolonging effects when administered in patients with acute overdosage of quetiapine.

Similarly it is reasonable to expect that the alpha-adrenergic-blocking properties of bretylium might be additive to those of quetiapine, resulting in problematic hypotension.

There is no specific antidote to quetiapine.

Therefore, appropriate supportive measures should be instituted.

The possibility of multiple drug involvement should be considered.

Hypotension and circulatory collapse should be treated with appropriate measures such as intravenous fluids and/or sympathomimetic agents (epinephrine and dopamine should not be used, since beta stimulation may worsen hypotension in the setting of quetiapine-induced alpha blockade).

In cases of severe extrapyramidal symptoms, anticholinergic medication should be administered.

Close medical supervision and monitoring should continue until the patient recovers.

DESCRIPTION

Description Section Quetiapine fumarate is a psychotropic agent belonging to a chemical class, the dibenzothiazepine derivatives.

The chemical designation is 2-[2-(4-dibenzo [b,f ] [1,4]thiazepin-11-yl-1-piperazinyl)ethoxy]-ethanol fumarate (2:1) (salt).

It is present in tablets as the fumarate salt.

All doses and tablet strengths are expressed as milligrams of base, not as fumarate salt.

Its molecular formula is C 42 H 50 N 6 O 4 S 2 •C 4 H 4 O 4 and it has a molecular weight of 883.10 (fumarate salt).

The structural formula is: Quetiapine fumarate is a white to off-white powder which is insoluble in water.

Quetiapine fumarate tablets are supplied for oral administration as 25 mg (round, peach), 50 mg (round, white), 100 mg (round, yellow), 200 mg (round, white), 300 mg (capsule-shaped, white), and 400 mg (capsule-shaped, yellow) tablets.

Inactive ingredients are microcrystalline cellulose, colloidal silicon dioxide, silicon dioxide, crospovidone, anhydrous citric acid, polysorbate 80, magnesium stearate, lactose monohydrate, hypromellose, polyethylene glycol and titanium dioxide.

The 25 mg tablets contain red ferric oxide and yellow ferric oxide and the 100 mg and 400 mg tablets contain only yellow ferric oxide.

CLINICAL STUDIES

Clinical Studies Section Short-term Trials – Adults The efficacy of quetiapine in the treatment of schizophrenia was established in 3 short-term (6-­week) controlled trials of inpatients with schizophrenia who met DSM III-R criteria for schizophrenia.

Although a single fixed dose haloperidol arm was included as a comparative treatment in one of the three trials, this single haloperidol dose group was inadequate to provide a reliable and valid comparison of quetiapine and haloperidol.

Several instruments were used for assessing psychiatric signs and symptoms in these studies, among them the Brief Psychiatric Rating Scale (BPRS), a multi-item inventory of general psychopathology traditionally used to evaluate the effects of drug treatment in schizophrenia.

The BPRS psychosis cluster (conceptual disorganization, hallucinatory behavior, suspiciousness, and unusual thought content) is considered a particularly useful subset for assessing actively psychotic schizophrenic patients.

A second traditional assessment, the Clinical Global Impression (CGI), reflects the impression of a skilled observer, fully familiar with the manifestations of schizophrenia, about the overall clinical state of the patient.

The results of the trials follow: In a 6-week, placebo-controlled trial (n=361) (study 1) involving 5 fixed doses of quetiapine (75 mg/day, 150 mg/day, 300 mg/day, 600 mg/day and 750 mg/day given in divided doses three times per day), the 4 highest doses of quetiapine were generally superior to placebo on the BPRS total score, the BPRS psychosis cluster and the CGI severity score, with the maximal effect seen at 300 mg/day, and the effects of doses of 150 mg/day to 750 mg/day were generally indistinguishable.

In a 6-week, placebo-controlled trial (n=286) (study 2) involving titration of quetiapine in high (up to 750 mg/day given in divided doses three times per day) and low (up to 250 mg/day given in divided doses three times per day) doses, only the high dose quetiapine group (mean dose, 500 mg/day) was superior to placebo on the BPRS total score, the BPRS psychosis cluster, and the CGI severity score.

In a 6-week dose and dose regimen comparison trial (n=618) (study 3) involving two fixed doses of quetiapine (450 mg/day given in divided doses both twice daily and three times daily and 50 mg/day given in divided doses twice daily), only the 450 mg/day (225 mg given twice daily) dose group was superior to the 50 mg/day (25 mg given twice daily) quetiapine dose group on the BPRS total score, the BPRS psychosis cluster, and the CGI severity score.

The primary efficacy results of these three studies in the treatment of schizophrenia in adults is presented in Table 19.

Examination of population subsets (race, gender, and age) did not reveal any differential responsiveness on the basis of race or gender, with an apparently greater effect in patients under the age of 40 years compared to those older than 40.

The clinical significance of this finding is unknown.

Adolescents (ages 13 to 17) The efficacy of quetiapine in the treatment of schizophrenia in adolescents (13 to 17 years of age) was demonstrated in a 6-week, double-blind, placebo-controlled trial (study 4).

Patients who met DSM-IV diagnostic criteria for schizophrenia were randomized into one of three treatment groups: quetiapine 400 mg/day (n = 73), quetiapine 800 mg/day (n = 74), or placebo (n = 75).

Study medication was initiated at 50 mg/day and on day 2 increased to 100 mg/per day (divided and given two or three times per day).

Subsequently, the dose was titrated to the target dose of 400 mg/day or 800 mg/day using increments of 100 mg/day, divided and given two or three times daily.

The primary efficacy variable was the mean change from baseline in total Positive and Negative Syndrome Scale (PANSS).

Quetiapine at 400 mg/day and 800 mg/day was superior to placebo in the reduction of PANSS total score.

The primary efficacy results of this study in the treatment of schizophrenia in adolescents is presented in Table 19.

Table 19: Schizophrenia Short-Term Trials Study Number Treatment Group Primary Efficacy Endpoint: BPRS Total Mean Baseline Score (SD) LS Mean Change from Baseline (SE) Placebo-subtracted Difference * (95% CI) Study 1 Quetiapine(75 mg/day) 45.7 (10.9) -2.2 (2) -4 (-11.2, 3.3) Quetiapine(150 mg/day) † 47.2 (10.1) -8.7 (2.1) -10.4 (-17.8, -3) Quetiapine(300 mg/day) 45.3 (10.9) -8.6 (2.1) -10.3 (-17.6, -3) Quetiapine(600 mg/day) 43.5 (11.3) -7.7 (2.1) -9.4 (-16.7, -2.1) Quetiapine(750 mg/day) 45.7 (11) -6.3 (2) -8 (-15.2, -0.8) Placebo 45.3 (9.2) 1.7 (2.1) — Study 2 Quetiapine(250 mg/day) 38.9 (9.8) -4.2 (1.6) -3.2 (-7.6, 1.2) Quetiapine(750 mg/day) 41 (9.6) -8.7 (1.6) -7.8 (-12.2, -3.4) Placebo 38.4 (9.7) -1 (1.6) — Study 3 Quetiapine(450 mg/day BID) 42.1 (10.7) -10 (1.3) -4.6 (-7.8, -1.4) Quetiapine(450 mg/day TID) 42.7 (10.4) -8.6 (1.3) -3.2 (-6.4, 0) Quetiapine (50 mg BID) 41.7 (10) -5.4 (1.3) — Primary Efficacy Endpoint: PANSS Total Mean Baseline Score (SD) LS Mean Change from Baseline (SE) Placebo-subtracted Difference (95% CI) Study 4 Quetiapine(400 mg/day) 96.2 (17.7) -27.3 (2.6) -8.2 (-16.1, -0.3) Quetiapine(800 mg/day) 96.9 (15.3) -28.4 (1.8) -9.3 (-16.2, -2.4) Placebo 96.2 (17.7) -19.2 (3) — SD: standard deviation; SE: standard error; LS Mean: least-squares mean; CI: unadjusted confidence interval.

# Doses that are statistically significant superior to quetiapine 50 mg BID.

Difference (drug minus placebo) in least-squares mean change from baseline.

Doses that are statistically significant superior to placebo.

Bipolar I disorder, manic or mixed episodes Adults The efficacy of quetiapine in the acute treatment of manic episodes was established in 3 placebo-controlled trials in patients who met DSM-IV criteria for bipolar I disorder with manic episodes.

These trials included patients with or without psychotic features and excluded patients with rapid cycling and mixed episodes.

Of these trials, 2 were monotherapy (12 weeks) and 1 was adjunct therapy (3 weeks) to either lithium or divalproex.

Key outcomes in these trials were change from baseline in the Young Mania Rating Scale (YMRS) score at 3 and 12 weeks for monotherapy and at 3 weeks for adjunct therapy.

Adjunct therapy is defined as the simultaneous initiation or subsequent administration of quetiapine with lithium or divalproex.

The primary rating instrument used for assessing manic symptoms in these trials was YMRS, an 11-­item clinician-rated scale traditionally used to assess the degree of manic symptomatology (irritability, disruptive/aggressive behavior, sleep, elevated mood, speech, increased activity, sexual interest, language/thought disorder, thought content, appearance, and insight) in a range from 0 (no manic features) to 60 (maximum score).

The results of the trials follow: Monotherapy The efficacy of quetiapine in the acute treatment of bipolar mania was established in 2 placebo-controlled trials.

In two 12-week trials (n=300, n=299) comparing quetiapine to placebo, quetiapine was superior to placebo in the reduction of the YMRS total score at weeks 3 and 12.

The majority of patients in these trials taking quetiapine were dosed in a range between 400 mg/day and 800 mg per day (studies 1 and 2 in Table 20).

Adjunct Therapy In this 3-week placebo-controlled trial, 170 patients with bipolar mania (YMRS ≥ 20) were randomized to receive quetiapine or placebo as adjunct treatment to lithium or divalproex.

Patients may or may not have received an adequate treatment course of lithium or divalproex prior to randomization.

Quetiapine was superior to placebo when added to lithium or divalproex alone in the reduction of YMRS total score.

(study 3 in Table 20).

The majority of patients in this trial taking quetiapine were dosed in a range between 400 mg/day and 800 mg per day.

In a similarly designed trial (n=200), quetiapine was associated with an improvement in YMRS scores but did not demonstrate superiority to placebo, possibly due to a higher placebo effect.

The primary efficacy results of these studies in the treatment of mania in adults is presented in Table 20.

Children and Adolescents (ages 10 to 17) The efficacy of quetiapine in the acute treatment of manic episodes associated with bipolar I disorder in children and adolescents (10 to 17 years of age) was demonstrated in a 3-week, double-blind, placebo-controlled, multicenter trial (study 4 in Table 20).

Patients who met DSM-IV diagnostic criteria for a manic episode were randomized into one of three treatment groups: quetiapine 400 mg/day (n = 95), quetiapine 600 mg/day (n = 98), or placebo (n = 91).

Study medication was initiated at 50 mg/day and on day 2 increased to 100 mg/day (divided doses given two or three times daily).

Subsequently, the dose was titrated to a target dose of 400 mg/day or 600 mg/day using increments of 100 mg/day, given in divided doses two or three times daily.

The primary efficacy variable was the mean change from baseline in total YMRS score.

Quetiapine 400 mg/day and 600 mg/day were superior to placebo in the reduction of YMRS total score (Table 20).

Table 20: Mania Trials Study Number Treatment Group Primary Efficacy Measure: YMRS Total Mean Baseline Score (SD) * LS Mean Change from Baseline (SE) Placebo-subtracted Difference † (95% CI) Study 1 Quetiapine(200 to 800 mg/day) ‡ § 34 (6.1) -12.3 (1.3) -4 (-7, -1) Haloperidol 32.3 (6) -15.7 (1.3) -7.4 (-10.4, -4.4) Placebo 33.1 (6.6) -8.3 (1.3) — Study 2 Quetiapine(200 to 800 mg/day) 32.7 (6.5) -14.6 (1.5) -7.9 (-10.9, -5) Lithium 33.3 (7.1) -15.2 (1.6) -8.5 (-11.5, -5.5) Placebo 34 (6.9) -6.7 (1.6) — Study 3 Quetiapine(200 to 800 mg/day) + mood stabilizer 31.5 (5.8) -13.8 (1.6) -3.8 (-7.1, -0.6) Placebo + mood stabilizer 31.1 (5.5) -10 (1.5) — Study 4 Quetiapine(400 mg/day) 29.4 (5.9) -14.3 (0.96) -5.2 (-8.1, -2.3) Quetiapine(600 mg/day) 29.6 (6.4) -15.6 (0.97) -6.6 (-9.5, -3.7) Placebo 30.7 (5.9) -9 (1.1) — Mood stabilizer: lithium or divalproex; SD: standard deviation; SE: standard error; LS Mean: least-squares mean; CI: unadjusted confidence interval.

Adult data mean baseline score is based on patients included in the primary analysis; pediatric mean baseline score is based on all patients in the ITT population Difference (drug minus placebo) in least-squares mean change from baseline.

Doses that are statistically significantly superior to placebo.

Included in the trial as an active comparator Bipolar Disorder, Depressive Episodes Adults The efficacy of quetiapine for the acute treatment of depressive episodes associated with bipolar disorder was established in 2 identically designed 8-week, randomized, double-blind, placebo-controlled studies (N=1045) (studies 5 and 6 in Table 21).

These studies included patients with either bipolar I or II disorder and those with or without a rapid cycling course.

Patients randomized to quetiapine were administered fixed doses of either 300 mg or 600 mg once daily.

The primary rating instrument used to assess depressive symptoms in these studies was the Montgomery-Asberg Depression Rating Scale (MADRS), a 10-item clinician-rated scale with scores ranging from 0 to 60.

The primary endpoint in both studies was the change from baseline in MADRS score at week 8.

In both studies, quetiapine was superior to placebo in reduction of MADRS score.

Improvement in symptoms, as measured by change in MADRS score relative to placebo, was seen in both studies at Day 8 (week 1) and onwards.

In these studies, no additional benefit was seen with the 600 mg dose.

For the 300 mg dose group, statistically significant improvements over placebo were seen in overall quality of life and satisfaction related to various areas of functioning, as measured using the Q-LES-Q(SF).

The primary efficacy results of these studies in the acute treatment of depressive episodes associated with bipolar disorder in adults is presented in Table 21.

Table 21: Depressive Episodes Associated with Bipolar Disorder Study Number Treatment Group Primary Efficacy Measure: MADRS Total Mean Baseline Score (SD) LS Mean Change from Baseline (SE) Placebo-subtracted Difference * (95% CI) Study 5 Quetiapine (300 mg/day) † 30.3 (5) -16.4 (0.9) -6.1 (-8.3, -3.9) Quetiapine (600 mg/day) 30.3 (5.3) -16.7 (0.9) -6.5 (-8.7, -4.3) Placebo 30.6 (5.3) -10.3 (0.9) — Study 6 Quetiapine (300 mg/day) 31.1 (5.7) -16.9 (1) -5 (-7.3, -2.7) Quetiapine (600 mg/day) 29.9 (5.6) -16 (1) -4.1 (-6.4, -1.8) Placebo 29.6 (5.4) -11.9 (1) — SD: standard deviation; SE: standard error; LS Mean: least-squares mean; CI: unadjusted confidence interval.

Difference (drug minus placebo) in least-squares mean change from baseline.

Doses that are statistically significantly superior to placebo.

Maintenance Treatment as an Adjunct to Lithium or Divalproex The efficacy of quetiapine in the maintenance treatment of bipolar I disorder was established in 2 placebo-controlled trials in patients (n=1326) who met DSM-IV criteria for bipolar I disorder (studies 7 and 8 in Figures 1 and 2).

The trials included patients whose most recent episode was manic, depressed, or mixed, with or without psychotic features.

In the open-label phase, patients were required to be stable on quetiapine plus lithium or divalproex for at least 12 weeks in order to be randomized.

On average, patients were stabilized for 15 weeks.

In the randomization phase, patients continued treatment with lithium or divalproex and were randomized to receive either quetiapine (administered twice daily totaling 400 mg/day to 800 mg/day) or placebo.

Approximately 50% of the patients had discontinued from the quetiapine group by day 280 and 50% of the placebo group had discontinued by day 117 of double-blind treatment.

The primary endpoint in these studies was time to recurrence of a mood event (manic, mixed or depressed episode).

A mood event was defined as medication initiation or hospitalization for a mood episode; YMRS score ≥ 20 or MADRS score ≥ 20 at 2 consecutive assessments; or study discontinuation due to a mood event.

(Figure 1 and Figure 2) In both studies, quetiapine was superior to placebo in increasing the time to recurrence of any mood event.

The treatment effect was present for increasing time to recurrence of both manic and depressed episodes.

The effect of quetiapine was independent of any specific subgroup (assigned mood stabilizer, sex, age, race, most recent bipolar episode, or rapid cycling course).

HOW SUPPLIED

How Supplied Section 25 mg tablets are peach, round, biconvex, film-coated tablets, debossed with ‘25’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-902-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-902-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-902-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-902-61 50 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘50’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-903-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-903-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-903-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-903-61 100 mg tablets are yellow, round, biconvex, film-coated tablets, debossed with ‘904’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-904-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-904-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-904-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-904-61 200 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘905’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-905-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-905-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-905-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-905-61 300 mg tablets are white, capsule-shaped, biconvex, film-coated tablets, debossed with ‘906’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-906-83 Bottles of 60’s with Child Resistant Cap ……………… NDC 47335-906-86 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-906-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-906-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-906-61 400 mg tablets are yellow, capsule-shaped, biconvex, film-coated tablets, debossed with ‘907’ on one side and plain on the other side and are supplied as: Bottles of 30’s with Child Resistant Cap ……………… NDC 47335-907-83 Bottles of 100’s with Child Resistant Cap ……………..

NDC 47335-907-88 Bottles of 1000’s with Non Child Resistant Cap …..…..

NDC 47335-907-18 Unit-dose blister pack of 100 (10 × 10) tablets ..……….

NDC 47335-907-61 Store at 20° to 25°C (68° to 77°F); excursions permitted between 15° and 30°C (59° and 86°F) [see USP Controlled Room Temperature].

RECENT MAJOR CHANGES

Recent Major Changes Section Warnings and Precautions, Cerebrovascular Adverse Reactions, Including Stroke, in Elderly Patients with Dementia-Related Psychosis (5.3 ) ———————4/2013

DOSAGE FORMS AND STRENGTHS

Dosage Forms & Strengths Section 25 mg tablets are peach, round, biconvex, film-coated tablets, debossed with ‘25’ on one side and plain on the other side 50 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘50’ on one side and plain on the other side 100 mg tablets are yellow, round, biconvex, film-coated tablets, debossed with ‘904’ on one side and plain on the other side 200 mg tablets are white, round, biconvex, film-coated tablets, debossed with ‘905’ on one side and plain on the other side 300 mg tablets are white, capsule-shaped, biconvex, film-coated tablets, debossed with ‘906’ on one side and plain on the other side 400 mg tablets are yellow, capsule-shaped, biconvex, film-coated tablets, debossed with ‘907’ on one side and plain on the other side

INDICATIONS AND USAGE

Indications & Usage Section Quetiapine fumarate tablets are atypical antipsychotic indicated for the treatment of: Schizophrenia ( 1.1 ) Bipolar I disorder manic episodes ( 1.2 ) Bipolar disorder, depressive episodes ( 1.2 ) Quetiapine fumarate tablets are indicated for the treatment of schizophrenia.

The efficacy of quetiapine fumarate tablets in schizophrenia was established in three 6-week trials in adults and one 6-week trial in adolescents (13 to ¬17 years).

The effectiveness of quetiapine fumarate tablets for the maintenance treatment of schizophrenia has not been systematically evaluated in controlled clinical trials [ see Clinical Studies ( 14.1 ) ].

Quetiapine fumarate tablets are indicated for the acute treatment of manic episodes associated with bipolar I disorder, both as monotherapy and as an adjunct to lithium or divalproex.

Efficacy was established in two 12-week monotherapy trials in adults, in one 3-week adjunctive trial in adults, and in one 3-week monotherapy trial in pediatric patients (10 to 17 years) [ see Clinical Studies ( 14.2 ) ].

Quetiapine fumarate tablets are indicated as monotherapy for the acute treatment of depressive episodes associated with bipolar disorder.

Efficacy was established in two 8-week monotherapy trials in adult patients with bipolar I and bipolar II disorder [ see Clinical Studies ( 14.2 ) ].

Quetiapine fumarate tablets are indicated for the maintenance treatment of bipolar I disorder, as an adjunct to lithium or divalproex.

Efficacy was established in two maintenance trials in adults.

The effectiveness of quetiapine fumarate tablets as monotherapy for the maintenance treatment of bipolar disorder has not been systematically evaluated in controlled clinical trials [ see Clinical Studies ( 14.2 ) ].

Pediatric schizophrenia and bipolar I disorder are serious mental disorders, however, diagnosis can be challenging.

For pediatric schizophrenia, symptom profiles can be variable, and for bipolar I disorder, patients may have variable patterns of periodicity of manic or mixed symptoms.

It is recommended that medication therapy for pediatric schizophrenia and bipolar I disorder be initiated only after a thorough diagnostic evaluation has been performed and careful consideration given to the risks associated with medication treatment.

Medication treatment for both pediatric schizophrenia and bipolar I disorder is indicated as part of a total treatment program that often includes psychological, educational and social interventions.

BOXED WARNING

Boxed Warning Section Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death [see Warnings and Precautions (5.1)] .

Quetiapine is not approved for the treatment of patients with dementia-related psychosis [see Warnings and Precautions (5.1)] .

Suicidal Thoughts and Behaviors Antidepressants increased the risk of suicidal thoughts and behavior in children, adolescents, and young adults in short-term studies.

These studies did not show an increase in the risk of suicidal thoughts and behavior with antidepressant use in patients over age 24; there was a reduction in risk with antidepressant use in patients aged 65 and older [see Warnings and Precautions (5.2)] .

In patients of all ages who are started on antidepressant therapy, monitor closely for worsening, and for emergence of suicidal thoughts and behaviors.

Advise families and caregivers of the need for close observation and communication with the prescriber [see Warnings and Precautions (5.2)] .

Quetiapine is not approved for use in pediatric patients under ten years of age [see Use in Specific Populations (8.4)] .

WARNING AND CAUTIONS

Warnings And Precautions Section Cerebrovascular Adverse Reactions: Increased incidence of cerebrovascular adverse events (e.g., stroke, transient ischemic attack) has been seen in elderly patients with dementia-related psychoses treated with atypical antipsychotic drugs ( 5.3 ) Neuroleptic Malignant Syndrome (NMS): Manage with immediate discontinuation and close monitoring ( 5.4 ) Metabolic Changes: Atypical antipsychotics have been associated with metabolic changes.

These metabolic changes include hyperglycemia, dyslipidemia, and weight gain ( 5.5 ) Hyperglycemia and Diabetes Mellitus: Monitor patients for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Monitor glucose regularly in patients with diabetes or at risk for diabetes Dyslipidemia: Undesirable alterations have been observed in patients treated with atypical antipsychotics.

Appropriate clinical monitoring is recommended, including fasting blood lipid testing at the beginning of, and periodically, during treatment Weight Gain: Gain in body weight has been observed; clinical monitoring of weight is recommended Tardive Dyskinesia: Discontinue if clinically appropriate ( 5.6 ) Hypotension: Use with caution in patients with known cardiovascular or cerebrovascular disease ( 5.7 ) Increased Blood Pressure in Children and Adolescents: Monitor blood pressure at the beginning of, and periodically during treatment in children and adolescents ( 5.8 ) Leukopenia, Neutropenia and Agranulocytosis: Monitor complete blood count frequently during the first few months of treatment in patients with a preexisting low white cell count or a history of leukopenia/neutropenia and discontinue quetiapine at the first sign of a decline in WBC in absence of other causative factors ( 5.9 ) Cataracts: Lens changes have been observed in patients during long-term quetiapine treatment.

Lens examination is recommended when starting treatment and at 6-month intervals during chronic treatment ( 5.10 ) Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

Analysis of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients.

Over the course of a typical 10-­week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature.

Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.

The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear.

Quetiapine fumarate tablets are not approved for the treatment of patients with dementia-related psychosis [ see Boxed Warning ] .

Patients with major depressive disorder (MDD), both adult and pediatric, may experience worsening of their depression and/or the emergence of suicidal ideation and behavior (suicidality) or unusual changes in behavior, whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs.

Suicide is a known risk of depression and certain other psychiatric disorders, and these disorders themselves are the strongest predictors of suicide.

There has been a long-standing concern, however, that antidepressants may have a role in inducing worsening of depression and the emergence of suicidality in certain patients during the early phases of treatment.

Pooled analyses of short-term placebo-controlled trials of antidepressant drugs (SSRIs and others) showed that these drugs increase the risk of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults (ages 18 to 24) with major depressive disorder (MDD) and other psychiatric disorders.

Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction with antidepressants compared to placebo in adults aged 65 and older.

The pooled analyses of placebo-controlled trials in children and adolescents with MDD, obsessive compulsive disorder (OCD), or other psychiatric disorders included a total of 24 short-term trials of 9 antidepressant drugs in over 4400 patients.

The pooled analyses of placebo-controlled trials in adults with MDD or other psychiatric disorders included a total of 295 short-term trials (median duration of 2 months) of 11 antidepressant drugs in over 77,000 patients.

There was considerable variation in risk of suicidality among drugs, but a tendency toward an increase in the younger patients for almost all drugs studied.

There were differences in absolute risk of suicidality across the different indications, with the highest incidence in MDD.

The risk differences (drug vs.

placebo), however, were relatively stable within age strata and across indications.

These risk differences (drug-placebo difference in the number of cases of suicidality per 1000 patients treated) are provided in Table 2.

Table 2 Drug-Placebo Difference in Number of Cases of Suicidality per 1000 Patients Treated Age Range Drug-Placebo Difference in Number of Cases of Suicidality per 1000 Patients Treated Increases Compared to Placebo <18 14 additional cases 18 to 24 5 additional cases Decreases Compared to Placebo 25 to 64 1 fewer case ≥65 6 fewer cases No suicides occurred in any of the pediatric trials.

There were suicides in the adult trials, but the number was not sufficient to reach any conclusion about drug effect on suicide.

It is unknown whether the suicidality risk extends to longer-term use, i.e., beyond several months.

However, there is substantial evidence from placebo-controlled maintenance trials in adults with depression that the use of antidepressants can delay the recurrence of depression.

All patients being treated with antidepressants for any indication should be monitored appropriately and observed closely for clinical worsening, suicidality, and unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases.

The following symptoms, anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric.

Although a causal link between the emergence of such symptoms and either the worsening of depression and/or the emergence of suicidal impulses has not been established, there is concern that such symptoms may represent precursors to emerging suicidality.

Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse, or who are experiencing emergent suicidality or symptoms that might be precursors to worsening depression or suicidality, especially if these symptoms are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Families and caregivers of patients being treated with antidepressants for major depressive disorder or other indications, both psychiatric and nonpsychiatric, should be alerted about the need to monitor patients for the emergence of agitation, irritability, unusual changes in behavior, and the other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to healthcare providers.

Such monitoring should include daily observation by families and caregivers.

Prescriptions for quetiapine fumarate tablets should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

Screening Patients for Bipolar Disorder: A major depressive episode may be the initial presentation of bipolar disorder.

It is generally believed (though not established in controlled trials) that treating such an episode with an antidepressant alone may increase the likelihood of precipitation of a mixed/manic episode in patients at risk for bipolar disorder.

Whether any of the symptoms described above represent such a conversion is unknown.

However, prior to initiating treatment with an antidepressant, including quetiapine, patients with depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression In placebo-controlled trials with risperidone, aripiprazole, and olanzapine in elderly subjects with dementia, there was a higher incidence of cerebrovascular adverse reactions (cerebrovascular accidents and transient ischemic attacks) including fatalities compared to placebo-treated subjects.

Quetiapine is not approved for the treatment of patients with dementia-related psychosis [see also Boxed Warning and Warnings and Precautions (5.1)].

A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with administration of antipsychotic drugs, including quetiapine fumarate tablets.

Rare cases of NMS have been reported with quetiapine fumarate tablets.

Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).

Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis) and acute renal failure.

The diagnostic evaluation of patients with this syndrome is complicated.

In arriving at a diagnosis, it is important to exclude cases where the clinical presentation includes both serious medical illness (e.g., pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and symptoms (EPS).

Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever and primary central nervous system (CNS) pathology.

The management of NMS should include: 1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; 2) intensive symptomatic treatment and medical monitoring; and 3) treatment of any concomitant serious medical problems for which specific treatments are available.

There is no general agreement about specific pharmacological treatment regimens for NMS.

If a patient requires antipsychotic drug treatment after recovery from NMS, the potential reintroduction of drug therapy should be carefully considered.

The patient should be carefully monitored since recurrences of NMS have been reported.

Atypical antipsychotic drugs have been associated with metabolic changes that include hyperglycemia/diabetes mellitus, dyslipidemia, and body weight gain.

While all of the drugs in the class have been shown to produce some metabolic changes, each drug has its own specific risk profile.

In some patients, a worsening of more than one of the metabolic parameters of weight, blood glucose, and lipids was observed in clinical studies.

Changes in these metabolic profiles should be managed as clinically appropriate.

Hyperglycemia and Diabetes Mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics, including quetiapine.

Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population.

Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse reactions is not completely understood.

However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse reactions in patients treated with the atypical antipsychotics.

Precise risk estimates for hyperglycemia-related adverse reactions in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics should be monitored regularly for worsening of glucose control.

Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment.

Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should undergo fasting blood glucose testing.

In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of the suspect drug.

Adults : Table 3: Fasting Glucose—Proportion of Patients Shifting to ≥ 126 mg/dL in Short-Term (≤ 12 weeks) Placebo-Controlled Studies * Laboratory Analyte Category Change (At Least Once) from Baseline Treatment Arm N Patients n(%) Fasting Glucose Normal to High (<100 mg/dL to ≥ 126 mg/dL) Quetiapine 2907 71 (2.4%) Placebo 1346 19 (1.4%) Borderline to High (≥ 100 mg/dL and <126 mg/dL to ≥ 126 mg/dL) Quetiapine 572 67 (11.7%) Placebo 279 33 (11.8%) Includes quetiapine fumarate tablets and quetiapine fumarate extended-release tablets data.

In a 24-week trial (active-controlled, 115 patients treated with quetiapine) designed to evaluate glycemic status with oral glucose tolerance testing of all patients, at week 24 the incidence of a treatment-emergent post-glucose challenge glucose level ≥ 200 mg/dL was 1.7% and the incidence of a fasting treatment-emergent blood glucose level ≥ 126 mg/dL was 2.6%.

The mean change in fasting glucose from baseline was 3.2 mg/dL and mean change in 2 hour glucose from baseline was -1.8 mg/dL for quetiapine.

In 2 long-term placebo-controlled randomized withdrawal clinical trials for bipolar I disorder maintenance, mean exposure of 213 days for quetiapine (646 patients) and 152 days for placebo (680 patients), the mean change in glucose from baseline was +5 mg/dL for quetiapine and –0.05 mg/dL for placebo.

The exposure-adjusted rate of any increased blood glucose level (≥ 126 mg/dL) for patients more than 8 hours since a meal (however, some patients may not have been precluded from calorie intake from fluids during fasting period) was 18 per 100 patient years for quetiapine (10.7% of patients; n=556) and 9.5 for placebo per 100 patient years (4.6% of patients; n=581).

Children and Adolescents : In a placebo-controlled quetiapine monotherapy study of adolescent patients (13 to 17 years of age) with schizophrenia (6 weeks duration), the mean change in fasting glucose levels for quetiapine (n=138) compared to placebo (n=67) was –0.75 mg/dL versus –1.7 mg/dL.

In a placebo-controlled quetiapine monotherapy study of children and adolescent patients (10 to 17 years of age) with bipolar mania (3 weeks duration), the mean change in fasting glucose level for quetiapine (n=170) compared to placebo (n=81) was 3.62 mg/dL versus –1.17 mg/dL.

No patient in either study with a baseline normal fasting glucose level (<100 mg/dL) or a baseline borderline fasting glucose level (≥100 mg/dL and <126 mg/dL) had a treatment-emergent blood glucose level of ≥126 mg/dL.

In a placebo-controlled quetiapine fumarate extended-release tablets monotherapy study (8 weeks duration) of children and adolescent patients (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the mean change in fasting glucose levels for quetiapine fumarate extended-release tablets (n = 60) compared to placebo (n = 62) was 1.8 mg/dL versus 1.6 mg/dL.

In this study, there were no patients in the quetiapine fumarate extended-release tablets or placebo-treated groups with a baseline normal fasting glucose level ( 126 mg/dL.

There was one patient in the quetiapine fumarate extended-release tablets group with a baseline borderline fasting glucose level ( > 100 mg/dL) and ( 126 mg/dL compared to zero patients in the placebo group.

Dyslipidemia Adults : Table 4 shows the percentage of adult patients with changes in total cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol from baseline by indication in clinical trials with quetiapine.

Table 4: Percentage of Adult Patients with Shifts in Total Cholesterol, Triglycerides, LDL-Cholesterol and HDL-Cholesterol from Baseline to Clinically Significant Levels by Indication Laboratory Analyte Indication Treatment Arm N Patients n (%) Total Cholesterol ≥240 mg/dL Schizophrenia * Quetiapine 137 24 (18%) Placebo 92 6 (7%) Bipolar Depression † Quetiapine 463 41 (9%) Placebo 250 15 (6%) Triglycerides ≥200 mg/dL Schizophrenia Quetiapine 120 26 (22%) Placebo 70 11 (16%) Bipolar Depression Quetiapine 436 59 (14%) Placebo 232 20 (9%) LDL-Cholesterol ≥ 160 mg/dL Schizophrenia Quetiapine na ‡ na Placebo na na Bipolar Depression Quetiapine 465 29 (6%) Placebo 256 12 (5%) HDL-Cholesterol ≤ 40 mg/dL Schizophrenia Quetiapine na na Placebo na na Bipolar Depression Quetiapine 393 56 (14%) Placebo 214 29 (14%) 6 weeks duration 8 weeks duration Parameters not measured in the quetiapine registration studies for schizophrenia.

Lipid parameters also were not measured in the bipolar mania registration studies.

Children and Adolescents : Table 5 shows the percentage of children and adolescents with changes in total cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol from baseline in clinical trials with quetiapine.

Table 5: Percentage of Children and Adolescents with Shifts in Total Cholesterol, Triglycerides, LDL-Cholesterol and HDL-Cholesterol from Baseline to Clinically Significant Levels Laboratory Analyte Indication Treatment Arm N Patients n (%) Total Cholesterol ≥200 mg/dL Schizophrenia * Quetiapine 107 13 (12%) Placebo 56 1 (2%) Bipolar Mania † Quetiapine 159 16 (10%) Placebo 66 2 (3%) Triglycerides ≥150 mg/dL Schizophrenia Quetiapine 103 17 (17%) Placebo 51 4 (8%) Bipolar Mania Quetiapine 149 32 (22%) Placebo 60 8 (13%) LDL-Cholesterol ≥ 130 mg/dL Schizophrenia Quetiapine 112 4 (4%) Placebo 60 1 (2%) Bipolar Mania Quetiapine 169 13 (8%) Placebo 74 4 (5%) HDL-Cholesterol ≤ 40 mg/dL Schizophrenia Quetiapine 104 16 (15%) Placebo 54 10 (19%) Bipolar Mania Quetiapine 154 16 (10%) Placebo 61 4 (7%) 13 to 17 years, 6 weeks duration 10 to 17 years, 3 weeks duration In a placebo-controlled quetiapine fumarate extended-release tablets monotherapy study (8 weeks duration) of children and adolescent patients (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the percentage of children and adolescents with shifts in total cholesterol (≥200 mg/dL), triglycerides (≥150 mg/dL), LDL-cholesterol (≥ 130 mg/dL) and HDL-cholesterol (≤40 mg/dL) from baseline to clinically significant levels were: total cholesterol 8% (7/83) for quetiapine fumarate extended-release tablets vs.

6% (5/84) for placebo; triglycerides 28% (22/80) for quetiapine fumarate extended-release tablets vs.

9% (7/82) for placebo; LDL-cholesterol 2% (2/86) for quetiapine fumarate extended-release tablets vs.

4% (3/85) for placebo and HDL-cholesterol 20% (13/65) for quetiapine fumarate extended-release tablets vs.

15% (11/74) for placebo.

Weight Gain Increases in weight have been observed in clinical trials.

Patients receiving quetiapine should receive regular monitoring of weight.

Adults : In clinical trials with quetiapine the following increases in weight have been reported.

Table 6: Proportion of Patients with Weight Gain ≥7% of Body Weight (Adults) Vital Sign Indication Treatment Arm N Patients n (%) Weight Gain ≥ 7% of Body Weight Schizophrenia * Quetiapine 391 89 (23%) Placebo 206 11 (6%) Bipolar Mania (monotherapy) † Quetiapine 209 44 (21%) Placebo 198 13 (7%) Bipolar Mania (adjunct therapy) ‡ Quetiapine 196 25 (13%) Placebo 203 8 (4%) Bipolar Depression § Quetiapine 554 47 (8%) Placebo 295 7 (2%) up to 6 weeks duration up to 12 weeks duration up to 3 weeks duration up to 8 weeks duration Children and Adolescents : In two clinical trials with quetiapine, one in bipolar mania and one in schizophrenia, reported increases in weight are included in table 7.

Table 7: Proportion of Patients with Weight Gain ≥7% of Body Weight (Children and Adolescents) Vital Sign Indication Treatment Arm N Patients n (%) Weight Gain ≥ 7% of Body Weight Schizophrenia * Quetiapine 111 23 (21%) Placebo 44 3 (7%) Bipolar Mania † Quetiapine 157 18 (12%) Placebo 68 0 (0%) 6 weeks duration 3 weeks duration The mean change in body weight in the schizophrenia trial was 2 kg in the quetiapine group and -0.4 kg in the placebo group and in the bipolar mania trial it was 1.7 kg in the quetiapine group and 0.4 kg in the placebo group.

In an open-label study that enrolled patients from the above two pediatric trials, 63% of patients (241/380) completed 26 weeks of therapy with quetiapine.

After 26 weeks of treatment, the mean increase in body weight was 4.4 kg.

Forty-five percent of the patients gained ≥ 7% of their body weight, not adjusted for normal growth.

In order to adjust for normal growth over 26 weeks an increase of at least 0.5 standard deviation from baseline in BMI was used as a measure of a clinically significant change; 18.3% of patients on quetiapine met this criterion after 26 weeks of treatment.

In a clinical trial for quetiapine fumarate extended-release tablets in children and adolescents (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the percentage of patients with weight gain ≥7% of body weight at any time was 15% (14/92) for quetiapine fumarate extended-release tablets vs.

10% (10/100) for placebo.

The mean change in body weight was 1.4 kg in the quetiapine fumarate extended-release tablets group vs.

0.6 kg in the placebo group.

When treating pediatric patients with quetiapine fumarate tablets for any indication, weight gain should be assessed against that expected for normal growth.

A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs, including quetiapine.

Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.

Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.

The risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase.

However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses or may even arise after discontinuation of treatment.

There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.

Antipsychotic treatment, itself, however, may suppress (or partially suppress) the signs and symptoms of the syndrome and thereby may possibly mask the underlying process.

The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown.

Given these considerations, quetiapine should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.

Chronic antipsychotic treatment should generally be reserved for patients who appear to suffer from a chronic illness that (1) is known to respond to antipsychotic drugs, and (2) for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.

In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

The need for continued treatment should be reassessed periodically.

If signs and symptoms of tardive dyskinesia appear in a patient on quetiapine, drug discontinuation should be considered.

However, some patients may require treatment with quetiapine despite the presence of the syndrome.

Quetiapine may induce orthostatic hypotension associated with dizziness, tachycardia and, in some patients, syncope, especially during the initial dose-titration period, probably reflecting its α 1 ­-adrenergic antagonist properties.

Syncope was reported in 1% (28/3265) of the patients treated with quetiapine, compared with 0.2% (2/954) on placebo and about 0.4% (2/527) on active control drugs.

Orthostatic hypotension, dizziness, and syncope may lead to falls.

Quetiapine should be used with particular caution in patients with known cardiovascular disease (history of myocardial infarction or ischemic heart disease, heart failure or conduction abnormalities), cerebrovascular disease or conditions which would predispose patients to hypotension (dehydration, hypovolemia and treatment with antihypertensive medications).

The risk of orthostatic hypotension and syncope may be minimized by limiting the initial dose to 25 mg twice daily [ s ee Dosage and Administration ( 2.2 )] .

If hypotension occurs during titration to the target dose, a return to the previous dose in the titration schedule is appropriate.

In placebo-controlled trials in children and adolescents with schizophrenia (6-week duration) or bipolar mania (3-week duration), the incidence of increases at any time in systolic blood pressure (≥20 mmHg) was 15.2% (51/335) for quetiapine and 5.5% (9/163) for placebo; the incidence of increases at any time in diastolic blood pressure (≥10 mmHg) was 40.6% (136/335) for quetiapine and 24.5% (40/163) for placebo.

In the 26-week open-label clinical trial, one child with a reported history of hypertension experienced a hypertensive crisis.

Blood pressure in children and adolescents should be measured at the beginning of, and periodically during treatment.

In a placebo-controlled quetiapine fumarate extended-release tablets clinical trial (8 weeks duration) in children and adolescents (10 to 17 years of age) with bipolar depression, in which efficacy was not established, the incidence of increases at any time in systolic blood pressure (≥20 mmHg) was 6.5% (6/92) for quetiapine fumarate extended-release tablets and 6% (6/100) for placebo; the incidence of increases at any time in diastolic blood pressure (≥10 mmHg) was 46.7% (43/92) for quetiapine fumarate extended-release tablets and 36% (36/100) for placebo.

In clinical trial and postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to atypical antipsychotic agents, including quetiapine.

Agranulocytosis (including fatal cases) has also been reported.

Possible risk factors for leukopenia/neutropenia include preexisting low white cell count (WBC) and history of drug induced leukopenia/neutropenia.

Patients with a preexisting low WBC or a history of drug induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and should discontinue quetiapine at the first sign of a decline in WBC in absence of other causative factors.

Patients with neutropenia should be carefully monitored for fever or other symptoms or signs of infection and treated promptly if such symptoms or signs occur.

Patients with severe neutropenia (absolute neutrophil count <1000/mm 3 ) should discontinue quetiapine and have their WBC followed until recovery.

The development of cataracts was observed in association with quetiapine treatment in chronic dog studies [ see Nonclinical Toxicology ( 13.2 )].

Lens changes have also been observed in adults, children and adolescents during long-term quetiapine treatment, but a causal relationship to quetiapine use has not been established.

Nevertheless, the possibility of lenticular changes cannot be excluded at this time.

Therefore, examination of the lens by methods adequate to detect cataract formation, such as slit lamp exam or other appropriately sensitive methods, is recommended at initiation of treatment or shortly thereafter, and at 6-month intervals during chronic treatment.

In clinical trials quetiapine was not associated with a persistent increase in QT intervals.

However, the QT effect was not systematically evaluated in a thorough QT study.

In post marketing experience, there were cases reported of QT prolongation in patients who overdosed on quetiapine [see Overdosage (10.1)] , in patients with concomitant illness, and in patients taking medicines known to cause electrolyte imbalance or increase QT interval [see Drug Interactions (7.1)] .

The use of quetiapine should be avoided in combination with other drugs that are known to prolong QTc including Class 1A antiarrythmics (e.g., quinidine, procainamide) or Class III antiarrythmics (e.g., amiodarone, sotalol), antipsychotic medications (e.g., ziprasidone, chlorpromazine, thioridazine), antibiotics (e.g., gatifloxacin, moxifloxacin), or any other class of medications known to prolong the QTc interval (e.g., pentamidine, levomethadyl acetate, methadone).

Quetiapine should also be avoided in circumstances that may increase the risk of occurrence of torsade de pointes and/or sudden death including (1) a history of cardiac arrhythmias such as bradycardia; (2) hypokalemia or hypomagnesemia; (3) concomitant use of other drugs that prolong the QTc interval; and (4) presence of congenital prolongation of the QT interval.

Caution should also be exercised when quetiapine is prescribed in patients with increased risk of QT prolongation (e.g.

cardiovascular disease, family history of QT prolongation, the elderly, congestive heart failure and heart hypertrophy).

During clinical trials, seizures occurred in 0.5% (20/3490) of patients treated with quetiapine compared to 0.2% (2/954) on placebo and 0.7% (4/527) on active control drugs.

As with other antipsychotics, quetiapine should be used cautiously in patients with a history of seizures or with conditions that potentially lower the seizure threshold, e.g., Alzheimer’s dementia.

Conditions that lower the seizure threshold may be more prevalent in a population of 65 years or older.

Adults: Clinical trials with quetiapine demonstrated dose-related decreases in thyroid hormone levels.

The reduction in total and free thyroxine (T4) of approximately 20% at the higher end of the therapeutic dose range was maximal in the first six weeks of treatment and maintained without adaptation or progression during more chronic therapy.

In nearly all cases, cessation of quetiapine treatment was associated with a reversal of the effects on total and free T4, irrespective of the duration of treatment.

The mechanism by which quetiapine effects the thyroid axis is unclear.

If there is an effect on the hypothalamic-pituitary axis, measurement of TSH alone may not accurately reflect a patient’s thyroid status.

Therefore, both TSH and free T4, in addition to clinical assessment, should be measured at baseline and at follow-up.

In the mania adjunct studies, where quetiapine was added to lithium or divalproex, 12% (24/196) of quetiapine treated patients compared to 7% (15/203) of placebo-treated patients had elevated TSH levels.

Of the quetiapine treated patients with elevated TSH levels, 3 had simultaneous low free T4 levels (free T4 <0.8 LLN).

About 0.7% (26/3489) of quetiapine patients did experience TSH increases in monotherapy studies.

Some patients with TSH increases needed replacement thyroid treatment.

In all quetiapine trials, the incidence of significant shifts in thyroid hormones and TSH were*: decrease in free T4 (free T4 <0.8 LLN), 2% (357/17513); decrease in total T4, 4% (75/1861); decrease in free T3, 0.4% (53/13766); decrease in total T3, 2% (26/1312), and increase in TSH, 4.9% (956/19412).

In eight patients, where TBG was measured, levels of TBG were unchanged.

Table 8 shows the incidence of these shifts in short-term placebo-controlled clinical trials.

Table 8: Incidence of shifts in thyroid hormone levels and TSH in short-term placebo-controlled clinical trials * , † Total T4 Free T4 Total T3 Free T3 TSH Quetiapine Placebo Quetiapine Placebo Quetiapine Placebo Quetiapine Placebo Quetiapine Placebo 3.4 % (37/1097) 0.6% (4/651) 0.7% (52/7218) 0.1% (4/3668) 0.5% (2/369) 0% (0/113) 0.2% (11/5673) 0% (1/2679) 3.2% (240/7587) 2.7% (105/3912) Based on shifts from normal baseline to potentially clinically important value at anytime post-baseline.

Shifts in total T Includes quetiapine fumarate tablets and quetiapine fumarate extended-release tablets data.

In short-term placebo-controlled monotherapy trials, the incidence of reciprocal, shifts in T 3 and TSH was 0 % for both quetiapine (1/4800) and placebo (0/2190) and for T 4 and TSH the shifts were 0.1% (7/6154) for quetiapine versus 0% (1/3007) for placebo.

Children and Adolescents : In acute placebo-controlled trials in children and adolescent patients with schizophrenia (6-week duration) or bipolar mania (3-week duration), the incidence of shifts for thyroid function values at any time for quetiapine treated patients and placebo-treated patients for elevated TSH was 2.9% (8/280) vs.

0.7% (1/138), respectively and for decreased total thyroxine was 2.8% (8/289) vs.

0% (0/145, respectively).

Of the quetiapine treated patients with elevated TSH levels, 1 had simultaneous low free T4 level at end of treatment.

Adults : During clinical trials with quetiapine, the incidence of shifts in prolactin levels to a clinically significant value occurred in 3.6% (158/4416) of patients treated with quetiapine compared to 2.6% (51/1968) on placebo.

Children and Adolescents : In acute placebo-controlled trials in children and adolescent patients with bipolar mania (3-week duration) or schizophrenia (6-week duration), the incidence of shifts in prolactin levels to a value (>20 mcg/L males; > 26 mcg/L females at any time) was 13.4% (18/134) for quetiapine compared to 4% (3/75) for placebo in males and 8.7% (9/104) for quetiapine compared to 0% (0/39) for placebo in females.

Like other drugs that antagonize dopamine D 2 receptors, quetiapine elevates prolactin levels in some patients and the elevation may persist during chronic administration.

Hyperprolactinemia, regardless of etiology, may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotrophin secretion.

This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is considered in a patient with previously detected breast cancer.

As is common with compounds which increase prolactin release, mammary gland, and pancreatic islet cell neoplasia (mammary adenocarcinomas, pituitary and pancreatic adenomas) was observed in carcinogenicity studies conducted in mice and rats.

Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans, but the available evidence is too limited to be conclusive [see Nonclinical Toxicology (13.1)] .

Somnolence was a commonly reported adverse event reported in patients treated with quetiapine especially during the 3 to 5 day period of initial dose-titration.

In schizophrenia trials, somnolence was reported in 18% (89/510) of patients on quetiapine compared to 11% (22/206) of placebo patients.

In acute bipolar mania trials using quetiapine as monotherapy, somnolence was reported in 16% (34/209) of patients on quetiapine compared to 4% of placebo patients.

In acute bipolar mania trials using quetiapine as adjunct therapy, somnolence was reported in 34% (66/196) of patients on quetiapine compared to 9% (19/203) of placebo patients.

In bipolar depression trials, somnolence was reported in 57% (398/698) of patients on quetiapine compared to 15% (51/347) of placebo patients.

Since quetiapine has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about performing activities requiring mental alertness, such as operating a motor vehicle (including automobiles) or operating hazardous machinery until they are reasonably certain that quetiapine therapy does not affect them adversely.

Somnolence may lead to falls.

Although not reported with quetiapine, disruption of the body’s ability to reduce core body temperature has been attributed to antipsychotic agents.

Appropriate care is advised when prescribing quetiapine for patients who will be experiencing conditions which may contribute to an elevation in core body temperature, e.g., exercising strenuously, exposure to extreme heat, receiving concomitant medication with anticholinergic activity, or being subject to dehydration.

Esophageal dysmotility and aspiration have been associated with antipsychotic drug use.

Aspiration pneumonia is a common cause of morbidity and mortality in elderly patients, in particular those with advanced Alzheimer’s dementia.

Quetiapine and other antipsychotic drugs should be used cautiously in patients at risk for aspiration pneumonia.

Acute withdrawal symptoms, such as insomnia, nausea, and vomiting have been described after abrupt cessation of atypical antipsychotic drugs, including quetiapine.

In short-term placebo-controlled, monotherapy clinical trials with quetiapine fumarate extended-release tablets that included a discontinuation phase which evaluated discontinuation symptoms, the aggregated incidence of patients experiencing one or more discontinuation symptoms after abrupt cessation was 12.1% (241/1993) for quetiapine fumarate extended-release tablets and 6.7% (71/1065) for placebo.

The incidence of the individual adverse events (i.e., insomnia, nausea, headache, diarrhea, vomiting, dizziness and irritability) did not exceed 5.3% in any treatment group and usually resolved after 1 week post-discontinuation.

Gradual withdrawal is advised.

INFORMATION FOR PATIENTS

Information For Patients Section See FDA-approved patient labeling (Medication Guide) Prescribers or other health professionals should inform patients, their families, and their caregivers about the benefits and risks associated with treatment with quetiapine fumarate tablets and should counsel them in its appropriate use.

A patient Medication Guide about “Antidepressant Medicines, Depression and other Serious Mental Illness, and Suicidal Thoughts or Actions” is available for quetiapine fumarate tablets.

The prescriber or health professional should instruct patients, their families, and their caregivers to read the Medication Guide and should assist them in understanding its contents.

Patients should be given the opportunity to discuss the contents of the Medication Guide and to obtain answers to any questions they may have.

The complete text of the Medication Guide is reprinted at the end of this document.

Patients should be advised of the following issues and asked to alert their prescriber if these occur while taking quetiapine fumarate tablets.

Increased Mortality in Elderly Patients with Dementia-Related Psychosis Patients and caregivers should be advised that elderly patients with dementia-related psychosis treated with atypical antipsychotic drugs are at increased risk of death compared with placebo.

Quetiapine is not approved for elderly patients with dementia-related psychosis [see Warnings and Precautions (5.1)] .

Suicidal Thoughts and Behaviors Patients, their families, and their caregivers should be encouraged to be alert to the emergence of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, mania, other unusual changes in behavior, worsening of depression, and suicidal ideation, especially early during antidepressant treatment and when the dose is adjusted up or down.

Families and caregivers of patients should be advised to look for the emergence of such symptoms on a day-to-day basis, since changes may be abrupt.

Such symptoms should be reported to the patient’s prescriber or health professional, especially if they are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Symptoms such as these may be associated with an increased risk for suicidal thinking and behavior and indicate a need for very close monitoring and possibly changes in the medication [ s ee Warnings and Precautions (5.2)] .

Neuroleptic Malignant Syndrome (NMS) Patients should be advised to report to their physician any signs or symptoms that may be related to NMS.

These may include muscle stiffness and high fever [ s ee Warnings and Precautions (5.4)] .

Hyperglycemia and Diabetes Mellitus Patients should be aware of the symptoms of hyperglycemia (high blood sugar) and diabetes mellitus.

Patients who are diagnosed with diabetes, those with risk factors for diabetes, or those that develop these symptoms during treatment should have their blood glucose monitored at the beginning of and periodically during treatment [ s ee Warnings and Precautions (5.5)] .

Hyperlipidemia Patients should be advised that elevations in total cholesterol, LDL-cholesterol and triglycerides and decreases in HDL-cholesterol may occur.

Patients should have their lipid profile monitored at the beginning of and periodically during treatment [ s ee Warnings and Precautions (5.5)].

Weight Gain Patients should be advised that they may experience weight gain.

Patients should have their weight monitored regularly [ s ee Warnings and Precautions (5.5)].

Orthostatic Hypotension Patients should be advised of the risk of orthostatic hypotension (symptoms include feeling dizzy or lightheaded upon standing, which may lead to falls), especially during the period of initial dose titration, and also at times of re-initiating treatment or increases in dose [ s ee Warnings and Precautions (5.7)].

Increased Blood Pressure in Children and Adolescents Children and adolescent patients should have their blood pressure measured at the beginning of, and periodically during, treatment [ s ee Warnings and Precautions (5.8)] .

Leukopenia/Neutropenia Patients with a preexisting low WBC or a history of drug induced leukopenia/neutropenia should be advised that they should have their CBC monitored while taking quetiapine fumarate tablets [ s ee Warnings and Precautions (5.9)].

Interference with Cognitive and Motor Performance Patients should be advised of the risk of somnolence or sedation (which may lead to falls), especially during the period of initial dose titration.

Patients should be cautioned about performing any activity requiring mental alertness, such as operating a motor vehicle (including automobiles) or operating machinery, until they are reasonably certain quetiapine therapy does not affect them adversely.

[ s ee Warnings and Precautions (5.15)].

Heat Exposure and Dehydration Patients should be advised regarding appropriate care in avoiding overheating and dehydration [ s ee Warnings and Precautions (5.16)].

Concomitant Medication As with other medications, patients should be advised to notify their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs .

[ s ee Drug Interactions (7.1)] .

Pregnancy and Nursing Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy with quetiapine fumarate tablets.

[see Use in Specific Populations (8.1) and (8.3)].

Need for Comprehensive Treatment Program Quetiapine fumarate tablets are indicated as an integral part of a total treatment program for adolescents with schizophrenia and pediatric bipolar disorder that may include other measures (psychological, educational, and social).

Effectiveness and safety of quetiapine fumarate tablets have not been established in pediatric patients less than 13 years of age for schizophrenia or less than 10 years of age for bipolar mania.

Appropriate educational placement is essential and psychosocial intervention is often helpful.

The decision to prescribe atypical antipsychotic medication will depend upon the physician’s assessment of the chronicity and severity of the patient’s symptoms [see Indications and Usage (1.3)] .

DOSAGE AND ADMINISTRATION

Dosage & Administration Section Quetiapine fumarate tablets can be taken with or without food ( 2.1 ) Indication Initial Dose Recommended Dose Maximum Dose Schizophrenia-Aults ( 2.2 ) 25 mg twice daily 150 to 750 mg/day 750 mg/day Schizophrenia-Adolescents (13 to 17 years) ( 2.2 ) 25 mg twice daily 400 to 800 mg/day 800 mg/day Bipolar Mania- Adults Monotherapy or as an adjunct to lithium or divalproex ( 2.2 ) 50 mg twice daily 400 to 800 mg/day 800 mg/day Bipolar Mania- Children and Adolescents (10 to 17 years), Monotherapy ( 2.2 ) 25 mg twice daily 400 to 600 mg/day 600 mg/day Bipolar Depression-Adults ( 2.2 ) 50 mg once daily at bedtime 300 mg/day 300 mg/day Geriatric Use: Consider a lower starting dose (50 mg/day), slower titration and careful monitoring during the initial dosing period in the elderly ( 2.3 , 8.5 ) Hepatic Impairment: Lower starting dose (25 mg/day) and slower titration may be needed ( 2.4 , 8.7 , 12.3 ) Quetiapine fumarate tablets can be taken with or without food.

The recommended initial dose, titration, dose range and maximum quetiapine fumarate tablets dose for each approved indication is displayed in Table 1.

After initial dosing, adjustments can be made upwards or downwards, if necessary, depending upon the clinical response and tolerability of the patient [see Clinical Studies (14.1 and 14.2)].

Table 1: Recommended Dosing for Quetiapine Fumarate Tablets Indication Initial Dose and Titration Recommended Dose Maximum Dose Schizophrenia-Adults Day 1: 25 mg twice daily.

Increase in increments of 25 mg to 50 mg divided two or three times on Days 2 and 3 to range of 300 to 400 mg by Day 4.

Further adjustments can be made in increments of 25 to 50 mg twice a day, in intervals of not less than 2 days.

150 to 750 mg/day 750 mg/day Schizophrenia- Adolescents (13 to 17 years) Day 1: 25 mg twice daily.

Day 2: Twice daily dosing totaling 100 mg.

Day 3: Twice daily dosing totaling 200 mg.

Day 4: Twice daily dosing totaling 300 mg.

Day 5: Twice daily dosing totaling 400 mg.

Further adjustments should be in increments no greater than 100 mg/day within the recommended dose range of 400 to 800 mg/day.

Based on response and tolerability, may be administered three times daily.

400 to 800 mg/day 800 mg/day Schizophrenia-Maintenance N/A * 400 to 800 mg/day 800 mg/day Bipolar Mania- Adults Monotherapy or as an adjunct to lithium or divalproex Day 1: Twice daily dosing totaling 100 mg.

Day 2: Twice daily dosing totaling 200 mg.

Day 3: Twice daily dosing totaling 300 mg.

Day 4: Twice daily dosing totaling 400 mg.

Further dosage adjustments up to 800 mg/day by Day 6 should be in increments of no greater than 200 mg/day.

400 to 800 mg/day 800 mg/day Bipolar Mania-Children and Adolescents (10 to 17 years), Monotherapy Day 1: 25 mg twice daily.

Day 2: Twice daily dosing totaling 100 mg.

Day 3: Twice daily dosing totaling 200 mg.

Day 4: Twice daily dosing totaling 300 mg.

Day 5: Twice daily dosing totaling 400 mg.

Further adjustments should be in increments no greater than 100 mg/day within the recommended dose range of 400 to 600 mg/day.

Based on response and tolerability, may be administered three times daily.

400 to 600 mg/day 600 mg/day Bipolar Depression- Adults Administer once daily at bedtime.

Day 1: 50 mg Day 2: 100 mg Day 3: 200 mg Day 4: 300 mg 300 mg/day 300 mg/day Bipolar I Disorder Maintenance Therapy- Adults Administer twice daily totaling 400 to 800 mg/day as adjunct to lithium or divalproex.

Generally, in the maintenance phase, patients continued on the same dose on which they were stabilized.

400 to 800 mg/day 800 mg/day N/A Not applicable Maintenance Treatment for Schizophrenia and Bipolar I Disorder Maintenance Treatment —Patients should be periodically reassessed to determine the need for maintenance treatment and the appropriate dose for such treatment [see Clinical Studies (14.2)].

Consideration should be given to a slower rate of dose titration and a lower target dose in the elderly and in patients who are debilitated or who have a predisposition to hypotensive reactions [see Clinical Pharmacology (12.3)] .

When indicated, dose escalation should be performed with caution in these patients.

Elderly patients should be started on quetiapine fumarate tablets 50 mg/day and the dose can be increased in increments of 50 mg/day depending on the clinical response and tolerability of the individual patient .

Patients with hepatic impairment should be started on 25 mg/day.

The dose should be increased daily in increments of 25 mg/day to 50 mg/day to an effective dose, depending on the clinical response and tolerability of the patient.

Quetiapine fumarate tablets dose should be reduced to one sixth of original dose when co-medicated with a potent CYP3A4 inhibitor (e.g., ketoconazole, itraconazole, indinavir, ritonavir, nefazodone, etc.).

When the CYP3A4 inhibitor is discontinued, the dose of quetiapine fumarate tablets should be increased by 6 fold [see Clinical Pharmacology (12.3) and Drug Interactions (7.1)] .

Quetiapine fumarate tablets dose should be increased up to 5 fold of the original dose when used in combination with a chronic treatment (e.g., greater than 7 to 14 days) of a potent CYP3A4 inducer (e.g., phenytoin, carbamazepine, rifampin, avasimibe, St.

John’s wort etc.).

The dose should be titrated based on the clinical response and tolerability of the individual patient.

When the CYP3A4 inducer is discontinued, the dose of quetiapine fumarate tablets should be reduced to the original level within 7 to 14 days [see Clinical Pharmacology (12.3) and Drug Interactions (7.1)] .

Although there are no data to specifically address re-initiation of treatment, it is recommended that when restarting therapy of patients who have been off quetiapine fumarate tablets for more than one week, the initial dosing schedule should be followed.

When restarting patients who have been off quetiapine fumarate tablets for less than one week, gradual dose escalation may not be required and the maintenance dose may be reinitiated.

There are no systematically collected data to specifically address switching patients with schizophrenia from antipsychotics to quetiapine fumarate tablets, or concerning concomitant administration with antipsychotics.

While immediate discontinuation of the previous antipsychotic treatment may be acceptable for some patients with schizophrenia, more gradual discontinuation may be most appropriate for others.

In all cases, the period of overlapping antipsychotic administration should be minimized.

When switching patients with schizophrenia from depot antipsychotics, if medically appropriate, initiate quetiapine fumarate tablets therapy in place of the next scheduled injection.

The need for continuing existing EPS medication should be re-evaluated periodically.

DRUG INTERACTIONS

7 Due to CNS effects, use caution when administering with other centrally-acting drugs.

Avoid alcohol.

( 7.1 ) Due to hypotensive effects, hypotensive effects of other drugs with this potential may be enhanced.

( 7.2 ) Effects of levodopa and dopamine agonists may be antagonized.

( 7.3 ) Cimetidine and ranitidine increase the bioavailability of risperidone.

( 7.5 ) Clozapine may decrease clearance of risperidone.

( 7.6 ) Fluoxetine and paroxetine increase plasma concentrations of risperidone.

( 7.10 ) Carbamazepine and other enzyme inducers decrease plasma concentrations of risperidone.

( 7.11 ) 7.1 Centrally-Acting Drugs and Alcohol Given the primary CNS effects of risperidone, caution should be used when RISPERDAL ® is taken in combination with other centrally-acting drugs and alcohol.

7.2 Drugs with Hypotensive Effects Because of its potential for inducing hypotension, RISPERDAL ® may enhance the hypotensive effects of other therapeutic agents with this potential.

7.3 Levodopa and Dopamine Agonists RISPERDAL ® may antagonize the effects of levodopa and dopamine agonists.

7.4 Amitriptyline Amitriptyline did not affect the pharmacokinetics of risperidone or risperidone and 9-hydroxyrisperidone combined.

7.5 Cimetidine and Ranitidine Cimetidine and ranitidine increased the bioavailability of risperidone by 64% and 26%, respectively.

However, cimetidine did not affect the AUC of risperidone and 9-hydroxyrisperidone combined, whereas ranitidine increased the AUC of risperidone and 9-hydroxyrisperidone combined by 20%.

7.6 Clozapine Chronic administration of clozapine with RISPERDAL ® may decrease the clearance of risperidone.

7.7 Lithium Repeated oral doses of RISPERDAL ® (3 mg twice daily) did not affect the exposure (AUC) or peak plasma concentrations (C max ) of lithium (n=13).

7.8 Valproate Repeated oral doses of RISPERDAL ® (4 mg once daily) did not affect the pre-dose or average plasma concentrations and exposure (AUC) of valproate (1000 mg/day in three divided doses) compared to placebo (n=21).

However, there was a 20% increase in valproate peak plasma concentration (C max ) after concomitant administration of RISPERDAL ® .

7.9 Digoxin RISPERDAL ® (0.25 mg twice daily) did not show a clinically relevant effect on the pharmacokinetics of digoxin.

7.10 Drugs That Inhibit CYP 2D6 and Other CYP Isozymes Risperidone is metabolized to 9-hydroxyrisperidone by CYP 2D6, an enzyme that is polymorphic in the population and that can be inhibited by a variety of psychotropic and other drugs [see Clinical Pharmacology (12.3) ] .

Drug interactions that reduce the metabolism of risperidone to 9-hydroxyrisperidone would increase the plasma concentrations of risperidone and lower the concentrations of 9-hydroxyrisperidone.

Analysis of clinical studies involving a modest number of poor metabolizers (n≅70) does not suggest that poor and extensive metabolizers have different rates of adverse effects.

No comparison of effectiveness in the two groups has been made.

In vitro studies showed that drugs metabolized by other CYP isozymes, including 1A1, 1A2, 2C9, 2C19, and 3A4, are only weak inhibitors of risperidone metabolism.

Fluoxetine and Paroxetine Fluoxetine (20 mg once daily) and paroxetine (20 mg once daily) have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

When either concomitant fluoxetine or paroxetine is initiated or discontinued, the physician should re-evaluate the dosing of RISPERDAL ® .

The effects of discontinuation of concomitant fluoxetine or paroxetine therapy on the pharmacokinetics of risperidone and 9-hydroxyrisperidone have not been studied.

Erythromycin There were no significant interactions between RISPERDAL ® and erythromycin.

7.11 Carbamazepine and Other Enzyme Inducers Carbamazepine co-administration decreased the steady-state plasma concentrations of risperidone and 9-hydroxyrisperidone by about 50%.

Plasma concentrations of carbamazepine did not appear to be affected.

The dose of RISPERDAL ® may need to be titrated accordingly for patients receiving carbamazepine, particularly during initiation or discontinuation of carbamazepine therapy.

Co-administration of other known enzyme inducers (e.g., phenytoin, rifampin, and phenobarbital) with RISPERDAL ® may cause similar decreases in the combined plasma concentrations of risperidone and 9-hydroxyrisperidone, which could lead to decreased efficacy of RISPERDAL ® treatment.

7.12 Drugs Metabolized by CYP 2D6 In vitro studies indicate that risperidone is a relatively weak inhibitor of CYP 2D6.

Therefore, RISPERDAL ® is not expected to substantially inhibit the clearance of drugs that are metabolized by this enzymatic pathway.

In drug interaction studies, RISPERDAL ® did not significantly affect the pharmacokinetics of donepezil and galantamine, which are metabolized by CYP 2D6.

OVERDOSAGE

10 10.1 Human Experience Premarketing experience included eight reports of acute RISPERDAL ® overdosage with estimated doses ranging from 20 to 300 mg and no fatalities.

In general, reported signs and symptoms were those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness and sedation, tachycardia and hypotension, and extrapyramidal symptoms.

One case, involving an estimated overdose of 240 mg, was associated with hyponatremia, hypokalemia, prolonged QT, and widened QRS.

Another case, involving an estimated overdose of 36 mg, was associated with a seizure.

Postmarketing experience includes reports of acute RISPERDAL ® overdosage, with estimated doses of up to 360 mg.

In general, the most frequently reported signs and symptoms are those resulting from an exaggeration of the drug’s known pharmacological effects, i.e., drowsiness, sedation, tachycardia, hypotension, and extrapyramidal symptoms.

Other adverse reactions reported since market introduction related to RISPERDAL ® overdose include prolonged QT interval and convulsions.

Torsade de pointes has been reported in association with combined overdose of RISPERDAL ® and paroxetine.

10.2 Management of Overdosage In case of acute overdosage, establish and maintain an airway and ensure adequate oxygenation and ventilation.

Gastric lavage (after intubation, if patient is unconscious) and administration of activated charcoal together with a laxative should be considered.

Because of the rapid disintegration of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets, pill fragments may not appear in gastric contents obtained with lavage.

The possibility of obtundation, seizures, or dystonic reaction of the head and neck following overdose may create a risk of aspiration with induced emesis.

Cardiovascular monitoring should commence immediately and should include continuous electrocardiographic monitoring to detect possible arrhythmias.

If antiarrhythmic therapy is administered, disopyramide, procainamide, and quinidine carry a theoretical hazard of QT-prolonging effects that might be additive to those of risperidone.

Similarly, it is reasonable to expect that the alpha-blocking properties of bretylium might be additive to those of risperidone, resulting in problematic hypotension.

There is no specific antidote to RISPERDAL ® .

Therefore, appropriate supportive measures should be instituted.

The possibility of multiple drug involvement should be considered.

Hypotension and circulatory collapse should be treated with appropriate measures, such as intravenous fluids and/or sympathomimetic agents (epinephrine and dopamine should not be used, since beta stimulation may worsen hypotension in the setting of risperidone-induced alpha blockade).

In cases of severe extrapyramidal symptoms, anticholinergic medication should be administered.

Close medical supervision and monitoring should continue until the patient recovers.

DESCRIPTION

11 RISPERDAL ® contains risperidone, a psychotropic agent belonging to the chemical class of benzisoxazole derivatives.

The chemical designation is 3-[2-[4-(6-fluoro-1,2-benzisoxazol-3-yl)-1-piperidinyl]ethyl]-6,7,8,9-tetrahydro-2-methyl-4H-pyrido[1,2-a]pyrimidin-4-one.

Its molecular formula is C 23 H 27 FN 4 O 2 and its molecular weight is 410.49.

The structural formula is: Risperidone is a white to slightly beige powder.

It is practically insoluble in water, freely soluble in methylene chloride, and soluble in methanol and 0.1 N HCl.

RISPERDAL ® Tablets are available in 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green) strengths.

RISPERDAL ® tablets contain the following inactive ingredients: colloidal silicon dioxide, hypromellose, lactose, magnesium stearate, microcrystalline cellulose, propylene glycol, sodium lauryl sulfate, and starch (corn).

The 0.25 mg, 0.5 mg, 2 mg, 3 mg, and 4 mg tablets also contain talc and titanium dioxide.

The 0.25 mg tablets contain yellow iron oxide; the 0.5 mg tablets contain red iron oxide; the 2 mg tablets contain FD&C Yellow No.

6 Aluminum Lake; the 3 mg and 4 mg tablets contain D&C Yellow No.

10; the 4 mg tablets contain FD&C Blue No.

2 Aluminum Lake.

RISPERDAL ® is also available as a 1 mg/mL oral solution.

RISPERDAL ® Oral Solution contains the following inactive ingredients: tartaric acid, benzoic acid, sodium hydroxide, and purified water.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in 0.5 mg (light coral), 1 mg (light coral), 2 mg (coral), 3 mg (coral), and 4 mg (coral) strengths.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain the following inactive ingredients: Amberlite ® resin, gelatin, mannitol, glycine, simethicone, carbomer, sodium hydroxide, aspartame, red ferric oxide, and peppermint oil.

In addition, the 2 mg, 3 mg, and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets contain xanthan gum.

Chemical Structure

CLINICAL STUDIES

14 14.1 Schizophrenia Adults Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of schizophrenia was established in four short-term (4- to 8-week) controlled trials of psychotic inpatients who met DSM-III-R criteria for schizophrenia.

Several instruments were used for assessing psychiatric signs and symptoms in these studies, among them the Brief Psychiatric Rating Scale (BPRS), a multi-item inventory of general psychopathology traditionally used to evaluate the effects of drug treatment in schizophrenia.

The BPRS psychosis cluster (conceptual disorganization, hallucinatory behavior, suspiciousness, and unusual thought content) is considered a particularly useful subset for assessing actively psychotic schizophrenic patients.

A second traditional assessment, the Clinical Global Impression (CGI), reflects the impression of a skilled observer, fully familiar with the manifestations of schizophrenia, about the overall clinical state of the patient.

In addition, the Positive and Negative Syndrome Scale (PANSS) and the Scale for Assessing Negative Symptoms (SANS) were employed.

The results of the trials follow: (1)In a 6-week, placebo-controlled trial (n=160) involving titration of RISPERDAL ® in doses up to 10 mg/day (twice-daily schedule), RISPERDAL ® was generally superior to placebo on the BPRS total score, on the BPRS psychosis cluster, and marginally superior to placebo on the SANS.

(2)In an 8-week, placebo-controlled trial (n=513) involving 4 fixed doses of RISPERDAL ® (2 mg/day, 6 mg/day, 10 mg/day, and 16 mg/day, on a twice-daily schedule), all 4 RISPERDAL ® groups were generally superior to placebo on the BPRS total score, BPRS psychosis cluster, and CGI severity score; the 3 highest RISPERDAL ® dose groups were generally superior to placebo on the PANSS negative subscale.

The most consistently positive responses on all measures were seen for the 6 mg dose group, and there was no suggestion of increased benefit from larger doses.

(3)In an 8-week, dose comparison trial (n=1356) involving 5 fixed doses of RISPERDAL ® (1 mg/day, 4 mg/day, 8 mg/day, 12 mg/day, and 16 mg/day, on a twice-daily schedule), the four highest RISPERDAL ® dose groups were generally superior to the 1 mg RISPERDAL ® dose group on BPRS total score, BPRS psychosis cluster, and CGI severity score.

None of the dose groups were superior to the 1 mg group on the PANSS negative subscale.

The most consistently positive responses were seen for the 4 mg dose group.

(4)In a 4-week, placebo-controlled dose comparison trial (n=246) involving 2 fixed doses of RISPERDAL ® (4 and 8 mg/day on a once-daily schedule), both RISPERDAL ® dose groups were generally superior to placebo on several PANSS measures, including a response measure (>20% reduction in PANSS total score), PANSS total score, and the BPRS psychosis cluster (derived from PANSS).

The results were generally stronger for the 8 mg than for the 4 mg dose group.

Long-Term Efficacy In a longer-term trial, 365 adult outpatients predominantly meeting DSM-IV criteria for schizophrenia and who had been clinically stable for at least 4 weeks on an antipsychotic medication were randomized to RISPERDAL ® (2–8 mg/day) or to an active comparator, for 1 to 2 years of observation for relapse.

Patients receiving RISPERDAL ® experienced a significantly longer time to relapse over this time period compared to those receiving the active comparator.

Pediatrics The efficacy of RISPERDAL ® in the treatment of schizophrenia in adolescents aged 13–17 years was demonstrated in two short-term (6 and 8 weeks), double-blind controlled trials.

All patients met DSM-IV diagnostic criteria for schizophrenia and were experiencing an acute episode at time of enrollment.

In the first trial (study #1), patients were randomized into one of three treatment groups: RISPERDAL ® 1–3 mg/day (n = 55, mean modal dose = 2.6 mg), RISPERDAL ® 4–6 mg/day (n = 51, mean modal dose = 5.3 mg), or placebo (n = 54).

In the second trial (study #2), patients were randomized to either RISPERDAL ® 0.15–0.6 mg/day (n = 132, mean modal dose = 0.5 mg) or RISPERDAL ® 1.5–6 mg/day (n = 125, mean modal dose = 4 mg).

In all cases, study medication was initiated at 0.5 mg/day (with the exception of the 0.15–0.6 mg/day group in study #2, where the initial dose was 0.05 mg/day) and titrated to the target dosage range by approximately Day 7.

Subsequently, dosage was increased to the maximum tolerated dose within the target dose range by Day 14.

The primary efficacy variable in all studies was the mean change from baseline in total PANSS score.

Results of the studies demonstrated efficacy of RISPERDAL ® in all dose groups from 1–6 mg/day compared to placebo, as measured by significant reduction of total PANSS score.

The efficacy on the primary parameter in the 1–3 mg/day group was comparable to the 4–6 mg/day group in study #1, and similar to the efficacy demonstrated in the 1.5–6 mg/day group in study #2.

In study #2, the efficacy in the 1.5–6 mg/day group was statistically significantly greater than that in the 0.15–0.6 mg/day group.

Doses higher than 3 mg/day did not reveal any trend towards greater efficacy.

14.2 Bipolar Mania – Monotherapy Adults The efficacy of RISPERDAL ® in the treatment of acute manic or mixed episodes was established in two short-term (3-week) placebo-controlled trials in patients who met the DSM-IV criteria for Bipolar I Disorder with manic or mixed episodes.

These trials included patients with or without psychotic features.

The primary rating instrument used for assessing manic symptoms in these trials was the Young Mania Rating Scale (YMRS), an 11-item clinician-rated scale traditionally used to assess the degree of manic symptomatology (irritability, disruptive/aggressive behavior, sleep, elevated mood, speech, increased activity, sexual interest, language/thought disorder, thought content, appearance, and insight) in a range from 0 (no manic features) to 60 (maximum score).

The primary outcome in these trials was change from baseline in the YMRS total score.

The results of the trials follow: (1)In one 3-week placebo-controlled trial (n=246), limited to patients with manic episodes, which involved a dose range of RISPERDAL ® 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 4.1 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

(2)In another 3-week placebo-controlled trial (n=286), which involved a dose range of 1–6 mg/day, once daily, starting at 3 mg/day (mean modal dose was 5.6 mg/day), RISPERDAL ® was superior to placebo in the reduction of YMRS total score.

Pediatrics The efficacy of RISPERDAL ® in the treatment of mania in children or adolescents with Bipolar I disorder was demonstrated in a 3-week, randomized, double-blind, placebo-controlled, multicenter trial including patients ranging in ages from 10 to 17 years who were experiencing a manic or mixed episode of bipolar I disorder.

Patients were randomized into one of three treatment groups: RISPERDAL ® 0.5–2.5 mg/day (n = 50, mean modal dose = 1.9 mg), RISPERDAL ® 3–6 mg/day (n = 61, mean modal dose = 4.7 mg), or placebo (n = 58).

In all cases, study medication was initiated at 0.5 mg/day and titrated to the target dosage range by Day 7, with further increases in dosage to the maximum tolerated dose within the targeted dose range by Day 10.

The primary rating instrument used for assessing efficacy in this study was the mean change from baseline in the total YMRS score.

Results of this study demonstrated efficacy of RISPERDAL ® in both dose groups compared with placebo, as measured by significant reduction of total YMRS score.

The efficacy on the primary parameter in the 3–6 mg/day dose group was comparable to the 0.5–2.5 mg/day dose group.

Doses higher than 2.5 mg/day did not reveal any trend towards greater efficacy.

14.3 Bipolar Mania – Combination Therapy The efficacy of RISPERDAL ® with concomitant lithium or valproate in the treatment of acute manic or mixed episodes was established in one controlled trial in adult patients who met the DSM-IV criteria for Bipolar I Disorder.

This trial included patients with or without psychotic features and with or without a rapid-cycling course.

(1)In this 3-week placebo-controlled combination trial, 148 in- or outpatients on lithium or valproate therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® , placebo, or an active comparator, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.8 mg/day), combined with lithium or valproate (in a therapeutic range of 0.6 mEq/L to 1.4 mEq/L or 50 mcg/mL to 120 mcg/mL, respectively) was superior to lithium or valproate alone in the reduction of YMRS total score.

(2)In a second 3-week placebo-controlled combination trial, 142 in- or outpatients on lithium, valproate, or carbamazepine therapy with inadequately controlled manic or mixed symptoms were randomized to receive RISPERDAL ® or placebo, in combination with their original therapy.

RISPERDAL ® , in a dose range of 1–6 mg/day, once daily, starting at 2 mg/day (mean modal dose of 3.7 mg/day), combined with lithium, valproate, or carbamazepine (in therapeutic ranges of 0.6 mEq/L to 1.4 mEq/L for lithium, 50 mcg/mL to 125 mcg/mL for valproate, or 4–12 mcg/mL for carbamazepine, respectively) was not superior to lithium, valproate, or carbamazepine alone in the reduction of YMRS total score.

A possible explanation for the failure of this trial was induction of risperidone and 9-hydroxyrisperidone clearance by carbamazepine, leading to subtherapeutic levels of risperidone and 9-hydroxyrisperidone.

14.4 Irritability Associated with Autistic Disorder Short-Term Efficacy The efficacy of RISPERDAL ® in the treatment of irritability associated with autistic disorder was established in two 8-week, placebo-controlled trials in children and adolescents (aged 5 to 16 years) who met the DSM-IV criteria for autistic disorder.

Over 90% of these subjects were under 12 years of age and most weighed over 20 kg (16–104.3 kg).

Efficacy was evaluated using two assessment scales: the Aberrant Behavior Checklist (ABC) and the Clinical Global Impression – Change (CGI-C) scale.

The primary outcome measure in both trials was the change from baseline to endpoint in the Irritability subscale of the ABC (ABC-I).

The ABC-I subscale measured the emotional and behavioral symptoms of autism, including aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods.

The CGI-C rating at endpoint was a co-primary outcome measure in one of the studies.

The results of these trials are as follows: (1)In one of the 8-week, placebo-controlled trials, children and adolescents with autistic disorder (n=101), aged 5 to 16 years, received twice daily doses of placebo or RISPERDAL ® 0.5–3.5 mg/day on a weight-adjusted basis.

RISPERDAL ® , starting at 0.25 mg/day or 0.5 mg/day depending on baseline weight (< 20 kg and ≥ 20 kg, respectively) and titrated to clinical response (mean modal dose of 1.9 mg/day, equivalent to 0.06 mg/kg/day), significantly improved scores on the ABC-I subscale and on the CGI-C scale compared with placebo.

(2)In the other 8-week, placebo-controlled trial in children with autistic disorder (n=55), aged 5 to 12 years, RISPERDAL ® 0.02 to 0.06 mg/kg/day given once or twice daily, starting at 0.01 mg/kg/day and titrated to clinical response (mean modal dose of 0.05 mg/kg/day, equivalent to 1.4 mg/day), significantly improved scores on the ABC-I subscale compared with placebo.

Long-Term Efficacy Following completion of the first 8-week double-blind study, 63 patients entered an open-label study extension where they were treated with RISPERDAL ® for 4 or 6 months (depending on whether they received RISPERDAL ® or placebo in the double-blind study).

During this open-label treatment period, patients were maintained on a mean modal dose of RISPERDAL ® of 1.8–2.1 mg/day (equivalent to 0.05 – 0.07 mg/kg/day).

Patients who maintained their positive response to RISPERDAL ® (response was defined as ≥ 25% improvement on the ABC-I subscale and a CGI-C rating of ‘much improved’ or ‘very much improved’) during the 4–6 month open-label treatment phase for about 140 days, on average, were randomized to receive RISPERDAL ® or placebo during an 8-week, double-blind withdrawal study (n=39 of the 63 patients).

A pre-planned interim analysis of data from patients who completed the withdrawal study (n=32), undertaken by an independent Data Safety Monitoring Board, demonstrated a significantly lower relapse rate in the RISPERDAL ® group compared with the placebo group.

Based on the interim analysis results, the study was terminated due to demonstration of a statistically significant effect on relapse prevention.

Relapse was defined as ≥ 25% worsening on the most recent assessment of the ABC-I subscale (in relation to baseline of the randomized withdrawal phase).

HOW SUPPLIED

16 /STORAGE AND HANDLING RISPERDAL ® (risperidone) Tablets RISPERDAL ® (risperidone) Tablets are imprinted ” JANSSEN ” on one side and either “R1”, or “R3” according to their respective strengths.

1 mg white, capsule-shaped tablets: bottles of 15 NDC 21695-113-15 3 mg yellow, capsule-shaped tablets: bottles of 30 NDC 21695-115-30 and bottles of 60 NDC 21695-113-60.

Storage and Handling RISPERDAL ® Tablets should be stored at controlled room temperature 15°–25°C (59°–77°F).

Protect from light and moisture.

Keep out of reach of children.

RECENT MAJOR CHANGES

Warnings and Precautions, Leukopenia, Neutropenia, and Agranulocytosis ( 5.8 ) 07/2009

GERIATRIC USE

8.5 Geriatric Use Clinical studies of RISPERDAL ® in the treatment of schizophrenia did not include sufficient numbers of patients aged 65 and over to determine whether or not they respond differently than younger patients.

Other reported clinical experience has not identified differences in responses between elderly and younger patients.

In general, a lower starting dose is recommended for an elderly patient, reflecting a decreased pharmacokinetic clearance in the elderly, as well as a greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy [see Clinical Pharmacology (12.3) and Dosage and Administration (2.4 , 2.5) ] .

While elderly patients exhibit a greater tendency to orthostatic hypotension, its risk in the elderly may be minimized by limiting the initial dose to 0.5 mg twice daily followed by careful titration [see Warnings and Precautions (5.7) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

This drug is substantially excreted by the kidneys, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function.

Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see Dosage and Administration (2.4) ] .

Concomitant use with Furosemide in Elderly Patients with Dementia-Related Psychosis In two of four placebo-controlled trials in elderly patients with dementia-related psychosis, a higher incidence of mortality was observed in patients treated with furosemide plus RISPERDAL ® when compared to patients treated with RISPERDAL ® alone or with placebo plus furosemide.

No pathological mechanism has been identified to explain this finding, and no consistent pattern for cause of death was observed.

An increase of mortality in elderly patients with dementia-related psychosis was seen with the use of RISPERDAL ® regardless of concomitant use with furosemide.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See Boxed Warning and Warnings and Precautions (5.1) ]

DOSAGE FORMS AND STRENGTHS

3 RISPERDAL ® Tablets are available in the following strengths and colors: 0.25 mg (dark yellow), 0.5 mg (red-brown), 1 mg (white), 2 mg (orange), 3 mg (yellow), and 4 mg (green).

All are capsule shaped, and imprinted with “JANSSEN” on one side and either “Ris 0.25”, “Ris 0.5”, “R1”, “R2”, “R3”, or “R4” on the other side according to their respective strengths.

RISPERDAL ® Oral Solution is available in a 1 mg/mL strength.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets are available in the following strengths, colors, and shapes: 0.5 mg (light coral, round), 1 mg (light coral, square), 2 mg (coral, square), 3 mg (coral, round), and 4 mg (coral, round).

All are biconvex and etched on one side with “R0.5”, “R1”, “R2”, “R3”, or “R4” according to their respective strengths.

Tablets: 0.25 mg, 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 ) Oral solution: 1 mg/mL ( 3 ) Orally disintegrating tablets: 0.5 mg, 1 mg, 2 mg, 3 mg, and 4 mg ( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of action of RISPERDAL ® , as with other drugs used to treat schizophrenia, is unknown.

However, it has been proposed that the drug’s therapeutic activity in schizophrenia is mediated through a combination of dopamine Type 2 (D 2 ) and serotonin Type 2 (5HT 2 ) receptor antagonism.

RISPERDAL ® is a selective monoaminergic antagonist with high affinity (Ki of 0.12 to 7.3 nM) for the serotonin Type 2 (5HT 2 ), dopamine Type 2 (D 2 ), α 1 and α 2 adrenergic, and H 1 histaminergic receptors.

RISPERDAL ® acts as an antagonist at other receptors, but with lower potency.

RISPERDAL ® has low to moderate affinity (Ki of 47 to 253 nM) for the serotonin 5HT 1C , 5HT 1D , and 5HT 1A receptors, weak affinity (Ki of 620 to 800 nM) for the dopamine D 1 and haloperidol-sensitive sigma site, and no affinity (when tested at concentrations >10 -5 M) for cholinergic muscarinic or β 1 and β 2 adrenergic receptors.

INDICATIONS AND USAGE

1 RISPERDAL® is an atypical antipsychotic agent indicated for: Treatment of schizophrenia in adults and adolescents aged 13–17 years ( 1.1 ) Alone, or in combination with lithium or valproate, for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults, and alone in children and adolescents aged 10–17 years ( 1.2 ) Treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years ( 1.3 ) 1.1 Schizophrenia Adults RISPERDAL ® (risperidone) is indicated for the acute and maintenance treatment of schizophrenia [see Clinical Studies (14.1) ] .

Adolescents RISPERDAL ® is indicated for the treatment of schizophrenia in adolescents aged 13–17 years [see Clinical Studies (14.1) ] .

1.2 Bipolar Mania Monotherapy – Adults and Pediatrics RISPERDAL ® is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in adults and in children and adolescents aged 10–17 years [see Clinical Studies (14.2) ] .

Combination Therapy – Adults The combination of RISPERDAL ® with lithium or valproate is indicated for the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder [ see Clinical Studies (14.3) ] .

1.3 Irritability Associated with Autistic Disorder Pediatrics RISPERDAL ® is indicated for the treatment of irritability associated with autistic disorder in children and adolescents aged 5–16 years, including symptoms of aggression towards others, deliberate self-injuriousness, temper tantrums, and quickly changing moods [see Clinical Studies (14.4) ] .

PEDIATRIC USE

8.4 Pediatric Use The efficacy and safety of RISPERDAL ® in the treatment of schizophrenia were demonstrated in 417 adolescents, aged 13 – 17 years, in two short-term (6 and 8 weeks, respectively) double-blind controlled trials [see Indications and Usage (1.1) , Adverse Reactions (6.1) , and Clinical Studies (14.1) ].

Additional safety and efficacy information was also assessed in one long-term (6-month) open-label extension study in 284 of these adolescent patients with schizophrenia.

Safety and effectiveness of RISPERDAL ® in children less than 13 years of age with schizophrenia have not been established.

The efficacy and safety of RISPERDAL ® in the short-term treatment of acute manic or mixed episodes associated with Bipolar I Disorder in 169 children and adolescent patients, aged 10 – 17 years, were demonstrated in one double-blind, placebo-controlled, 3-week trial [see Indications and Usage (1.2) , Adverse Reactions (6.2) , and Clinical Studies (14.2) ] .

Safety and effectiveness of RISPERDAL ® in children less than 10 years of age with bipolar disorder have not been established.

The efficacy and safety of RISPERDAL ® in the treatment of irritability associated with autistic disorder were established in two 8-week, double-blind, placebo-controlled trials in 156 children and adolescent patients, aged 5 to 16 years [see Indications and Usage (1.3) , Adverse Reactions (6.3) and Clinical Studies (14.4) ] .

Additional safety information was also assessed in a long-term study in patients with autistic disorder, or in short- and long-term studies in more than 1200 pediatric patients with psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania who were of similar age and weight, and who received similar dosages of RISPERDAL ® as patients treated for irritability associated with autistic disorder.

The safety and effectiveness of RISPERDAL ® in pediatric patients less than 5 years of age with autistic disorder have not been established.

Tardive Dyskinesia In clinical trials in 1885 children and adolescents treated with RISPERDAL ® , 2 (0.1%) patients were reported to have tardive dyskinesia, which resolved on discontinuation of RISPERDAL ® treatment [see also Warnings and Precautions (5.4) ] .

Weight Gain In a long-term, open-label extension study in adolescent patients with schizophrenia, weight increase was reported as a treatment-emergent adverse event in 14% of patients.

In 103 adolescent patients with schizophrenia, a mean increase of 9.0 kg was observed after 8 months of RISPERDAL ® treatment.

The majority of that increase was observed within the first 6 months.

The average percentiles at baseline and 8 months, respectively, were 56 and 72 for weight, 55 and 58 for height, and 51 and 71 for body mass index.

In long-term, open-label trials (studies in patients with autistic disorder or other psychiatric disorders), a mean increase of 7.5 kg after 12 months of RISPERDAL ® treatment was observed, which was higher than the expected normal weight gain (approximately 3 to 3.5 kg per year adjusted for age, based on Centers for Disease Control and Prevention normative data).

The majority of that increase occurred within the first 6 months of exposure to RISPERDAL ® .

The average percentiles at baseline and 12 months, respectively, were 49 and 60 for weight, 48 and 53 for height, and 50 and 62 for body mass index.

In one 3-week, placebo-controlled trial in children and adolescent patients with acute manic or mixed episodes of bipolar I disorder, increases in body weight were higher in the RISPERDAL ® groups than the placebo group, but not dose related (1.90 kg in the RISPERDAL ® 0.5–2.5 mg group, 1.44 kg in the RISPERDAL ® 3–6 mg group, and 0.65 kg in the placebo group).

A similar trend was observed in the mean change from baseline in body mass index.

When treating pediatric patients with RISPERDAL ® for any indication, weight gain should be assessed against that expected with normal growth.

[See also Adverse Reactions (6.7) ] Somnolence Somnolence was frequently observed in placebo-controlled clinical trials of pediatric patients with autistic disorder.

Most cases were mild or moderate in severity.

These events were most often of early onset with peak incidence occurring during the first two weeks of treatment, and transient with a median duration of 16 days.

Somnolence was the most commonly observed adverse event in the clinical trial of bipolar disorder in children and adolescents, as well as in the schizophrenia trials in adolescents.

As was seen in the autistic disorder trials, these events were most often of early onset and transient in duration.

[See also Adverse Reactions (6.1 , 6.2 , 6.3) ] Patients experiencing persistent somnolence may benefit from a change in dosing regimen [ see Dosage and Administration (2.1 , 2.2 , 2.3) ] .

Hyperprolactinemia, Growth, and Sexual Maturation RISPERDAL ® has been shown to elevate prolactin levels in children and adolescents as well as in adults [se e Warnings and Precautions (5.6) ] .

In double-blind, placebo-controlled studies of up to 8 weeks duration in children and adolescents (aged 5 to 17 years) with autistic disorder or psychiatric disorders other than autistic disorder, schizophrenia, or bipolar mania, 49% of patients who received RISPERDAL ® had elevated prolactin levels compared to 2% of patients who received placebo.

Similarly, in placebo-controlled trials in children and adolescents (aged 10 to 17 years) with bipolar disorder, or adolescents (aged 13 to 17 years) with schizophrenia, 82–87% of patients who received RISPERDAL ® had elevated levels of prolactin compared to 3–7% of patients on placebo.

Increases were dose-dependent and generally greater in females than in males across indications.

In clinical trials in 1885 children and adolescents, galactorrhea was reported in 0.8% of RISPERDAL ® -treated patients and gynecomastia was reported in 2.3% of RISPERDAL ® -treated patients.

The long-term effects of RISPERDAL ® on growth and sexual maturation have not been fully evaluated.

PREGNANCY

8.1 Pregnancy Pregnancy Category C.

The teratogenic potential of risperidone was studied in three Segment II studies in Sprague-Dawley and Wistar rats (0.63–10 mg/kg or 0.4 to 6 times the maximum recommended human dose [MRHD] on a mg/m 2 basis) and in one Segment II study in New Zealand rabbits (0.31–5 mg/kg or 0.4 to 6 times the MRHD on a mg/m 2 basis).

The incidence of malformations was not increased compared to control in offspring of rats or rabbits given 0.4 to 6 times the MRHD on a mg/m 2 basis.

In three reproductive studies in rats (two Segment III and a multigenerational study), there was an increase in pup deaths during the first 4 days of lactation at doses of 0.16–5 mg/kg or 0.1 to 3 times the MRHD on a mg/m 2 basis.

It is not known whether these deaths were due to a direct effect on the fetuses or pups or to effects on the dams.

There was no no-effect dose for increased rat pup mortality.

In one Segment III study, there was an increase in stillborn rat pups at a dose of 2.5 mg/kg or 1.5 times the MRHD on a mg/m 2 basis.

In a cross-fostering study in Wistar rats, toxic effects on the fetus or pups, as evidenced by a decrease in the number of live pups and an increase in the number of dead pups at birth (Day 0), and a decrease in birth weight in pups of drug-treated dams were observed.

In addition, there was an increase in deaths by Day 1 among pups of drug-treated dams, regardless of whether or not the pups were cross-fostered.

Risperidone also appeared to impair maternal behavior in that pup body weight gain and survival (from Day 1 to 4 of lactation) were reduced in pups born to control but reared by drug-treated dams.

These effects were all noted at the one dose of risperidone tested, i.e., 5 mg/kg or 3 times the MRHD on a mg/m 2 basis.

Placental transfer of risperidone occurs in rat pups.

There are no adequate and well-controlled studies in pregnant women.

However, there was one report of a case of agenesis of the corpus callosum in an infant exposed to risperidone in utero .

The causal relationship to RISPERDAL ® therapy is unknown.

Reversible extrapyramidal symptoms in the neonate were observed following postmarketing use of RISPERDAL ® during the last trimester of pregnancy.

RISPERDAL ® should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

NUSRING MOTHERS

8.3 Nursing Mothers In animal studies, risperidone and 9-hydroxyrisperidone are excreted in milk.

Risperidone and 9-hydroxyrisperidone are also excreted in human breast milk.

Therefore, women receiving RISPERDAL ® should not breast-feed.

BOXED WARNING

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

Analyses of 17 placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients.

Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group.

Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature.

Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality.

The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear.

RISPERDAL ® (risperidone) is not approved for the treatment of patients with dementia-related psychosis.

[See Warnings and Precautions (5.1) ] WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS See full prescribing information for complete boxed warning.

Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis.

( 5.1 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Cerebrovascular events, including stroke, in elderly patients with dementia-related psychosis.

RISPERDAL ® is not approved for use in patients with dementia-related psychosis ( 5.2 ) Neuroleptic Malignant Syndrome ( 5.3 ) Tardive dyskinesia ( 5.4 ) Hyperglycemia and diabetes mellitus ( 5.5 ) Hyperprolactinemia ( 5.6 ) Orthostatic hypotension ( 5.7 ) Leukopenia, Neutropenia, and Agranulocytosis: has been reported with antipsychotics, including risperidone.

Patients with a history of a clinically significant low white blood cell count (WBC) or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

( 5.8 ) Potential for cognitive and motor impairment ( 5.9 ) Seizures ( 5.10 ) Dysphagia ( 5.11 ) Priapism ( 5.12 ) Thrombotic Thrombocytopenic Purpura (TTP) ( 5.13 ) Disruption of body temperature regulation ( 5.14 ) Antiemetic Effect ( 5.15 ) Suicide ( 5.16 ) Increased sensitivity in patients with Parkinson’s disease or those with dementia with Lewy bodies ( 5.17 ) Diseases or conditions that could affect metabolism or hemodynamic responses ( 5.17 ) 5.1 Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death.

RISPERDAL ® (risperidone) is not approved for the treatment of dementia-related psychosis [see Boxed Warning ] .

5.2 Cerebrovascular Adverse Events, Including Stroke, in Elderly Patients with Dementia-Related Psychosis Cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, were reported in patients (mean age 85 years; range 73–97) in trials of risperidone in elderly patients with dementia-related psychosis.

In placebo-controlled trials, there was a significantly higher incidence of cerebrovascular adverse events in patients treated with risperidone compared to patients treated with placebo.

RISPERDAL ® is not approved for the treatment of patients with dementia-related psychosis.

[See also Boxed Warnings and Warnings and Precautions (5.1) ] 5.3 Neuroleptic Malignant Syndrome (NMS) A potentially fatal symptom complex sometimes referred to as Neuroleptic Malignant Syndrome (NMS) has been reported in association with antipsychotic drugs.

Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).

Additional signs may include elevated creatine phosphokinase, myoglobinuria (rhabdomyolysis), and acute renal failure.

The diagnostic evaluation of patients with this syndrome is complicated.

In arriving at a diagnosis, it is important to identify cases in which the clinical presentation includes both serious medical illness (e.g., pneumonia, systemic infection, etc.) and untreated or inadequately treated extrapyramidal signs and symptoms (EPS).

Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever, and primary central nervous system pathology.

The management of NMS should include: (1) immediate discontinuation of antipsychotic drugs and other drugs not essential to concurrent therapy; (2) intensive symptomatic treatment and medical monitoring; and (3) treatment of any concomitant serious medical problems for which specific treatments are available.

There is no general agreement about specific pharmacological treatment regimens for uncomplicated NMS.

If a patient requires antipsychotic drug treatment after recovery from NMS, the potential reintroduction of drug therapy should be carefully considered.

The patient should be carefully monitored, since recurrences of NMS have been reported.

5.4 Tardive Dyskinesia A syndrome of potentially irreversible, involuntary, dyskinetic movements may develop in patients treated with antipsychotic drugs.

Although the prevalence of the syndrome appears to be highest among the elderly, especially elderly women, it is impossible to rely upon prevalence estimates to predict, at the inception of antipsychotic treatment, which patients are likely to develop the syndrome.

Whether antipsychotic drug products differ in their potential to cause tardive dyskinesia is unknown.

The risk of developing tardive dyskinesia and the likelihood that it will become irreversible are believed to increase as the duration of treatment and the total cumulative dose of antipsychotic drugs administered to the patient increase.

However, the syndrome can develop, although much less commonly, after relatively brief treatment periods at low doses.

There is no known treatment for established cases of tardive dyskinesia, although the syndrome may remit, partially or completely, if antipsychotic treatment is withdrawn.

Antipsychotic treatment, itself, however, may suppress (or partially suppress) the signs and symptoms of the syndrome and thereby may possibly mask the underlying process.

The effect that symptomatic suppression has upon the long-term course of the syndrome is unknown.

Given these considerations, RISPERDAL ® should be prescribed in a manner that is most likely to minimize the occurrence of tardive dyskinesia.

Chronic antipsychotic treatment should generally be reserved for patients who suffer from a chronic illness that: (1) is known to respond to antipsychotic drugs, and (2) for whom alternative, equally effective, but potentially less harmful treatments are not available or appropriate.

In patients who do require chronic treatment, the smallest dose and the shortest duration of treatment producing a satisfactory clinical response should be sought.

The need for continued treatment should be reassessed periodically.

If signs and symptoms of tardive dyskinesia appear in a patient treated with RISPERDAL ® , drug discontinuation should be considered.

However, some patients may require treatment with RISPERDAL ® despite the presence of the syndrome.

5.5 Hyperglycemia and Diabetes Mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics including RISPERDAL ® .

Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population.

Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse events is not completely understood.

However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse events in patients treated with the atypical antipsychotics.

Precise risk estimates for hyperglycemia-related adverse events in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics should be monitored regularly for worsening of glucose control.

Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment.

Any patient treated with atypical antipsychotics should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness.

Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics should undergo fasting blood glucose testing.

In some cases, hyperglycemia has resolved when the atypical antipsychotic was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of the suspect drug.

5.6 Hyperprolactinemia As with other drugs that antagonize dopamine D 2 receptors, RISPERDAL ® elevates prolactin levels and the elevation persists during chronic administration.

RISPERDAL ® is associated with higher levels of prolactin elevation than other antipsychotic agents.

Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion.

This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients.

Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds.

Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects.

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro , a factor of potential importance if the prescription of these drugs is contemplated in a patient with previously detected breast cancer.

An increase in pituitary gland, mammary gland, and pancreatic islet cell neoplasia (mammary adenocarcinomas, pituitary and pancreatic adenomas) was observed in the risperidone carcinogenicity studies conducted in mice and rats [see Non-Clinical Toxicology (13.1) ] .

Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans; the available evidence is considered too limited to be conclusive at this time.

5.7 Orthostatic Hypotension RISPERDAL ® may induce orthostatic hypotension associated with dizziness, tachycardia, and in some patients, syncope, especially during the initial dose-titration period, probably reflecting its alpha-adrenergic antagonistic properties.

Syncope was reported in 0.2% (6/2607) of RISPERDAL ® -treated patients in Phase 2 and 3 studies in adults with schizophrenia.

The risk of orthostatic hypotension and syncope may be minimized by limiting the initial dose to 2 mg total (either once daily or 1 mg twice daily) in normal adults and 0.5 mg twice daily in the elderly and patients with renal or hepatic impairment [see Dosage and Administration (2.1 , 2.4) ] .

Monitoring of orthostatic vital signs should be considered in patients for whom this is of concern.

A dose reduction should be considered if hypotension occurs.

RISPERDAL ® should be used with particular caution in patients with known cardiovascular disease (history of myocardial infarction or ischemia, heart failure, or conduction abnormalities), cerebrovascular disease, and conditions which would predispose patients to hypotension, e.g., dehydration and hypovolemia.

Clinically significant hypotension has been observed with concomitant use of RISPERDAL ® and antihypertensive medication.

5.8 Leukopenia, Neutropenia, and Agranulocytosis Class Effect: In clinical trial and/or postmarketing experience, events of leukopenia/neutropenia have been reported temporally related to antipsychotic agents, including RISPERDAL ® .

Agranulocytosis has also been reported.

Possible risk factors for leukopenia/neutropenia include pre-existing low white blood cell count (WBC) and history of drug-induced leukopenia/neutropenia.

Patients with a history of a clinically significant low WBC or a drug-induced leukopenia/neutropenia should have their complete blood count (CBC) monitored frequently during the first few months of therapy and discontinuation of RISPERDAL ® should be considered at the first sign of a clinically significant decline in WBC in the absence of other causative factors.

Patients with clinically significant neutropenia should be carefully monitored for fever or other symptoms or signs of infection and treated promptly if such symptoms or signs occur.

Patients with severe neutropenia (absolute neutrophil count <1000/mm 3 ) should discontinue RISPERDAL ® and have their WBC followed until recovery.

5.9 Potential for Cognitive and Motor Impairment Somnolence was a commonly reported adverse event associated with RISPERDAL ® treatment, especially when ascertained by direct questioning of patients.

This adverse event is dose-related, and in a study utilizing a checklist to detect adverse events, 41% of the high-dose patients (RISPERDAL ® 16 mg/day) reported somnolence compared to 16% of placebo patients.

Direct questioning is more sensitive for detecting adverse events than spontaneous reporting, by which 8% of RISPERDAL ® 16 mg/day patients and 1% of placebo patients reported somnolence as an adverse event.

Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely.

5.10 Seizures During premarketing testing in adult patients with schizophrenia, seizures occurred in 0.3% (9/2607) of RISPERDAL ® -treated patients, two in association with hyponatremia.

RISPERDAL ® should be used cautiously in patients with a history of seizures.

5.11 Dysphagia Esophageal dysmotility and aspiration have been associated with antipsychotic drug use.

Aspiration pneumonia is a common cause of morbidity and mortality in patients with advanced Alzheimer’s dementia.

RISPERDAL ® and other antipsychotic drugs should be used cautiously in patients at risk for aspiration pneumonia.

[See also Boxed Warning and Warnings and Precautions (5.1) ] 5.12 Priapism Rare cases of priapism have been reported.

While the relationship of the events to RISPERDAL ® use has not been established, other drugs with alpha-adrenergic blocking effects have been reported to induce priapism, and it is possible that RISPERDAL ® may share this capacity.

Severe priapism may require surgical intervention.

5.13 Thrombotic Thrombocytopenic Purpura (TTP) A single case of TTP was reported in a 28 year-old female patient receiving oral RISPERDAL ® in a large, open premarketing experience (approximately 1300 patients).

She experienced jaundice, fever, and bruising, but eventually recovered after receiving plasmapheresis.

The relationship to RISPERDAL ® therapy is unknown.

5.14 Body Temperature Regulation Disruption of body temperature regulation has been attributed to antipsychotic agents.

Both hyperthermia and hypothermia have been reported in association with oral RISPERDAL ® use.

Caution is advised when prescribing for patients who will be exposed to temperature extremes.

5.15 Antiemetic Effect Risperidone has an antiemetic effect in animals; this effect may also occur in humans, and may mask signs and symptoms of overdosage with certain drugs or of conditions such as intestinal obstruction, Reye’s syndrome, and brain tumor.

5.16 Suicide The possibility of a suicide attempt is inherent in patients with schizophrenia and bipolar mania, including children and adolescent patients, and close supervision of high-risk patients should accompany drug therapy.

Prescriptions for RISPERDAL ® should be written for the smallest quantity of tablets, consistent with good patient management, in order to reduce the risk of overdose.

5.17 Use in Patients with Concomitant Illness Clinical experience with RISPERDAL ® in patients with certain concomitant systemic illnesses is limited.

Patients with Parkinson’s Disease or Dementia with Lewy Bodies who receive antipsychotics, including RISPERDAL ® , are reported to have an increased sensitivity to antipsychotic medications.

Manifestations of this increased sensitivity have been reported to include confusion, obtundation, postural instability with frequent falls, extrapyramidal symptoms, and clinical features consistent with the neuroleptic malignant syndrome.

Caution is advisable in using RISPERDAL ® in patients with diseases or conditions that could affect metabolism or hemodynamic responses.

RISPERDAL ® has not been evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or unstable heart disease.

Patients with these diagnoses were excluded from clinical studies during the product’s premarket testing.

Increased plasma concentrations of risperidone and 9-hydroxyrisperidone occur in patients with severe renal impairment (creatinine clearance <30 mL/min/1.73 m 2 ), and an increase in the free fraction of risperidone is seen in patients with severe hepatic impairment.

A lower starting dose should be used in such patients [ see Dosage and Administration (2.4) ] .

5.18 Monitoring: Laboratory Tests No specific laboratory tests are recommended.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION Physicians are advised to discuss the following issues with patients for whom they prescribe RISPERDAL ® : 17.1 Orthostatic Hypotension Patients should be advised of the risk of orthostatic hypotension, especially during the period of initial dose titration [see Warnings and Precautions (5.7) ] .

17.2 Interference with Cognitive and Motor Performance Since RISPERDAL ® has the potential to impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that RISPERDAL ® therapy does not affect them adversely [see Warnings and Precautions (5.9) ] .

17.3 Pregnancy Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy [see Use in Specific Populations (8.1) ] .

17.4 Nursing Patients should be advised not to breast-feed an infant if they are taking RISPERDAL ® [see Use in Specific Populations (8.3) ] .

17.5 Concomitant Medication Patients should be advised to inform their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs, since there is a potential for interactions [see Drug Interactions (7) ] .

17.6 Alcohol Patients should be advised to avoid alcohol while taking RISPERDAL ® [see Drug Interactions (7.1) ] .

17.7 Phenylketonurics Phenylalanine is a component of aspartame.

Each 4 mg RISPERDAL ® M-TAB ® Orally Orally Disintegrating Tablet contains 0.14 mg phenylalanine.

DOSAGE AND ADMINISTRATION

2 Initial Dose Titration Target Dose Effective Dose Range Schizophrenia- adults ( 2.1 ) 2 mg/day 1–2 mg daily 4–8 mg daily 4–16 mg/day Schizophrenia – adolescents ( 2.1 ) 0.5mg/day 0.5– 1 mg daily 3mg/day 1–6 mg/day Bipolar mania – adults ( 2.2 ) 2–3 mg/day 1mg daily 1–6mg/day 1–6 mg/day Bipolar mania in children/adolescents ( 2.2 ) 0.5 mg/day 0.5–1mg daily 2.5mg/day 0.5–6 mg/day Irritability associated with autistic disorder ( 2.3 ) 0.25 mg/day (<20 kg) 0.5 mg/day (≥20 kg) 0.25–0.5 mg at ≥ 2 weeks 0.5 mg/day (<20 kg) 1 mg/day (≥20 kg) 0.5–3 mg/day 2.1 Schizophrenia Adults Usual Initial Dose RISPERDAL ® can be administered once or twice daily.

Initial dosing is generally 2 mg/day.

Dose increases should then occur at intervals not less than 24 hours, in increments of 1–2 mg/day, as tolerated, to a recommended dose of 4–8 mg/day.

In some patients, slower titration may be appropriate.

Efficacy has been demonstrated in a range of 4–16 mg/day [see Clinical Studies (14.1) ] .

However, doses above 6 mg/day for twice daily dosing were not demonstrated to be more efficacious than lower doses, were associated with more extrapyramidal symptoms and other adverse effects, and are generally not recommended.

In a single study supporting once-daily dosing, the efficacy results were generally stronger for 8 mg than for 4 mg.

The safety of doses above 16 mg/day has not been evaluated in clinical trials.

Maintenance Therapy While it is unknown how long a patient with schizophrenia should remain on RISPERDAL ® , the effectiveness of RISPERDAL ® 2 mg/day to 8 mg/day at delaying relapse was demonstrated in a controlled trial in patients who had been clinically stable for at least 4 weeks and were then followed for a period of 1 to 2 years [ see Clinical Studies (14.1) ] .

Patients should be periodically reassessed to determine the need for maintenance treatment with an appropriate dose.

Adolescents The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 3 mg/day.

Although efficacy has been demonstrated in studies of adolescent patients with schizophrenia at doses between 1 and 6 mg/day, no additional benefit was seen above 3 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

There are no controlled data to support the longer term use of RISPERDAL ® beyond 8 weeks in adolescents with schizophrenia.

The physician who elects to use RISPERDAL ® for extended periods in adolescents with schizophrenia should periodically re-evaluate the long-term usefulness of the drug for the individual patient.

Reinitiation of Treatment in Patients Previously Discontinued Although there are no data to specifically address reinitiation of treatment, it is recommended that after an interval off RISPERDAL ® , the initial titration schedule should be followed.

Switching From Other Antipsychotics There are no systematically collected data to specifically address switching schizophrenic patients from other antipsychotics to RISPERDAL ® , or treating patients with concomitant antipsychotics.

While immediate discontinuation of the previous antipsychotic treatment may be acceptable for some schizophrenic patients, more gradual discontinuation may be most appropriate for others.

The period of overlapping antipsychotic administration should be minimized.

When switching schizophrenic patients from depot antipsychotics, initiate RISPERDAL ® therapy in place of the next scheduled injection.

The need for continuing existing EPS medication should be re-evaluated periodically.

2.2 Bipolar Mania Usual Dose Adults RISPERDAL ® should be administered on a once-daily schedule, starting with 2 mg to 3 mg per day.

Dosage adjustments, if indicated, should occur at intervals of not less than 24 hours and in dosage increments/decrements of 1 mg per day, as studied in the short-term, placebo-controlled trials.

In these trials, short-term (3 week) anti-manic efficacy was demonstrated in a flexible dosage range of 1–6 mg per day [see Clinical Studies (14.2 , 14.3) ] .

RISPERDAL ® doses higher than 6 mg per day were not studied.

Pediatrics The dosage of RISPERDAL ® should be initiated at 0.5 mg once daily, administered as a single-daily dose in either the morning or evening.

Dosage adjustments, if indicated, should occur at intervals not less than 24 hours, in increments of 0.5 or 1 mg/day, as tolerated, to a recommended dose of 2.5 mg/day.

Although efficacy has been demonstrated in studies of pediatric patients with bipolar mania at doses between 0.5 and 6 mg/day, no additional benefit was seen above 2.5 mg/day, and higher doses were associated with more adverse events.

Doses higher than 6 mg/day have not been studied.

Patients experiencing persistent somnolence may benefit from administering half the daily dose twice daily.

Maintenance Therapy There is no body of evidence available from controlled trials to guide a clinician in the longer-term management of a patient who improves during treatment of an acute manic episode with RISPERDAL ® .

While it is generally agreed that pharmacological treatment beyond an acute response in mania is desirable, both for maintenance of the initial response and for prevention of new manic episodes, there are no systematically obtained data to support the use of RISPERDAL ® in such longer-term treatment (i.e., beyond 3 weeks).

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

2.3 Irritability Associated with Autistic Disorder – Pediatrics (Children and Adolescents) The safety and effectiveness of RISPERDAL ® in pediatric patients with autistic disorder less than 5 years of age have not been established.

The dosage of RISPERDAL ® should be individualized according to the response and tolerability of the patient.

The total daily dose of RISPERDAL ® can be administered once daily, or half the total daily dose can be administered twice daily.

Dosing should be initiated at 0.25 mg per day for patients < 20 kg and 0.5 mg per day for patients ≥ 20 kg.

After a minimum of four days from treatment initiation, the dose may be increased to the recommended dose of 0.5 mg per day for patients < 20 kg and 1 mg per day for patients ≥ 20 kg.

This dose should be maintained for a minimum of 14 days.

In patients not achieving sufficient clinical response, dose increases may be considered at ≥ 2-week intervals in increments of 0.25 mg per day for patients < 20 kg or 0.5 mg per day for patients ≥ 20 kg.

Caution should be exercised with dosage for smaller children who weigh less than 15 kg.

In clinical trials, 90% of patients who showed a response (based on at least 25% improvement on ABC-I, [see Clinical Studies (14.4) ] ) received doses of RISPERDAL ® between 0.5 mg and 2.5 mg per day.

The maximum daily dose of RISPERDAL ® in one of the pivotal trials, when the therapeutic effect reached plateau, was 1 mg in patients 45 kg.

No dosing data is available for children who weighed less than 15 kg.

Once sufficient clinical response has been achieved and maintained, consideration should be given to gradually lowering the dose to achieve the optimal balance of efficacy and safety.

The physician who elects to use RISPERDAL ® for extended periods should periodically re-evaluate the long-term risks and benefits of the drug for the individual patient.

Patients experiencing persistent somnolence may benefit from a once-daily dose administered at bedtime or administering half the daily dose twice daily, or a reduction of the dose.

2.4 Dosage in Special Populations The recommended initial dose is 0.5 mg twice daily in patients who are elderly or debilitated, patients with severe renal or hepatic impairment, and patients either predisposed to hypotension or for whom hypotension would pose a risk.

Dosage increases in these patients should be in increments of no more than 0.5 mg twice daily.

Increases to dosages above 1.5 mg twice daily should generally occur at intervals of at least 1 week.

In some patients, slower titration may be medically appropriate.

Elderly or debilitated patients, and patients with renal impairment, may have less ability to eliminate RISPERDAL ® than normal adults.

Patients with impaired hepatic function may have increases in the free fraction of risperidone, possibly resulting in an enhanced effect [see Clinical Pharmacology (12.3) ] .

Patients with a predisposition to hypotensive reactions or for whom such reactions would pose a particular risk likewise need to be titrated cautiously and carefully monitored [see Warnings and Precautions (5.2 , 5.7 , 5.17) ] .

If a once-daily dosing regimen in the elderly or debilitated patient is being considered, it is recommended that the patient be titrated on a twice-daily regimen for 2–3 days at the target dose.

Subsequent switches to a once-daily dosing regimen can be done thereafter.

2.5 Co-Administration of RISPERDAL ® with Certain Other Medications Co-administration of carbamazepine and other enzyme inducers (e.g., phenytoin, rifampin, phenobarbital) with RISPERDAL ® would be expected to cause decreases in the plasma concentrations of the sum of risperidone and 9-hydroxyrisperidone combined, which could lead to decreased efficacy of RISPERDAL ® treatment.

The dose of RISPERDAL ® needs to be titrated accordingly for patients receiving these enzyme inducers, especially during initiation or discontinuation of therapy with these inducers [see Drug Interactions (7.11) ] .

Fluoxetine and paroxetine have been shown to increase the plasma concentration of risperidone 2.5–2.8 fold and 3–9 fold, respectively.

Fluoxetine did not affect the plasma concentration of 9-hydroxyrisperidone.

Paroxetine lowered the concentration of 9-hydroxyrisperidone by about 10%.

The dose of RISPERDAL ® needs to be titrated accordingly when fluoxetine or paroxetine is co-administered [see Drug Interactions (7.10) ] .

2.6 Administration of RISPERDAL ® Oral Solution RISPERDAL ® Oral Solution can be administered directly from the calibrated pipette, or can be mixed with a beverage prior to administration.

RISPERDAL ® Oral Solution is compatible in the following beverages: water, coffee, orange juice, and low-fat milk; it is NOT compatible with either cola or tea.

2.7 Directions for Use of RISPERDAL ® M-TAB ® Orally Disintegrating Tablets Tablet Accessing RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 0.5 mg, 1 mg, and 2 mg are supplied in blister packs of 4 tablets each.

Do not open the blister until ready to administer.

For single tablet removal, separate one of the four blister units by tearing apart at the perforations.

Bend the corner where indicated.

Peel back foil to expose the tablet.

DO NOT push the tablet through the foil because this could damage the tablet.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg RISPERDAL ® M-TAB ® Orally Disintegrating Tablets 3 mg and 4 mg are supplied in a child-resistant pouch containing a blister with 1 tablet each.

The child-resistant pouch should be torn open at the notch to access the blister.

Do not open the blister until ready to administer.

Peel back foil from the side to expose the tablet.

DO NOT push the tablet through the foil, because this could damage the tablet.

Tablet Administration Using dry hands, remove the tablet from the blister unit and immediately place the entire RISPERDAL ® M-TAB ® Orally Disintegrating Tablet on the tongue.

The RISPERDAL ® M-TAB ® Orally Disintegrating Tablet should be consumed immediately, as the tablet cannot be stored once removed from the blister unit.

RISPERDAL ® M-TAB ® Orally Disintegrating Tablets disintegrate in the mouth within seconds and can be swallowed subsequently with or without liquid.

Patients should not attempt to split or to chew the tablet.

DRUG INTERACTIONS

7 MAOIs MAOIs should not be used within 14 days of trazodone [see Warnings and Precautions ( 5.8 )].

Central Nervous System (CNS) Depressants Trazodone may enhance the response to alcohol, barbiturates, and other CNS depressants.

Cytochrome P450 3A4 Inhibitors In vitro drug metabolism studies suggest that there is a potential for drug interactions when trazodone is given with cytochrome P450 3A4 (CYP3A4) inhibitors.

The effect of short-term administration of ritonavir (200 mg twice daily, 4 doses) on the pharmacokinetics of a single dose of trazodone (50 mg) has been studied in 10 healthy subjects.

The C max of trazodone increased by 34%, the AUC increased 2.4 fold, the half-life increased by 2.2 fold, and the clearance decreased by 52%.

Adverse effects including nausea, hypotension, and syncope were observed when ritonavir and trazodone were coadministered.

It is likely that ketoconazole, indinavir, and other CYP3A4 inhibitors such as itraconazole may lead to substantial increases in trazodone plasma concentrations with the potential for adverse effects.

If trazodone is used with a potent CYP3A4 inhibitor, the risk of cardiac arrhythmia may be increased [see Warnings and Precautions ( 5.4 )] and a lower dose of trazodone should be considered.

Cytochrome P450 Inducers (e.g., Carbamazepine) Carbamazepine induces CYP3A4.

Following coadministration of carbamazepine 400 mg per day with trazodone 100 mg to 300 mg daily, carbamazepine reduced plasma concentrations of trazodone and m-chlorophenlypiperazine (an active metabolite) by 76% and 60% respectively, compared to pre-carbamazepine values.

Patients should be closely monitored to see if there is a need for an increased dose of trazodone when taking both drugs.

Digoxin and Phenytoin Increased serum digoxin or phenytoin levels have been reported in patients receiving trazodone concurrently with either of these drugs.

Monitor serum levels and adjust dosages as needed.

Serotonergic Drugs Based on the mechanism of action of trazodone and the potential for serotonin syndrome, caution is advised when trazodone is coadministered with other drugs that may affect the neurotransmitter systems [ see Warnings and Precautions ( 5.2 ) ].

NSAIDs, Aspirin, or Other Drugs Affecting Coagulation or Bleeding Due to a possible association between serotonin modulating drugs and gastrointestinal bleeding, patients should be monitored for and cautioned about the potential risk of bleeding associated with the concomitant use of trazodone and NSAIDs, aspirin, or other drugs that affect coagulation or bleeding [s ee Warnings and Precautions ( 5.7 ) ].

Warfarin There have been reports of altered (either increased or decreased) prothrombin times in taking both warfarin and trazodone.

• CNS Depressants: Trazodone may enhance effects of alcohol, barbiturates, or other CNS depressants ( 7 ).

• CYP3A4 Inhibitors: May necessitate lower dose of trazodone hydrochloride tablets ( 7 ).

• CYP3A4 Inducers (e.g., Carbamazepine): May necessitate higher dose of trazodone hydrochloride tablets ( 7 ).

• Digoxin or Phenytoin: Monitor for increased serum levels ( 7 ).

• Warfarin: Monitor for increased or decreased prothrombin time ( 7 ).

OVERDOSAGE

10 10.1 Human Experience Death from overdose has occurred in patients ingesting trazodone and other CNS depressant drugs concurrently (alcohol; alcohol and chloral hydrate and diazepam; amobarbital; chlordiazepoxide; or meprobamate).

The most severe reactions reported to have occurred with overdose of trazodone alone have been priapism, respiratory arrest, seizures, and ECG changes, including QT prolongation.

The reactions reported most frequently have been drowsiness and vomiting.

Overdosage may cause an increase in incidence or severity of any of the reported adverse reactions.

10.2 Management of Overdose There is no specific antidote for trazodone hydrochloride overdose.

Treatment should consist of those general measures employed in the management of overdosage with any drug effective in the treatment of major depressive disorder.

Ensure an adequate airway, oxygenation and ventilation.

Monitor cardiac rhythm and vital signs.

General supportive and symptomatic measures are also recommended.

Induction of emesis is not recommended.

Gastric lavage with a large bore orogastric tube with appropriate airway protection, if needed, may be indicated if performed soon after ingestion, or in symptomatic patients.

Activated charcoal should be administered.

Forced diuresis may be useful in facilitating elimination of the drug.

In managing overdosage, consider the possibility of multiple drug involvement.

The physician should consider contacting a poison control center for additional information on the treatment of any overdose.

DESCRIPTION

11 Trazodone hydrochloride, USP is an antidepressant chemically unrelated to tricyclic, tetracyclic, or other known antidepressant agents.

Trazodone hydrochloride, USP is a triazolopyridine derivative designated as 2-[3-[4-(3-chlorophenyl)-1-piperazinyl]propyl]-1,2,4-triazolo[4, 3-a]pyridin-3(2 H )-one hydrochloride.

It is a white, odorless crystalline powder which is freely soluble in water.

The structural formula is represented as follows: C19H22ClN5O · HCl M.

W.

408.32 C19H22ClN5O · HCl M.

W.

408.32 Each tablet, for oral administration, contains 50 mg, 100 mg or 150 mg of trazodone hydrochloride, USP.

In addition, each tablet contains colloidal silicon dioxide, lactose anhydrous, magnesium stearate, microcrystalline cellulose and sodium starch glycolate.

structural formula

CLINICAL STUDIES

14 The efficacy and safety of trazodone hydrochloride was established from both inpatient and outpatient trials of the trazodone immediate release formulation in the treatment of major depressive disorder.

HOW SUPPLIED

16 /STORAGE AND HANDLING Trazodone Hydrochloride Tablets USP are available as follows: 50 mg: White, round, compressed tablet, debossed “PLIVA 433” on one side and scored on the other side.

Available in Cards of 28 tablets, NDC 55154-5764-3 Cards of 30 tablets, NDC 55154-5764-9 100 mg: White, round, compressed tablet, debossed “PLIVA 434” on one side and scored on the other side.

Available in Cards of 28 tablets, NDC 55154-5765-3 Cards of 30 tablets, NDC 55154-5765-9 150 mg: White, trapezoid, flat-face, beveled edge tablet, scored and debossed as “PLIVA” bisect “441” on one side and tri-scored and debossed as “50” in each section on the other side.

Available in Overbagged with 10 tablets per bag, NDC 55154-5762-0 Cartons of 100 tablets, NDC 55154-5762-4 Directions for using the correct score when breaking the tablet please refer to the following: – For 50 mg, break the score on either the left or right side of the tablet (one-third of a tablet).

– For 75 mg, break the score down the middle of the tablet (one-half of a tablet).

– For 100 mg, break the score on either the left or right side of the tablet (two-thirds of a tablet).

– For 150 mg, use the entire tablet.

Store at 20° to 25°C (68° to 77°F) [See USP Controlled Room Temperature].

Dispense in a tight, light-resistant container as defined in the USP, with a child-resistant closure (as required).

KEEP THIS AND ALL MEDICATIONS OUT OF THE REACH OF CHILDREN.

Image 1 Image 2 Image 3 Image 4

RECENT MAJOR CHANGES

Warnings and Precautions ( 5.12 ) 06/2014

GERIATRIC USE

8.5 Geriatric Use Reported clinical literature and experience with trazodone has not identified differences in responses between elderly and younger patients.

However, as experience in the elderly with trazodone hydrochloride is limited, it should be used with caution in geriatric patients.

Antidepressants have been associated with cases of clinically significant hyponatremia in elderly patients who may be at greater risk for this adverse reaction [ see Warnings and Precautions ( 5.10 ) ].

DOSAGE FORMS AND STRENGTHS

3 Trazodone hydrochloride tablets are available in the following strengths: 50 mg- White, round, compressed tablet, debossed “PLIVA 433” on one side and scored on the other side.

100 mg- White, round, compressed tablet, debossed “PLIVA 434” on one side and scored on the other side.

150 mg- White, trapezoid, flat-face, beveled edge tablet, scored and debossed as “PLIVA” bisect “441” on one side and tri-scored and debossed as “50” in each section on the other side.

Bisectable tablets of 50 mg, 100 mg and 150 mg ( 3 ).

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of trazodone’s antidepressant action is not fully understood, but is thought to be related to its potentiation of serotonergic activity in the CNS.

INDICATIONS AND USAGE

1 Trazodone Hydrochloride Tablets USP are indicated for the treatment of major depressive disorder (MDD) in adults.

The efficacy of Trazodone Hydrochloride Tablets USP has been established in trials with the immediate release formulation of trazodone [see Clinical Studies ( 14 )].

Trazodone Hydrochloride Tablets USP are indicated for the treatment of major depressive disorder ( 1 ).

• Efficacy was established in trials of trazodone immediate release formulation in patients with major depressive disorder ( 14 ).

PEDIATRIC USE

8.4 Pediatric Use Safety and effectiveness in the pediatric population have not been established [ see Boxed Warning and Warnings and Precautions ( 5.1 ) ].

Trazodone hydrochloride should not be used in children or adolescents.

PREGNANCY

8.1 Pregnancy Teratogenic Effects Pregnancy Category C Trazodone hydrochloride has been shown to cause increased fetal resorption and other adverse effects on the fetus in two studies using the rat when given at dose levels approximately 30 to 50 times the proposed maximum human dose.

There was also an increase in congenital anomalies in one of three rabbit studies at approximately 15 to 50 times the maximum human dose.

There are no adequate and well-controlled studies in pregnant women.

Trazodone hydrochloride should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

NUSRING MOTHERS

8.3 Nursing Mothers Trazodone and/or its metabolites have been found in the milk of lactating rats, suggesting that the drug may be secreted in human milk.

Caution should be exercised when trazodone is administered to a nursing woman.

BOXED WARNING

WARNING: SUICIDALITY AND ANTIDEPRESSANT DRUGS Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders.

Anyone considering the use of trazodone hydrochloride tablets or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need.

Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction in risk with antidepressants compared to placebo in adults aged 65 and older.

Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide.

Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior.

Families and caregivers should be advised of the need for close observation and communication with the prescriber.

Trazodone hydrochloride tablets are not approved for use in pediatric patients [see Warnings and Precautions (5.1) and Patient Counseling Information (17.1)] .

WARNING: SUICIDALITY AND ANTIDEPRESSANT DRUGS See full prescribing information for complete boxed warning.

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS • Clinical Worsening/Suicide Risk: Monitor for clinical worsening and suicidal thinking and behavior ( 5.1 ).

• Serotonin Syndrome or Neuroleptic Malignant Syndrome-Like Reactions: Have been reported with antidepressants.

Discontinue trazodone hydrochloride tablets and initiate supportive treatment ( 5.2 , 7 ).

• Activation of Mania/Hypomania: Screen for bipolar disorder and monitor for mania/hypomania ( 5.3 ).

• QT Prolongation: Increases the QT interval.

Avoid use with drugs that also increase the QT interval and in patients with risk factors for prolonged QT interval ( 5.4 ).

• Use in Patients With Heart Disease: Use with caution in patients with cardiac disease ( 5.5 ).

• Orthostatic Hypotension and Syncope: Have occurred.

Warn patients of risk and symptoms of hypotension ( 5.6 ).

• Abnormal Bleeding: May increase the risk of bleeding.

Use with NSAIDs, aspirin, or other drugs that affect coagulation may compound this risk ( 5.7 , 7 ).

• Interaction With MAOIs: Do not use concomitantly or within 14 days of monoamine oxidase inhibitors ( 5.8 , 7 ).

• Priapism: Has occurred.

Warn male patients of this risk and how/when to seek medical attention ( 5.9 ).

• Hyponatremia: Can occur in association with SIADH ( 5.10 ).

• Potential for Cognitive and Motor Impairment: Has potential to impair judgment, thinking, and motor skills.

Advise patients to use caution when operating machinery ( 5.11 ).

• Angle-Closure Glaucoma: Angle closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressants.

( 5.12 ) • Discontinuation Symptoms: May occur with abrupt discontinuation and include anxiety and sleep disturbance.

Upon discontinuation, taper trazodone hydrochloride tablets and monitor for symptoms ( 5.13 ).

5.1 Clinical Worsening and Suicide Risk Patients with major depressive disorder (MDD), both adult and pediatric, may experience worsening of their depression and/or the emergence of suicidal ideation and behavior (suicidality) or unusual changes in behavior, whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs.

Suicide is a known risk of depression and certain other psychiatric disorders and these disorders themselves are the strongest predictors of suicide.

There has been a long standing concern, however, that antidepressants may have a role in inducing worsening of depression and the emergence of suicidality in certain patients during the early phases of treatment.

Pooled analyses of short-term placebo-controlled trials of antidepressant drugs (SSRIs and others) showed that these drugs increase the risk of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults (ages 18 to 24) with MDD and other psychiatric disorders.

Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction with antidepressants compared to placebo in adults aged 65 and older.

The pooled analyses of placebo-controlled trials in children and adolescents with MDD, obsessive compulsive disorder (OCD), or other psychiatric disorders included a total of 24 short-term trials of 9 antidepressant drugs in over 4,400 patients.

The pooled analyses of placebo-controlled trials in adults with MDD or other psychiatric disorders included a total of 295 short-term trials (median duration of 2 months) of 11 antidepressant drugs in over 77,000 patients.

There was considerable variation in risk of suicidality among drugs, but a tendency toward an increase in the younger patients for almost all drugs studied.

There were differences in absolute risk of suicidality across the different indications, with the highest incidence in MDD.

The risk differences (drug vs.

placebo), however, were relatively stable within age strata and across indications.

These risk differences (drug-placebo difference in the number of cases of suicidality per 1,000 patients treated) are provided in Table 1 .

Table 1 Age Range Drug-Placebo Difference in Number of Cases of Suicidality per 1,000 Patients Treated Increases Compared to Placebo < 18 14 additional cases 18 to 24 5 additional cases Decreases Compared to Placebo 25 to 64 1 fewer case ≥ 65 6 fewer cases No suicides occurred in any of the pediatric trials.

There were suicides in the adult trials, but the number was not sufficient to reach any conclusion about drug effect on suicide.

It is unknown whether the suicidality risk extends to longer-term use, i.e., beyond several months.

However, there is substantial evidence from placebo-controlled maintenance trials in adults with depression that the use of antidepressants can delay the recurrence of depression.

All patients being treated with antidepressants for any indication should be monitored appropriately and observed closely for clinical worsening, suicidality, and unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases .

The following symptoms, anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric.

Although a causal link between the emergence of such symptoms and either the worsening of depression and/or the emergence of suicidal impulses has not been established, there is concern that such symptoms may represent precursors to emerging suicidality.

Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse, or who are experiencing emergent suicidality or symptoms that might be precursors to worsening depression or suicidality, especially if these symptoms are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Families and caregivers of patients being treated with antidepressants for major depressive disorder or other indications, both psychiatric and nonpsychiatric, should be alerted about the need to monitor patients for the emergence of agitation, irritability, unusual changes in behavior, and the other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to healthcare providers .

Such monitoring should include daily observation by families and caregivers .

Prescriptions for trazodone should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

5.2 Serotonin Syndrome or Neuroleptic Malignant Syndrome (NMS)-Like Reactions The development of a potentially life-threatening serotonin syndrome or neuroleptic malignant syndrome (NMS)-like reactions have been reported with antidepressants alone and may occur with trazodone treatment, but particularly with concomitant use of other serotoninergic drugs (including SSRIs, SNRIs and triptans) and with drugs that impair metabolism of serotonin (including monoamine oxidase inhibitors [MAOIs]), or with antipsychotics or other dopamine antagonists.

Serotonin syndrome symptoms may include mental status changes (e.g., agitation, hallucinations, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, and hyperthermia), neuromuscular aberrations (e.g., hyperreflexia, incoordination) and/or gastrointestinal symptoms (e.g., nausea, vomiting, and diarrhea).

Serotonin syndrome, in its most severe form, can resemble neuroleptic malignant syndrome, which includes hyperthermia, muscle rigidity, autonomic instability with possible rapid fluctuation of vital signs, and mental status changes.

Treatment with trazodone hydrochloride tablets and any concomitant serotonergic or antidopaminergic agents, including antipsychotics, should be discontinued immediately if the above reactions occur and supportive symptomatic treatment should be initiated.

Trazodone hydrochloride tablets should not be used within 14 days of an MAOI [see Warnings and Precautions ( 5.8 ) and Drug Interactions ( 7 )].

If concomitant treatment with trazodone hydrochloride tablets and an SSRI, SNRI or a 5-hydroxytryptamine receptor agonist (triptan) is clinically warranted, careful observation of the patient is advised, particularly during treatment initiation and dose increases.

The concomitant use of trazodone hydrochloride tablets with serotonin precursors (such as tryptophan) is not recommended.

5.3 Screening Patients for Bipolar Disorder and Monitoring for Mania/Hypomania A major depressive episode may be the initial presentation of bipolar disorder.

It is generally believed (though not established in controlled trials) that treating such an episode with an antidepressant alone may increase the likelihood of precipitation of a mixed/manic episode in patients at risk for bipolar disorder.

Whether any of the symptoms described for clinical worsening and suicide risk represent such a conversion is unknown.

However, prior to initiating treatment with an antidepressant, patients with depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression.

It should be noted that trazodone hydrochloride tablets are not approved for use in treating bipolar depression.

5.4 QT Prolongation and Risk of Sudden Death Trazodone is known to prolong the QT/QT c interval.

Some drugs that prolong the QT/QT c interval can cause torsade de pointes with sudden, unexplained death.

The relationship of QT prolongation is clearest for larger increases (20 msec and greater), but it is possible that smaller QT/QT c prolongations may also increase risk, especially in susceptible individuals, such as those with hypokalemia, hypomagnesemia, or a genetic predisposition to prolonged QT/QT c .

Although torsade de pointes has not been observed with the use of trazodone hydrochloride tablets at recommended doses in premarketing trials, experience is too limited to rule out an increased risk.

However, there have been postmarketing reports of torsade de pointes with the immediate-release form of trazodone (in the presence of multiple confounding factors), even at doses of 100 mg per day or less.

5.5 Use in Patients With Heart Disease Trazodone hydrochloride is not recommended for use during the initial recovery phase of myocardial infarction.

Caution should be used when administering trazodone hydrochloride tablets to patients with cardiac disease and such patients should be closely monitored, since antidepressant drugs (including trazodone hydrochloride) may cause cardiac arrhythmias.

QT prolongation has been reported with trazodone therapy [see Warnings and Precautions (5.4)] .

Clinical studies in patients with preexisting cardiac disease indicate that trazodone hydrochloride may be arrhythmogenic in some patients in that population.

Arrhythmias identified include isolated PVCs, ventricular couplets, tachycardia with syncope, and torsade de pointes.

Postmarketing events have been reported at doses of 100 mg or less with the immediate-release form of trazodone.

Concomitant administration of drugs that prolong the QT interval or that are inhibitors of CYP3A4 may increase the risk of cardiac arrhythmia.

5.6 Orthostatic Hypotension and Syncope Hypotension, including orthostatic hypotension and syncope has been reported in patients receiving trazodone hydrochloride.

Concomitant use with an antihypertensive may require a reduction in the dose of the antihypertensive drug.

5.7 Abnormal Bleeding Postmarketing data have shown an association between use of drugs that interfere with serotonin reuptake and the occurrence of gastrointestinal (GI) bleeding.

While no association between trazodone and bleeding events, in particular GI bleeding, was shown, patients should be cautioned about potential risk of bleeding associated with the concomitant use of trazodone and NSAIDs, aspirin, or other drugs that affect coagulation or bleeding.

Other bleeding events related to SSRIs and SNRIs have ranged from ecchymosis, hematoma, epistaxis, and petechiae to life-threatening hemorrhages.

5.8 Interaction With MAOIs In patients receiving serotonergic drugs in combination with a monoamine oxidase inhibitor (MAOI), there have been reports of serious, sometimes fatal reactions including hyperthermia, rigidity, myoclonus, autonomic instability with rapid fluctuation in vital signs, and mental status changes that include extreme agitation progressing to delirium and coma.

These reactions have also been reported in patients who have recently discontinued antidepressant treatment and have been started on an MAOI.

Some cases presented with features resembling neuroleptic malignant syndrome.

Furthermore, limited animal data on the effects of combined use of serotonergic antidepressants and MAOIs suggest that these drugs may act synergistically to elevate blood pressure and evoke behavioral excitation.

Therefore, it is recommended that trazodone hydrochloride tablets should not be used in combination with an MAOI or within 14 days of discontinuing treatment with an MAOI.

Similarly, at least 14 days should be allowed after stopping trazodone hydrochloride tablets before starting an MAOI.

5.9 Priapism Rare cases of priapism (painful erections greater than 6 hours in duration) were reported in men receiving trazodone.

Priapism, if not treated promptly, can result in irreversible damage to the erectile tissue.

Men who have an erection lasting greater than 6 hours, whether painful or not, should immediately discontinue the drug and seek emergency medical attention [see Adverse Reactions ( 6.2 ) and Overdosage ( 10 )].

Trazodone should be used with caution in men who have conditions that might predispose them to priapism (e.g., sickle cell anemia, multiple myeloma, or leukemia), or in men with anatomical deformation of the penis (e.g., angulation, cavernosal fibrosis, or Peyronie’s disease).

5.10 Hyponatremia Hyponatremia may occur as a result of treatment with antidepressants.

In many cases, this hyponatremia appears to be the result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Cases with serum sodium lower than 110 mmol/L have been reported.

Elderly patients may be at greater risk of developing hyponatremia with antidepressants.

Also, patients taking diuretics or who are otherwise volume-depleted can be at greater risk.

Discontinuation of trazodone hydrochloride tablets should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

Signs and symptoms of hyponatremia include headache, difficulty concentrating, memory impairment, confusion, weakness, and unsteadiness, which can lead to falls.

Signs and symptoms associated with more severe and/or acute cases have included hallucination, syncope, seizure, coma, respiratory arrest, and death.

5.11 Potential for Cognitive and Motor Impairment Trazodone hydrochloride tablets may cause somnolence or sedation and may impair the mental and/or physical ability required for the performance of potentially hazardous tasks.

Patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that the drug treatment does not affect them adversely 5.12 Angle-Closure Glaucoma Angle-Closure Glaucoma: The pupillary dilation that occurs following use of many antidepressant drugs including trazodone hydrochloride tablets may trigger an angle closure attack in a patient with anatomically narrow angles who does not have a patent iridectomy 5.13 Discontinuation Symptoms Withdrawal symptoms including anxiety, agitation and sleep disturbances, have been reported with trazodone.

Clinical experience suggests that the dose should be gradually reduced before complete discontinuation of the treatment.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION See FDA-approved Medication Guide 17.1 Information for Patients Prescribers or other health professionals should inform patients, their families, and their caregivers about the benefits and risks associated with treatment with trazodone hydrochloride and should counsel them in its appropriate use.

Patients should be warned that: • There is a potential for increased risk of suicidal thoughts especially in children, teenagers and young adults.

• The following symptoms should be reported to the physician: anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia, hypomania and mania.

• They should inform their physician if they have a history of bipolar disorder, cardiac disease or myocardial infarction.

• Serotonin syndrome could occur and symptoms may include changes in mental status (e.g., agitation, hallucinations, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, and hyperthermia), neuromuscular aberrations (e.g., hyperreflexia, incoordination) and/or gastrointestinal symptoms (e.g., nausea, vomiting, and diarrhea).

• Trazodone hydrochloride has been associated with the occurrence of priapism.

• There is a potential for hypotension, including orthostatic hypotension and syncope.

• There is a potential risk of bleeding (including life-threatening hemorrhages) and bleeding related events (including ecchymosis, hematoma, epistaxis, and petechiae) with the concomitant use of trazodone hydrochloride and NSAIDs, aspirin, or other drugs that affect coagulation or bleeding.

• Withdrawal symptoms including anxiety, agitation and sleep disturbances, have been reported with trazodone.

Clinical experience suggests that the dose should be gradually reduced.

• Patients should be advised that taking trazodone hydrochloride tablets can cause mild pupillary dilation, which in susceptible individuals, can lead to an episode of angle-closure glaucoma.

Pre-existing glaucoma is almost always open-angle glaucoma because angle closure glaucoma, when diagnosed, can be treated definitively with iridectomy.

Open-angle glaucoma is not a risk factor for angle-closure glaucoma.

Patients may wish to be examined to determine whether they are susceptible to angle closure, and have a prophylactic procedure (e.g., iridectomy), if they are susceptible.

[ see Warnings and Precautions ( 5.12 ) ] Patients should be counseled that: • Trazodone may cause somnolence or sedation and may impair the mental and/or physical ability required for the performance of potentially hazardous tasks.

Patients should be cautioned about operating hazardous machinery, including automobiles until they are reasonably certain that the drug treatment does not affect them.

• Trazodone may enhance the response to alcohol, barbiturates, and other CNS depressants.

• Women who intend to become pregnant or who are breastfeeding should discuss with a physician whether they should continue to use trazodone, since use in pregnant and nursing women is not recommended.

Important Administration Instructions: • Trazodone hydrochloride tablets should be swallowed whole or broken in half along the score line.

• Trazodone hydrochloride tablets should be taken shortly after a meal or light snack.

Manufactured In Croatia By: PLIVA HRVATSKA d.o.o.

Zagreb, Croatia Manufactured For: TEVA PHARMACEUTICALS USA Sellersville, PA 18960 Rev.

E 5/2014

DOSAGE AND ADMINISTRATION

2 The dosage should be initiated at a low-dose and increased gradually, noting the clinical response and any evidence of intolerance.

Occurrence of drowsiness may require the administration of a major portion of the daily dose at bedtime or a reduction of dosage.

Trazodone hydrochloride tablets should be taken shortly after a meal or light snack.

Dose Selection An initial dose of 150 mg/day in divided doses is suggested.

The dose may be increased by 50 mg/day every 3 to 4 days.

The maximum dose for outpatients usually should not exceed 400 mg/day in divided doses.

Inpatients (i.e., more severely depressed patients) may be given up to but not in excess of 600 mg/day in divided doses • Once an adequate response has been achieved, dosage may be gradually reduced, with subsequent adjustment depending on therapeutic response.

• Patients should be monitored for withdrawal symptoms when discontinuing treatment with trazodone hydrochloride tablets.

The dose should be gradually reduced whenever possible [see Warnings and Precautions ( 5.13 )] .

Maintenance Treatment The efficacy of trazodone hydrochloride tablets for the maintenance treatment of MDD has not been evaluated.

While there is no body of evidence available to answer the question of how long a patient treated with trazodone hydrochloride tablets should continue the drug, it is generally recommended that treatment be continued for several months after an initial response.

Patients should be maintained on the lowest effective dose and be periodically reassessed to determine the continued need for maintenance treatment.

Important Administration Instructions Trazodone hydrochloride tablets are scored to provide flexibility in dosing.

Trazodone hydrochloride tablets can be swallowed whole or administered as a half tablet by breaking the tablet along the score line.

• Starting dose: 150 mg in divided doses daily.

May be increased by 50 mg per day every three to four days.

Maximum dose: 400 mg per day in divided doses ( 2 ).

• Trazodone hydrochloride tablets should be taken shortly after a meal or light snack ( 2 ).

• Tablets should be swallowed whole or broken in half along the score line, and should not be chewed or crushed ( 2 ).

• When discontinued, gradual dose reduction is recommended ( 2 ).

DRUG INTERACTIONS

7 MAOI’s: concomitant use contraindicated ( 4 ).

Avoid MAOI’s 14 days before starting venlafaxine and 7 days after stopping venlafaxine ( 5.2 ).

Cimetidine: Caution in patients with pre-existing hypertension, in elderly patients and patients with hepatic dysfunction.

( 7.2 ) Haloperidol: Increase in Haloperidol AUC and Cmax.

( 7.4 ) Ketoconazole: Increase in venlafaxine and O-desmethylvenlafaxine AUC and Cmax.

Caution when using venlafaxine with substances that inhibit both CYP2D6 and CYP3A4.

( 7.7 ) Metoprolol: Possibly reduced blood-pressure lowering effect despite increased metoprolol plasma levels.

Caution should be exercised with co-administration of venlafaxine and metoprolol.

( 7.8 ) CNS-active drugs: Caution when using venlafaxine with such drugs.

( 7.10 ) Serotonergic drugs (e.g., triptans, SSRIs, other SNRIs, linezolid, lithium, tramadol, or St.

John’s Wort): Potential for serotonin syndrome.

Careful patient observation advised.

( 7.10 ) Tryptophan supplements: Concomitant use not recommended.

( 7.10 ) 7.1 Alcohol A single dose of ethanol (0.5 g/kg) had no effect on the pharmacokinetics of venlafaxine or O-desmethylvenlafaxine (ODV) when venlafaxine was administered at 150 mg/day in 15 healthy male subjects.

Additionally, administration of venlafaxine in a stable regimen did not exaggerate the psychomotor and psychometric effects induced by ethanol in these same subjects when they were not receiving venlafaxine.

7.2 Cimetidine Concomitant administration of cimetidine and venlafaxine in a steady-state study for both drugs resulted in inhibition of first-pass metabolism of venlafaxine in 18 healthy subjects.

The oral clearance of venlafaxine was reduced by about 43%, and the exposure (AUC) and maximum concentration (C max ) of the drug were increased by about 60%.

However, coadministration of cimetidine had no apparent effect on the pharmacokinetics of ODV, which is present in much greater quantity in the circulation than venlafaxine.

The overall pharmacological activity of venlafaxine plus ODV is expected to increase only slightly, and no dosage adjustment should be necessary for most normal adults.

However, for patients with pre-existing hypertension, and for elderly patients or patients with hepatic dysfunction, the interaction associated with the concomitant use of venlafaxine and cimetidine is not known and potentially could be more pronounced.

Therefore, caution is advised with such patients.

7.3 Diazepam Under steady-state conditions for venlafaxine administered at 150 mg/day, a single 10 mg dose of diazepam did not appear to affect the pharmacokinetics of either venlafaxine or ODV in 18 healthy male subjects.

Venlafaxine also did not have any effect on the pharmacokinetics of diazepam or its active metabolite, desmethyldiazepam, or affect the psychomotor and psychometric effects induced by diazepam.

7.4 Haloperidol Venlafaxine administered under steady-state conditions at 150 mg/day in 24 healthy subjects decreased total oral-dose clearance (Cl/F) of a single 2 mg dose of haloperidol by 42%, which resulted in a 70% increase in haloperidol AUC.

In addition, the haloperidol C max increased 88% when coadministered with venlafaxine, but the haloperidol elimination half-life (t 1/2 ) was unchanged.

The mechanism explaining this finding is unknown.

7.5 Lithium The steady-state pharmacokinetics of venlafaxine administered at 150 mg/day were not affected when a single 600 mg oral dose of lithium was administered to 12 healthy male subjects.

ODV also was unaffected.

Venlafaxine had no effect on the pharmacokinetics of lithium (see also CNS-Active Drugs, below).

7.6 Drugs Highly Bound to Plasma Proteins Venlafaxine is not highly bound to plasma proteins; therefore, administration of Venlafaxine Extended Release Tablets to a patient taking another drug that is highly protein bound should not cause increased free concentrations of the other drug.

7.7 Drugs that Inhibit Cytochrome P450 Isoenzymes CYP2D6 Inhibitors: In vitro and in vivo studies indicate that venlafaxine is metabolized to its active metabolite, ODV, by CYP2D6, the isoenzyme that is responsible for the genetic polymorphism seen in the metabolism of many antidepressants.

Therefore, the potential exists for a drug interaction between drugs that inhibit CYP2D6-mediated metabolism of venlafaxine, reducing the metabolism of venlafaxine to ODV, resulting in increased plasma concentrations of venlafaxine and decreased concentrations of the active metabolite.

CYP2D6 inhibitors such as quinidine would be expected to do this, but the effect would be similar to what is seen in patients who are genetically CYP2D6 poor metabolizers [ see Clinical Pharmacology (12.3) ].

Therefore, no dosage adjustment is required when venlafaxine is coadministered with a CYP2D6 inhibitor.

Ketoconazole: A pharmacokinetic study with ketoconazole 100 mg b.i.d.

with a single dose of venlafaxine 50 mg in extensive metabolizers (EM; n=14) and 25 mg in poor metabolizers (PM;n=6) of CYP2D6 resulted in higher plasma concentrations of both venlafaxine and O-desmethylvenlafaxine (ODV) in most subjects following administration of ketoconazole.

Venlafaxine Cmax increased by 26% in EM subjects and 48% in PM subjects.

Cmax values for ODV increased by 14% and 29% in EM and PM subjects, respectively.

Venlafaxine AUC increased by 21% in EM subjects and 70% in PM subjects (range in PM’s -2% to 206%), and AUC values for ODV increased by 23% and 33% in EM and PM (range in PM’s -38% to 105%) subjects, respectively.

Combined AUC’s of venlafaxine and ODV increased on average by approximately 23% in EM’s and 53% in PM’s, (range in PM’s 4% – 134%).

Concomitant use of CYP3A4 inhibitors and venlafaxine may increase levels of venlafaxine and ODV.

Therefore, caution is advised if a patient’s therapy includes a CYP3A4 inhibitor and venlafaxine concomitantly.

7.8 Drugs Metabolized by Cytochrome P450 Isoenzymes CYP2D6 In vitro studies indicate that venlafaxine is a relatively weak inhibitor of CYP2D6.

These findings have been confirmed in a clinical drug interaction study comparing the effect of venlafaxine with that of fluoxetine on the CYP2D6-mediated metabolism of dextromethorphan to dextrorphan.

Imipramine – Venlafaxine did not affect the pharmacokinetics of imipramine and 2-OH-imipramine.

However, desipramine AUC, C max , and C min increased by about 35% in the presence of venlafaxine.

The 2-OH-desipramine AUC’s increased by at least 2.5 fold (with venlafaxine 37.5 mg q12h) and by 4.5 fold (with venlafaxine 75 mg q12h).

Imipramine did not affect the pharmacokinetics of venlafaxine and ODV.

The clinical significance of elevated 2-OH-desipramine levels is unknown.

Metoprolol – Concomitant administration of venlafaxine (50 mg every 8 hours for 5 days) and metoprolol (100 mg every 24 hours for 5 days) to 18 healthy male subjects in a pharmacokinetic interaction study for both drugs resulted in an increase of plasma concentrations of metoprolol by approximately 30-40% without altering the plasma concentrations of its active metabolite, α-hydroxymetoprolol.

Metoprolol did not alter the pharmacokinetic profile of venlafaxine or its active metabolite, O-desmethylvenlafaxine.

Venlafaxine appeared to reduce the blood pressure lowering effect of metoprolol in this study.

The clinical relevance of this finding for hypertensive patients is unknown.

Caution should be exercised with co-administration of venlafaxine and metoprolol.

Venlafaxine treatment has been associated with dose-related increases in blood pressure in some patients.

It is recommended that patients receiving Venlafaxine Extended Release Tablets have regular monitoring of blood pressure [ see Warnings and Precautions (5.3) ].

Risperidone – Venlafaxine administered under steady-state conditions at 150 mg/day slightly inhibited the CYP2D6-mediated metabolism of risperidone (administered as a single 1 mg oral dose) to its active metabolite, 9-hydroxyrisperidone, resulting in an approximate 32% increase in risperidone AUC.

However, venlafaxine coadministration did not significantly alter the pharmacokinetic profile of the total active moiety (risperidone plus 9-hydroxyrisperidone).

CYP3A4 Venlafaxine did not inhibit CYP3A4 in vitro.

This finding was confirmed in vivo by clinical drug interaction studies in which venlafaxine did not inhibit the metabolism of several CYP3A4 substrates, including alprazolam, diazepam, and terfenadine.

Indinavir – In a study of 9 healthy volunteers, venlafaxine administered under steady-state conditions at 150 mg/day resulted in a 28% decrease in the AUC of a single 800 mg oral dose of indinavir and a 36% decrease in indinavir C max .

Indinavir did not affect the pharmacokinetics of venlafaxine and ODV.

The clinical significance of this finding is unknown.

CYP1A2 Venlafaxine did not inhibit CYP1A2 in vitro.

This finding was confirmed in vivo by a clinical drug interaction study in which venlafaxine did not inhibit the metabolism of caffeine, a CYP1A2 substrate.

CYP2C9 Venlafaxine did not inhibit CYP2C9 in vitro.

In vivo, venlafaxine 75 mg by mouth every 12 hours did not alter the pharmacokinetics of a single 500 mg dose of tolbutamide or the CYP2C9 mediated formation of 4-hydroxy-tolbutamide.

CYP2C19 Venlafaxine did not inhibit the metabolism of diazepam, which is partially metabolized by CYP2C19 (see Diazepam above).

7.9 Monoamine Oxidase Inhibitors (MAOIs) [See Dosage and Administration (2.6 and 2.7) , Contraindications (4.1) , and Warnings and Precautions (5.2) .] 7.10 Serotonergic Drugs [See Dosage and Administration (2.6 and 2.7) , Contraindications (4.1) , and Warnings and Precautions (5.2) .] 7.11 Drugs that Interfere with Hemostasis (e.g., NSAID’s, Aspirin, and Warfarin) Serotonin release by platelets plays an important role in hemostasis.

Epidemiological studies of the case-control and cohort design that have demonstrated an association between use of psychotropic drugs that interfere with serotonin reuptake and the occurrence of upper gastrointestinal bleeding.

These studies have also shown that concurrent use of an NSAID or aspirin may potentiate this risk of bleeding.

Altered anticoagulant effects, including increased bleeding, have been reported when SSRI’s and SNRI’s are coadministered with warfarin.

Patients receiving warfarin therapy should be carefully monitored when Venlafaxine Extended-Release Tablets are initiated or discontinued.

[ See Warnings and Precautions (5.13) .] 7.12 Electroconvulsive Therapy There are no clinical data establishing the benefit of electroconvulsive therapy combined with Venlafaxine Extended Release Tablets treatment.

7.13 Postmarketing Spontaneous Drug Interaction Reports There have been reports of elevated clozapine levels that were temporally associated with adverse reactions, including seizures, following the addition of venlafaxine.

There have been reports of increases in prothrombin time, partial thromboplastin time, or INR when venlafaxine was given to patients receiving warfarin therapy.

7.14 Drug-Laboratory Test Interactions False-positive urine immunoassay screening tests for phencyclidine (PCP) and amphetamine have been reported in patients taking venlafaxine.

This is due to lack of specificity of the screening tests.

False positive test results may be expected for several days following discontinuation of venlafaxine therapy.

Confirmatory tests, such as gas chromatography/mass spectrometry, will distinguish venlafaxine from PCP and amphetamine.

OVERDOSAGE

10 10.1 Human Experience Among the patients included in the premarketing evaluation of venlafaxine hydrochloride extended-release capsules, there were 2 reports of acute overdosage with venlafaxine hydrochloride extended-release capsules in major depressive disorder trials, either alone or in combination with other drugs.

One patient took a combination of 6 g of venlafaxine hydrochloride extended-release capsules and 2.5 mg of lorazepam.

This patient was hospitalized, treated symptomatically, and recovered without any untoward effects.

The other patient took 2.85 g of venlafaxine hydrochloride extended-release capsules.

This patient reported paresthesia of all four limbs but recovered without sequelae.

There were no reports of acute overdose with venlafaxine hydrochloride extended-release capsules in Social Anxiety Disorder trials.

Among the patients included in the premarketing evaluation with venlafaxine hydrochloride immediate-release tablets, there were 14 reports of acute overdose with venlafaxine, either alone or in combination with other drugs and/or alcohol.

The majority of the reports involved ingestion in which the total dose of venlafaxine taken was estimated to be no more than several-fold higher than the usual therapeutic dose.

The 3 patients who took the highest doses were estimated to have ingested approximately 6.75 g, 2.75 g, and 2.5 g.

The resultant peak plasma levels of venlafaxine for the latter 2 patients were 6.24 and 2.35 μg/mL, respectively, and the peak plasma levels of O-desmethylvenlafaxine were 3.37 and 1.30 μg/mL, respectively.

Plasma venlafaxine levels were not obtained for the patient who ingested 6.75 g of venlafaxine.

All 14 patients recovered without sequelae.

Most patients reported no symptoms.

Among the remaining patients, somnolence was the most commonly reported symptom.

The patient who ingested 2.75 g of venlafaxine was observed to have 2 generalized convulsions and a prolongation of QTc to 500 msec, compared with 405 msec at baseline.

Mild sinus tachycardia was reported in 2 of the other patients.

In postmarketing experience, overdose with venlafaxine has occurred predominantly in combination with alcohol and/or other drugs.

The most commonly reported reactions in overdosage include tachycardia, changes in level of consciousness (ranging from somnolence to coma), mydriasis, seizures, and vomiting.

Electrocardiogram changes (e.g., prolongation of QT interval, bundle branch block, QRS prolongation), ventricular tachycardia, bradycardia, hypotension, rhabdomyolysis, vertigo, liver necrosis, serotonin syndrome, and death have been reported.

Published retrospective studies report that venlafaxine overdosage may be associated with an increased risk of fatal outcomes compared to that observed with SSRI antidepressant products, but lower than that for tricyclic antidepressants.

Epidemiological studies have shown that venlafaxine-treated patients have a higher pre-existing burden of suicide risk factors than SSRI-treated patients.

The extent to which the finding of an increased risk of fatal outcomes can be attributed to the toxicity of venlafaxine in overdosage as opposed to some characteristic(s) of venlafaxine-treated patients is not clear.

Prescriptions for Venlafaxine Extended Release Tablets should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

10.2 Management of Overdosage Treatment should consist of those general measures employed in the management of overdosage with any antidepressant.

Ensure an adequate airway, oxygenation, and ventilation.

Monitor cardiac rhythm and vital signs.

General supportive and symptomatic measures are also recommended.

Induction of emesis is not recommended.

Gastric lavage with a large bore orogastric tube with appropriate airway protection, if needed, may be indicated if performed soon after ingestion or in symptomatic patients.

Activated charcoal should be administered.

Due to the large volume of distribution of this drug, forced diuresis, dialysis, hemoperfusion, and exchange transfusion are unlikely to be of benefit.

No specific antidotes for venlafaxine are known.

In managing overdosage, consider the possibility of multiple drug involvement.

The physician should consider contacting a poison control center for additional information on the treatment of any overdose.

Telephone numbers for certified poison control centers are listed in the Physicians’ Desk Reference ® ( PDR ).

DESCRIPTION

11 Venlafaxine Extended Release Tablets (venlafaxine hydrochloride) are extended-release tablets for oral administration that contain venlafaxine hydrochloride, a structurally novel antidepressant.

Venlafaxine hydrochloride is a selective serotonin and norepinephrine reuptake inhibitor (SNRI).

It is designated (R/S)-1-[2-(dimethylamino)-1-(4-methoxyphenyl)ethyl] cyclohexanol hydrochloride or (±)-1-[α- [(dimethylamino)methyl]-p-methoxybenzyl] cyclohexanol hydrochloride and has the empirical formula of C 17 H 27 NO 2 HCl.

Its molecular weight is 313.87.

The structural formula is shown below.

Venlafaxine hydrochloride is a white to off-white crystalline solid with a solubility of 572 mg/mL in water (adjusted to ionic strength of 0.2 M with sodium chloride).

Its octanol:water (0.2 M sodium chloride) partition coefficient is 0.43.

Venlafaxine Extended Release Tablets are formulated as extended-release tablet for once-a-day oral administration.

Venlafaxine Extended Release Tablets use osmotic pressure to deliver venlafaxine hydrochloride at a controlled rate over approximately 24 hours.

The system, which resembles a conventional tablet in appearance, comprises an osmotically active core surrounded by a semipermeable membrane.

The unitary tablet core is composed of the drug and excipients (including the osmotically active components).

There is a precision-laser drilled orifice in the semipermeable membrane on the side of the tablet.

In an aqueous environment, such as the gastrointestinal tract, water permeates through the membrane into the tablet core, causing the drug to dissolve and the osmotic components to expand.

This expansion pushes the drug out through the orifice.

The semipermeable membrane controls the rate at which water permeates into the tablet core, which in turn controls the rate of drug delivery.

The controlled rate of drug delivery into the gastrointestinal lumen is thus independent of pH or gastrointestinal motility.

The function of Venlafaxine Extended Release Tablets depends on the existence of an osmotic gradient between the contents of the core and the fluid in the gastrointestinal tract.

Since the osmotic gradient remains constant, drug delivery remains essentially constant.

The biologically inert components of the tablet remain intact during gastrointestinal transit and are eliminated in the feces as an insoluble shell.

Tablets contain venlafaxine hydrochloride equivalent to 37.5 mg, 75 mg, 150 mg, or 225 mg venlafaxine.

Inactive ingredients consist of mannitol, povidone, microcrystalline cellulose, polyethylene glycol, colloidal silicon dioxide, magnesium stearate, cellulose acetate, hypromellose , lactose, titanium dioxide, triacetin, black iron oxide, and propylene glycol.

Chemical Structure

CLINICAL STUDIES

14 14.1 Major Depressive Disorder The efficacy of venlafaxine hydrochloride extended-release capsules as a treatment for major depressive disorder was established in two placebo-controlled, short-term, flexible-dose studies in adult outpatients meeting DSM-III-R or DSM-IV criteria for major depressive disorder.

A 12-week study utilizing venlafaxine hydrochloride extended-release capsules doses in a range 75 to 150 mg/day (mean dose for completers was 136 mg/day) and an 8-week study utilizing venlafaxine hydrochloride extended-release capsules doses in a range 75 to 225 mg/day (mean dose for completers was 177 mg/day) both demonstrated superiority of venlafaxine hydrochloride extended-release capsules over placebo on the HAM-D total score, HAM-D Depressed Mood Item, the MADRS total score, the Clinical Global Impressions (CGI) Severity of Illness item, and the CGI Global Improvement item.

In both studies, venlafaxine hydrochloride extended-release capsules were also significantly better than placebo for certain factors of the HAM-D, including the anxiety/somatization factor, the cognitive disturbance factor, and the retardation factor, as well as for the psychic anxiety score.

A 4-week study of inpatients meeting DSM-III-R criteria for major depressive disorder with melancholia utilizing venlafaxine hydrochloride immediate-release tablets in a range of 150 to 375 mg/day (t.i.d.

schedule) demonstrated superiority of venlafaxine hydrochloride immediate-release tablets over placebo.

The mean dose in completers was 350 mg/day.

Examination of gender subsets of the population studied did not reveal any differential responsiveness on the basis of gender.

In one longer-term study, adult outpatients meeting DSM-IV criteria for major depressive disorder who had responded during an 8-week open trial on venlafaxine hydrochloride extended-release capsules (75, 150, or 225 mg, qAM) were randomized to continuation of their same venlafaxine hydrochloride extended-release capsules dose or to placebo, for up to 26 weeks of observation for relapse.

Response during the open phase was defined as a CGI Severity of Illness item score of ≤3 and a HAM-D-21 total score of ≤10 at the day 56 evaluation.

Relapse during the double-blind phase was defined as follows: (1) a reappearance of major depressive disorder as defined by DSM-IV criteria and a CGI Severity of Illness item score of ≥4 (moderately ill), (2) 2 consecutive CGI Severity of Illness item scores of ≥4, or (3) a final CGI Severity of Illness item score of ≥4 for any patient who withdrew from the study for any reason.

Patients receiving continued venlafaxine hydrochloride extended-release capsules treatment experienced significantly lower relapse rates over the subsequent 26 weeks compared with those receiving placebo.

In a second longer-term trial, adult outpatients meeting DSM-III-R criteria for major depressive disorder, recurrent type, who had responded (HAM-D-21 total score ≤12 at the day 56 evaluation) and continued to be improved [defined as the following criteria being met for days 56 through 180: (1) no HAM-D-21 total score ≥20; (2) no more than 2 HAM-D-21 total scores >10, and (3) no single CGI Severity of Illness item score ≥4 (moderately ill)] during an initial 26 weeks of treatment on venlafaxine hydrochloride immediate-release tablets (100 to 200 mg/day, on a b.i.d.

schedule) were randomized to continuation of their same dose of venlafaxine hydrochloride immediate-release tablets or to placebo.

The follow-up period to observe patients for relapse, defined as a CGI Severity of Illness item score ≥4, was for up to 52 weeks.

Patients receiving continued treatment with venlafaxine hydrochloride immediate-release tablets experienced significantly lower relapse rates over the subsequent 52 weeks compared with those receiving placebo.

14.2 Social Anxiety Disorder (Social Phobia) The efficacy of venlafaxine hydrochloride extended-release capsules as a treatment for Social Anxiety Disorder (also known as Social Phobia) was established in two double-blind, parallel group, 12-week, multicenter, placebo-controlled, flexible-dose studies in adult outpatients meeting DSM-IV criteria for Social Anxiety Disorder.

Patients received doses in a range of 75 to 225 mg/day.

Efficacy was assessed with the Liebowitz Social Anxiety Scale (LSAS).

In these two trials, venlafaxine hydrochloride extended-release capsules were significantly more effective than placebo on change from baseline to endpoint on the LSAS total score.

Examination of subsets of the population studied did not reveal any differential responsiveness on the basis of gender.

There was insufficient information to determine the effect of age or race on outcome in these studies.

HOW SUPPLIED

16 /STORAGE AND HANDLING Venlafaxine Extended Release Tablets 37.5 mg are round, biconvex, white coated tablets with OS301 printed on one side.

They are supplied as follows: Unit of Use Bottles of 30 Tablets NDC 65580-301-03 Unit of Use Bottles of 90 Tablets NDC 65580-301-09 Venlafaxine Extended Release Tablets 75 mg are round, biconvex, white coated tablets with OS302 printed on one side.

They are supplied as follows: Unit of Use Bottles of 30 Tablets NDC 65580-302-03 Unit of Use Bottles of 90 Tablets NDC 65580-302-09 Venlafaxine Extended Release Tablets 150 mg are round, biconvex, white coated tablets with OS303 printed on one side.

They are supplied as follows: Unit of Use Bottles of 30 Tablets NDC 65580-303-03 Unit of Use Bottles of 90 Tablets NDC 65580-303-09 Venlafaxine Extended Release Tablets 225 mg are round, biconvex, white coated tablets with OS304 printed on one side.

They are supplied as follows: Unit of Use Bottles of 30 Tablets NDC 65580-304-03 Unit of Use Bottles of 90 Tablets NDC 65580-304-09 Store at 25°C (77°F); excursions permitted to 15-30°C (59-86°F) [see USP Controlled Room Temperature].

Protect from moisture and humidity.

GERIATRIC USE

8.5 Geriatric Use Approximately 4% (14/357) and 2% (6/277) of patients treated with venlafaxine hydrochloride extended-release capsules in placebo-controlled premarketing major depressive disorder and Social Anxiety Disorder trials, respectively, were 65 years of age or over.

Of 2,897 patients treated with venlafaxine hydrochloride immediate-release tablets in premarketing phase major depressive disorder studies, 12% (357) were 65 years of age or over.

No overall differences in effectiveness or safety were observed between geriatric patients and younger patients, and other reported clinical experience generally has not identified differences in response between the elderly and younger patients.

However, greater sensitivity of some older individuals cannot be ruled out.

SSRIs and SNRIs, including venlafaxine hydrochloride extended-release capsules have been associated with cases of clinically significant hyponatremia in elderly patients, who may be at greater risk for this adverse reaction [ see Warnings and Precautions (5.11) ].

The pharmacokinetics of venlafaxine and ODV are not substantially altered in the elderly [ see Clinical Pharmacology (12.3) ].

No dose adjustment is recommended for the elderly on the basis of age alone, although other clinical circumstances, some of which may be more common in the elderly, such as renal or hepatic impairment, may warrant a dose reduction [ see Dosage and Administration (2.3) ].

DOSAGE FORMS AND STRENGTHS

3 Venlafaxine Extended Release Tablets are available as: – 37.5 mg tablets (round, biconvex, white coated tablets with OS301 printed on one side) – 75 mg tablets (round, biconvex, white coated tablets with OS302 printed on one side) – 150 mg tablets (round, biconvex, white coated tablets with OS303 printed on one side) – 225 mg tablets (round, biconvex, white coated tablets with OS304 printed on one side) 37.5 mg, 75 mg, 150 mg, and 225 mg tablets ( 3 )

MECHANISM OF ACTION

12.1 Mechanism of Action The mechanism of the antidepressant action of venlafaxine in humans is believed to be associated with its potentiation of neurotransmitter activity in the CNS.

Preclinical studies have shown that venlafaxine and its active metabolite, O-desmethylvenlafaxine (ODV), are potent inhibitors of neuronal serotonin and norepinephrine reuptake and weak inhibitors of dopamine reuptake.

INDICATIONS AND USAGE

1 Venlafaxine Extended Release Tablets are a selective serotonin and norepinephrine reuptake inhibitor (SNRI) indicated for: Major Depressive Disorder (MDD) ( 1.1 ) Social Anxiety Disorder (SAD) ( 1.2 ) 1.1 Major Depressive Disorder Venlafaxine Extended Release Tablets (venlafaxine hydrochloride) are indicated for the treatment of major depressive disorder (MDD).

Efficacy of venlafaxine in MDD was shown in both short-term trials and a longer-term trial in MDD [ see Clinical Studies (14.1) ].

A major depressive episode (DSM-IV) implies a prominent and relatively persistent (nearly every day for at least 2 weeks) depressed mood or the loss of interest or pleasure in nearly all activities, representing a change from previous functioning, and includes the presence of at least five of the following nine symptoms during the same two-week period: depressed mood, markedly diminished interest or pleasure in usual activities, significant change in weight and/or appetite, insomnia or hypersomnia, psychomotor agitation or retardation, increased fatigue, feelings of guilt or worthlessness, slowed thinking or impaired concentration, a suicide attempt or suicidal ideation.

1.2 Social Anxiety Disorder Venlafaxine Extended Release Tablets are indicated for the treatment of Social Anxiety Disorder (SAD), also known as Social Phobia, as defined in DSM-IV.

Social Anxiety Disorder (DSM-IV) is characterized by a marked and persistent fear of 1 or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others.

Exposure to the feared situation almost invariably provokes anxiety, which may approach the intensity of a panic attack.

The feared situations are avoided or endured with intense anxiety or distress.

The avoidance, anxious anticipation, or distress in the feared situation(s) interferes significantly with the person’s normal routine, occupational or academic functioning, or social activities or relationships, or there is a marked distress about having the phobias.

Lesser degrees of performance anxiety or shyness generally do not require psychopharmacological treatment.

Efficacy of venlafaxine extended release in the treatment of SAD was established in short-term SAD trials [ see Clinical Studies (14.2) ].

PEDIATRIC USE

8.4 Pediatric Use Safety and effectiveness in the pediatric population have not been established [ see BOXED WARNING and Warnings and Precautions (5.1) ].

Two placebo-controlled trials in 766 pediatric patients with MDD and two placebo-controlled trials in another disorder in 793 pediatric patients have been conducted with venlafaxine hydrochloride extended-release capsules, and the data were not sufficient to support a claim for use in pediatric patients.

Anyone considering the use of Venlafaxine Extended Release Tablets in a child or adolescent must balance the potential risks with the clinical need.

Although no studies have been designed to primarily assess impact of venlafaxine hydrochloride extended-release capsules on the growth, development, and maturation of children and adolescents, the studies that have been done suggest that Venlafaxine Extended Release Tablets may adversely affect weight and height [ see Warnings and Precautions (5.7 , 5.8 , and 5.9) ].

Should the decision be made to treat a pediatric patient with Venlafaxine Extended Release Tablets, regular monitoring of weight and height is recommended during treatment, particularly if it is to be continued long term.

The safety of Venlafaxine Extended Release Tablets treatment for pediatric patients has not been systematically assessed for chronic treatment longer than six months in duration.

In the studies conducted in pediatric patients (ages 6-17), the occurrence of blood pressure and cholesterol increases considered to be clinically relevant in pediatric patients was similar to that observed in adult patients.

Consequently, the precautions for adults apply to pediatric patients [ see Warnings and Precautions (5.3 and 5.14) ].

PREGNANCY

8.1 Pregnancy Teratogenic Effects Pregnancy Category C Venlafaxine did not cause malformations in offspring of rats or rabbits given doses up to 2.5 times (rat) or 4 times (rabbit) the maximum recommended human daily dose on a mg/m 2 basis.

However, in rats, there was a decrease in pup weight, an increase in stillborn pups, and an increase in pup deaths during the first 5 days of lactation, when dosing began during pregnancy and continued until weaning.

The cause of these deaths is not known.

These effects occurred at 2.5 times (mg/m 2 ) the maximum human daily dose.

The no effect dose for rat pup mortality was 0.25 times the human dose on a mg/m 2 basis.

There are no adequate and well-controlled studies in pregnant women.

Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.

Non-Teratogenic Effects Neonates exposed to venlafaxine hydrochloride extended-release capsules, other SNRIs (Serotonin and Norepinephrine Reuptake Inhibitors), or SSRIs (Selective Serotonin Reuptake Inhibitors), late in the third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding.

Such complications can arise immediately upon delivery.

Reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying.

These features are consistent with either a direct toxic effect of SSRIs and SNRIs or, possibly, a drug discontinuation syndrome.

It should be noted that, in some cases, the clinical picture is consistent with serotonin syndrome [ see Warnings and Precautions (5.2) ].

When treating a pregnant woman with Venlafaxine Extended-Release Tablets during the third trimester, the physician should carefully consider the potential risks and benefits of treatment [ see Dosage and Administration (2) ].

NUSRING MOTHERS

8.3 Nursing Mothers Venlafaxine and ODV have been reported to be excreted in human milk.

Because of the potential for serious adverse reactions in nursing infants from Venlafaxine Extended Release Tablets, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

BOXED WARNING

WARNING: SUICIDALITY AND ANTIDEPRESSANT DRUGS Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of Major Depressive Disorder (MDD) and other psychiatric disorders.

Anyone considering the use of Venlafaxine Extended Release Tablets or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need.

Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction in risk with antidepressants compared to placebo in adults aged 65 and older.

Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide.

Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior.

Families and caregivers should be advised of the need for close observation and communication with the prescriber.

Venlafaxine Extended Release Tablets are not approved for use in pediatric patients.

[ See Warnings and Precautions (5.1) and Patient Counseling Information (17.1) ] WARNING: Suicidality and Antidepressants See full prescribing information for complete boxed warning.

Increased risk of suicidal thinking and behavior in children, adolescents and young adults taking antidepressants for major depressive disorder (MDD) and other psychiatric disorders.

Venlafaxine Extended Release Tablets are not approved for use in pediatric patients.

( 5.1 )

WARNING AND CAUTIONS

5 WARNINGS AND PRECAUTIONS Serotonin Syndrome: Serotonin syndrome has been reported with SSRIs and SNRIs, including Venlafaxine Extended Release Tablets, both when taken alone, but especially when co-administered with other serotonergic agents (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone and St.

John’s Wort).

If such symptoms occur, discontinue Venlafaxine Extended-Release tablets and initiate supportive treatment.

If concomitant use of Venlafaxine Extended Release Tablets with other serotonergic drugs is clinically warranted, patients should be made aware of a potential increased risk for serotonin syndrome, particularly during treatment initiation and dose increases.

( 5.2 ).

Suicidality: Monitor for clinical worsening and suicide risk.

( 5.1 ) Sustained hypertension may occur.

Blood pressure monitoring recommended.

( 5.3 ) Angle Closure Glaucoma: Angle closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressants.

( 5.4 ) Abrupt discontinuation or dose reduction: Discontinuation symptoms may occur (generally self-limiting; serious symptoms possible).

Dose reduction recommended to be gradual.

( 5.5 ) Activation of Mania/Hypomania has occurred.

( 5.10 ) Symptomatic hyponatremia may occur.

( 5.11 ) Seizures have been reported.

Use with caution in patients with seizure history.

( 5.12 ) Abnormal bleeding (most commonly ecchymosis) has been reported.

( 5.13 ) Serum cholesterol: Clinically relevant cholesterol increases may occur.

Cholesterol measurements should be considered during long-term therapy.

( 5.14 ) Interstitial lung disease and eosinophilic pneumonia have been reported.

( 5.15 ) 5.1 Clinical Worsening and Suicide Risk Patients with major depressive disorder (MDD), both adult and pediatric, may experience worsening of their depression and/or the emergence of suicidal ideation and behavior (suicidality) or unusual changes in behavior, whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs.

Suicide is a known risk of depression and certain other psychiatric disorders, and these disorders themselves are the strongest predictors of suicide.

There has been a long standing concern, however, that antidepressants may have a role in inducing worsening of depression and the emergence of suicidality in certain patients during the early phases of treatment.

Pooled analyses of short-term placebo-controlled trials of antidepressant drugs (SSRIs and others) showed that these drugs increase the risk of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults (ages 18-24) with major depressive disorder (MDD) and other psychiatric disorders.

Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction with antidepressants compared to placebo in adults aged 65 and older.

The pooled analyses of placebo-controlled trials in children and adolescents with MDD, obsessive compulsive disorder (OCD), or other psychiatric disorders included a total of 24 short-term trials of 9 antidepressant drugs in over 4400 patients.

The pooled analyses of placebo-controlled trials in adults with MDD or other psychiatric disorders included a total of 295 short-term trials (median duration of 2 months) of 11 antidepressant drugs in over 77,000 patients.

There was considerable variation in risk of suicidality among drugs, but a tendency toward an increase in the younger patients for almost all drugs studied.

There were differences in absolute risk of suicidality across the different indications, with the highest incidence in MDD.

The risk differences (drug vs placebo), however, were relatively stable within age strata and across indications.

These risk differences (drug-placebo difference in the number of cases of suicidality per 1000 patients treated) are provided in Table 1.

Table 1 Age Range Drug-Placebo Difference in Number of Cases of Suicidality per 1000 Patients Treated Increases Compared to Placebo <18 14 additional cases 18-24 5 additional cases Decreases Compared to Placebo 25-64 1 fewer case ≥65 6 fewer cases No suicides occurred in any of the pediatric trials.

There were suicides in the adult trials, but the number was not sufficient to reach any conclusion about drug effect on suicide.

It is unknown whether the suicidality risk extends to longer-term use, i.e., beyond several months.

However, there is substantial evidence from placebo-controlled maintenance trials in adults with depression that the use of antidepressants can delay the recurrence of depression.

All patients being treated with antidepressants for any indication should be monitored appropriately and observed closely for clinical worsening, suicidality, and unusual changes in behavior, especially during the initial few months of a course of drug therapy, or at times of dose changes, either increases or decreases.

The following symptoms, anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have been reported in adult and pediatric patients being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and nonpsychiatric.

Although a causal link between the emergence of such symptoms and either the worsening of depression and/or the emergence of suicidal impulses has not been established, there is concern that such symptoms may represent precursors to emerging suicidality.

Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse, or who are experiencing emergent suicidality or symptoms that might be precursors to worsening depression or suicidality, especially if these symptoms are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

If the decision has been made to discontinue treatment, medication should be tapered, as rapidly as is feasible, but with recognition that abrupt discontinuation can be associated with certain symptoms [ see Dosage and Administration (2.5 ) and Warnings and Precautions (5.5) ].

Families and caregivers of patients being treated with antidepressants for major depressive disorder or other indications, both psychiatric and nonpsychiatric, should be alerted about the need to monitor patients for the emergence of agitation, irritability, unusual changes in behavior, and the other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to health care providers.

Such monitoring should include daily observation by families and caregivers.

Prescriptions for Venlafaxine Extended Release Tablets should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

A major depressive episode may be the initial presentation of bipolar disorder.

It is generally believed (though not established in controlled trials) that treating such an episode with an antidepressant alone may increase the likelihood of precipitation of a mixed/manic episode in patients at risk for bipolar disorder.

Whether any of the symptoms described above represent such a conversion is unknown.

However, prior to initiating treatment with an antidepressant, patients with depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder, and depression.

It should be noted that Venlafaxine Extended Release Tablets are not approved for use in treating bipolar depression.

5.2 Serotonin Syndrome The development of a potentially life-threatening serotonin syndrome has been reported with SNRIs and SSRIs, including Venlafaxine Extended Release Tablets, alone but particularly with concomitant use of other serotonergic drugs (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, busipirone, and St.

John’s Wort), and with drugs that impair metabolism of serotonin (in particular, MAOIs, both those intended to treat psychiatric disorders and also others, such as linezolid and intravenous methylene blue).

Serotonin syndrome symptoms may include mental status changes (e.g., agitation, hallucinations, delirium, and coma), autonomic instability (e.g., tachycardia, labile blood pressure, dizziness, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (e.g., tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea).

Patients should be monitored for the emergence of serotonin syndrome.

The concomitant use of Venlafaxine Extended Release Tablets with MAOIs intended to treat psychiatric disorders is contraindicated.

Venlafaxine Extended Release Tablets should also not be started in a patient who is being treated with MAOIs such as linezolid or intravenous methylene blue.

All reports with methylene blue that provided information on the route of administration involved intravenous administration in the dose range of 1 mg/kg to 8 mg/kg.

No reports involved the administration of methylene blue by other routes (such as oral tablets or local tissue injection) or at lower doses.

There may be circumstances when it is necessary to initiate treatment with a MAOI such as linezolid or intravenous methylene blue in a patient taking Venlafaxine Extended Release Tablets.

Venlafaxine Extended Release Tablets should be discontinued before initiating treatment with the MAOI.

[ see CONTRAINDICATIONS (4.1) and DOSAGE AND ADMINISTRATION (2.6 and 2.7) ].

If concomitant use of Venlafaxine Extended Release Tablets with other serotonergic drugs including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, buspirone, tryptophan and St.

John’s Wort is clinically warranted, patients should be aware of a potential increased risk for serotonin syndrome, particularly during treatment initiation and dose increases.

Treatment with Venlafaxine Extended Release Tablets and any concomitant serotonergic agents should be discontinued immediately if the above events occur and supportive symptomatic treatment should be initiated.

5.3 Sustained Hypertension Venlafaxine hydrochloride extended-release capsule treatment is associated with sustained hypertension (defined as treatment-emergent supine diastolic blood pressure (SDBP) ≥90 mm Hg and ≥10 mm Hg above baseline for 3 consecutive on-therapy visits) (see Table 2 ).

An analysis for patients in venlafaxine hydrochloride immediate-release tablet studies meeting criteria for sustained hypertension revealed a dose-dependent increase in the incidence of sustained hypertension for immediate-release venlafaxine hydrochloride (see Table 3 ).

An insufficient number of patients received mean doses of venlafaxine hydrochloride extended-release capsules over 300 mg/day to fully evaluate the incidence of sustained increases in blood pressure at these higher doses.

Table 2: Number (%) of Sustained Elevations in SDBP in Venlafaxine Hydrochloride Extended-Release Capsule Premarketing Studies by Indication Major Depressive Disorder (75-375 mg/day) Other Clinical Trials (75-225 mg/day) 19/705 (3) 5/771 (0.6) Table 3: Incidence (%) of Sustained Elevations in SDBP in Venlafaxine Hydrochloride Immediate-Release Tablet Studies Venlafaxine mg/day Incidence 100 to ≤200 5% >200 to ≤300 7% >300 13% In premarketing major depressive disorder studies, 0.7% (5/705) of the venlafaxine hydrochloride extended-release capsule-treated patients discontinued treatment because of elevated blood pressure.

Among these patients, most of the blood pressure increases were in a modest range (12 to 16 mm Hg, SDBP).

In other clinical studies, 0.6% (5/771) of the venlafaxine hydrochloride extended-release capsule-treated patients discontinued treatment because of elevated blood pressure.

In these patients, the blood pressure increases were modest (1 to 24 mm Hg, SDBP).

Sustained increases of SDBP could have adverse consequences.

Cases of elevated blood pressure requiring immediate treatment have been reported in post marketing experience.

Pre-existing hypertension should be controlled before treatment with venlafaxine.

It is recommended that patients receiving venlafaxine hydrochloride extended-release tablets have regular monitoring of blood pressure.

For patients who experience a sustained increase in blood pressure while receiving venlafaxine, either dose reduction or discontinuation should be considered.

Elevations in Systolic and Diastolic Blood Pressure In placebo-controlled premarketing studies, there were changes in mean blood pressure (see Table 4 for mean change in supine systolic and supine diastolic blood pressure).

Across most indications, a dose-related increase in supine systolic and diastolic blood pressure was evident in venlafaxine hydrochloride extended-release capsule-treated patients.

Table 4: Final On-Therapy Mean Changes from Baseline in Supine Systolic and Diastolic Blood Pressure (mm Hg) Results by Indication, Study Duration, and Dose in Placebo-Controlled Trials Venlafaxine Hydrochloride Extended-Release Capsules mg/day Placebo ≤75 >75 SSBP Supine Systolic Blood Pressure SDBP Supine Diastolic Blood Pressure SSBP SDBP SSBP SDBP Major Depressive Disorder 8-12 weeks -0.28 0.37 2.93 3.56 -1.08 -0.10 Other Clinical Trials 12 weeks -0.29 -1.26 1.18 1.34 -1.96 -1.22 Across all clinical trials, 1.4% of patients in the venlafaxine hydrochloride extended-release capsule-treated groups experienced a ≥15 mm Hg increase in supine diastolic blood pressure with blood pressure ≥105 mm Hg compared to 0.9% of patients in the placebo groups.

Similarly, 1% of patients in the venlafaxine hydrochloride extended-release capsule-treated groups experienced a ≥20 mm Hg increase in supine systolic blood pressure with blood pressure ≥180 mm Hg compared to 0.3% of patients in the placebo groups.

5.4 Angle Closure Glaucoma Angle-Closure Glaucoma: The pupillary dilation that occurs following use of many antidepressant drugs including Venlafaxine may trigger an angle closure attack in a patient with anatomically narrow angles who does not have a patent iridectomy.

5.5 Discontinuation of Treatment with Venlafaxine Extended Release Tablets Discontinuation symptoms have been systematically evaluated in patients taking venlafaxine, to include prospective analyses of clinical trials and retrospective surveys of trials in major depressive disorder and social anxiety disorder.

Abrupt discontinuation or dose reduction of venlafaxine at various doses has been found to be associated with the appearance of new symptoms, the frequency of which increased with increased dose level and with longer duration of treatment.

Reported symptoms include agitation, anorexia, anxiety, confusion, impaired coordination and balance, diarrhea, dizziness, dry mouth, dysphoric mood, fasciculation, fatigue, headaches, hypomania, insomnia, nausea, nervousness, nightmares, sensory disturbances (including shock-like electrical sensations), somnolence, sweating, tremor, vertigo, and vomiting.

During marketing of venlafaxine hydrochloride extended-release capsules, other SNRI’s (Serotonin and Norepinephrine Reuptake Inhibitors), and SSRI’s (Selective Serotonin Reuptake Inhibitors), there have been spontaneous reports of adverse reactions occurring upon discontinuation of these drugs, particularly when abrupt, including the following: dysphoric mood, irritability, agitation, dizziness, sensory disturbances (e.g.

paresthesias such as electric shock sensations), anxiety, confusion, headache, lethargy, emotional lability, insomnia, hypomania, tinnitus, and seizures.

While these reactions are generally self-limiting, there have been reports of serious discontinuation symptoms.

Patients should be monitored for these symptoms when discontinuing treatment with Venlafaxine Extended Release Tablets.

A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible.

If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered.

Subsequently, the physician may continue decreasing the dose but at a more gradual rate [ see Dosage and Administration (2.4) ].

5.6 Insomnia and Nervousness Treatment-emergent insomnia and nervousness were more commonly reported for patients treated with venlafaxine hydrochloride extended-release capsules than with placebo in pooled analyses of short-term major depressive disorder and other clinical studies, as shown in Table 5.

Table 5 Incidence of Insomnia and Nervousness in Placebo-Controlled Major Depressive Disorder and Other Trials Major Depressive Disorder Other Trials Venlafaxine Hydrochloride Extended-Release Capsules Placebo Venlafaxine Hydrochloride Extended-Release Capsules Placebo Symptom n = 357 n = 285 N = 819 n = 695 Insomnia 17% 11% 24% 8% Nervousness 10% 5% 10% 5% Insomnia and nervousness each led to drug discontinuation in 0.9% of the patients treated with venlafaxine hydrochloride extended-release capsules in major depressive disorder studies.

In other clinical trials, insomnia and nervousness led to drug discontinuation in 2% and 1%, respectively, of the patients treated with venlafaxine hydrochloride extended-release capsules up to 12 weeks.

5.7 Changes in Weight Adult Patients: A loss of 5% or more of body weight occurred in 7% of patients treated with venlafaxine hydrochloride extended-release capsules and 2% of placebo-treated patients in the short-term placebo-controlled major depressive disorder trials.

The discontinuation rate for weight loss associated with venlafaxine hydrochloride extended-release capsules was 0.1% in major depressive disorder studies.

In other placebo-controlled trials, 4% of the patients treated with venlafaxine hydrochloride extended-release capsules and 1% of the placebo-treated patients sustained a loss of 7% or more of body weight during up to 6 months of treatment.

None of the patients receiving venlafaxine hydrochloride extended-release capsules in other studies discontinued for weight loss.

The safety and efficacy of venlafaxine therapy in combination with weight loss agents, including phentermine, have not been established.

Co-administration of Venlafaxine Extended Release Tablets and weight loss agents is not recommended.

Venlafaxine Extended Release Tablets are not indicated for weight loss alone or in combination with other products.

Pediatric Patients: Weight loss has been observed in pediatric patients (ages 6-17) receiving venlafaxine hydrochloride extended-release capsules.

In a pooled analysis of four eight-week, double-blind, placebo-controlled, flexible dose outpatient trials for major depressive disorder (MDD) and another disorder, patients treated with venlafaxine hydrochloride extended-release capsules lost an average of 0.45 kg (n = 333), while placebo-treated patients gained an average of 0.77 kg (n = 333).

More patients treated with venlafaxine hydrochloride extended-release capsules than with placebo experienced a weight loss of at least 3.5% in the studies (18% of patients treated with venlafaxine hydrochloride extended-release capsules vs.

3.6% of placebo-treated patients; p<0.001).

In a 16-week, double-blind, placebo-controlled, flexible dose outpatient study for another disorder, venlafaxine hydrochloride extended-release capsule-treated patients lost an average of 0.75 kg (n=137), while placebo-treated patients gained an average of 0.76 kg (n=148).

More patients treated with venlafaxine hydrochloride extended-release capsules than with placebo experienced a weight loss of at least 3.5% in the study (47% of patients treated with venlafaxine hydrochloride extended-release capsules vs.

14% of placebo-treated patients; p<0.001).

Weight loss was not limited to patients with treatment-emergent anorexia [ see Warnings and Precautions (5.9) ].

The risks associated with longer-term use of venlafaxine hydrochloride extended-release capsules were assessed in an open-label MDD study of children and adolescents who received venlafaxine hydrochloride extended-release capsules for up to six months.

The children and adolescents in the study had increases in weight that were less than expected based on data from age- and sex-matched peers.

The difference between observed weight gain and expected weight gain was larger for children (<12 years old) than for adolescents (≥12 years old).

5.8 Changes in Height Pediatric Patients: During an eight-week, placebo-controlled non-MDD study, venlafaxine hydrochloride extended-release capsule-treated patients (ages 6-17) grew an average of 0.3 cm (n=122), while placebo-treated patients grew an average of 1.0 cm (n=132); p=0.041.

This difference in height increase was most notable in patients younger than twelve.

During the eight-week placebo-controlled MDD studies, venlafaxine hydrochloride extended-release capsule-treated patients grew an average of 0.8 cm (n = 146), while placebo-treated patients grew an average of 0.7 cm (n = 147).

During a 16-week, placebo-controlled non-MDD study, both the venlafaxine hydrochloride extended-release capsule-treated patients (n=109) and the placebo-treated (n=112) patients each grew an average of 1.0 cm.

In the six-month, open-label MDD study, children and adolescents had height increases that were less than expected based on data from age- and sex-matched peers.

The difference between observed growth rates and expected growth rates was larger for children (<12 years old) than for adolescents (≥12 years old).

5.9 Changes in Appetite Adult Patients: Treatment-emergent anorexia was more commonly reported for patients treated with venlafaxine hydrochloride extended-release capsules (8%) than for placebo-treated patients (4%) in the pool of short-term, double-blind, placebo-controlled major depressive disorder studies.

The discontinuation rate for anorexia associated with venlafaxine hydrochloride extended-release capsules was 1.0% in major depressive disorder studies.

Treatment-emergent anorexia was more commonly reported for patients treated with venlafaxine hydrochloride extended-release capsules (20%) than for placebo-treated patients (2%) in the pool of short-term, double-blind, placebo-controlled Social Anxiety Disorder studies.

The discontinuation rate for anorexia was 0.4% for patients receiving venlafaxine hydrochloride extended-release capsules for up to 12 weeks in Social Anxiety Disorder studies.

Pediatric Patients: Decreased appetite has been observed in pediatric patients receiving venlafaxine hydrochloride extended-release capsules.

In placebo-controlled trials in MDD and another disorder, 10% of patients aged 6-17 treated with venlafaxine hydrochloride extended-release capsules for up to eight weeks and 3% of patients treated with placebo reported treatment-emergent anorexia (decreased appetite).

None of the patients receiving venlafaxine hydrochloride extended-release capsules discontinued for anorexia or weight loss.

In a placebo-controlled non-MDD trial, 22% and 3% of patients aged 8-17 treated for up to 16 weeks with venlafaxine hydrochloride extended-release capsules and placebo, respectively, reported treatment-emergent anorexia (decreased appetite).

The discontinuation rates for anorexia were 0.7% and 0.0% for patients receiving venlafaxine hydrochloride extended-release capsules and placebo, respectively; the discontinuation rates for weight loss were 0.7% for patients receiving either venlafaxine hydrochloride extended-release capsules or placebo.

5.10 Activation of Mania/Hypomania During premarketing major depressive disorder studies, mania or hypomania occurred in 0.3% of patients treated with venlafaxine hydrochloride extended-release capsules and 0.0% placebo patients.

In premarketing Social Anxiety Disorder studies, no patients treated with venlafaxine hydrochloride extended-release capsules and no placebo-treated patients experienced mania or hypomania.

In all premarketing major depressive disorder trials with venlafaxine hydrochloride immediate-release tablets, mania or hypomania occurred in 0.5% of venlafaxine-treated patients compared with 0% of placebo patients.

Mania/hypomania has also been reported in a small proportion of patients with mood disorders who were treated with other marketed drugs to treat major depressive disorder.

As with all drugs effective in the treatment of major depressive disorder, Venlafaxine Extended Release Tablets should be used cautiously in patients with a history of mania.

5.11 Hyponatremia Hyponatremia may occur as a result of treatment with SSRI’s and SNRI’s, including Venlafaxine Extended Release Tablets.

In many cases, this hyponatremia appears to be the result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Cases with serum sodium lower than 110 mmol/L have been reported.

Elderly patients may be at greater risk of developing hyponatremia with SSRIs and SNRIs.

Also, patients taking diuretics or who are otherwise volume depleted may be at greater risk [ see Use in Specific Populations (8.5) ].

Discontinuation of Venlafaxine Extended Release Tablets should be considered in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

Signs and symptoms of hyponatremia include headache, difficulty concentrating, memory impairment, confusion, weakness, and unsteadiness, which may lead to falls.

Signs and symptoms associated with more severe and/or acute cases have included hallucination, syncope, seizure, coma, respiratory arrest, and death.

5.12 Seizures During premarketing experience, no seizures occurred among 705 patients treated with venlafaxine hydrochloride extended-release capsules in the major depressive disorder studies or among 277 patients treated with venlafaxine hydrochloride extended-release capsules in Social Anxiety Disorder studies.

In all premarketing major depressive disorder trials with venlafaxine hydrochloride immediate-release tablets, seizures were reported at various doses in 0.3% (8/3082) of venlafaxine-treated patients.

Venlafaxine Extended Release Tablets, like many antidepressants, should be used cautiously in patients with a history of seizures and should be discontinued in any patient who develops seizures.

5.13 Abnormal Bleeding SSRIs and SNRIs, including Venlafaxine Extended Release Tablets, may increase the risk of bleeding events.

Concomitant use of aspirin, nonsteroidal anti-inflammatory drugs, warfarin, and other anticoagulants may add to this risk.

Case reports and epidemiological studies (case-control and cohort design) have demonstrated an association between use of drugs that interfere with serotonin reuptake and the occurrence of gastrointestinal bleeding.

Bleeding events related to SSRIs and SNRIs use have ranged from ecchymoses, hematomas, epistaxis, and petechiae to life-threatening hemorrhages.

Patients should be cautioned about the risk of bleeding associated with the concomitant use of Venlafaxine Extended Release Tablets and NSAIDs, aspirin, or other drugs that affect coagulation.

5.14 Serum Cholesterol Elevation Clinically relevant increases in serum cholesterol were recorded in 5.3% of venlafaxine-treated patients and 0.0% of placebo-treated patients treated for at least 3 months in placebo-controlled trials [ see Adverse Reactions (6.1) ].

Measurement of serum cholesterol levels should be considered during long-term treatment.

5.15 Interstitial Lung Disease and Eosinophilic Pneumonia Interstitial lung disease and eosinophilic pneumonia associated with venlafaxine therapy have been rarely reported.

The possibility of these adverse reactions should be considered in venlafaxine-treated patients who present with progressive dyspnea, cough or chest discomfort.

Such patients should undergo a prompt medical evaluation, and discontinuation of venlafaxine therapy should be considered.

5.16 Use in Patients With Heart Disease Premarketing experience with venlafaxine in patients with concomitant systemic illness is limited.

Caution is advised in administering Venlafaxine Extended Release Tablets to patients with diseases or conditions that could affect hemodynamic responses.

Venlafaxine has not been evaluated or used to any appreciable extent in patients with a recent history of myocardial infarction or unstable heart disease.

Patients with these diagnoses were systematically excluded from many clinical studies during venlafaxine’s premarketing testing.

The electrocardiograms were analyzed for 275 patients who received venlafaxine hydrochloride extended-release capsules and 220 patients who received placebo in 8- to 12-week double-blind, placebo-controlled trials in major depressive disorder as well as for 195 patients who received venlafaxine hydrochloride extended-release capsules and 228 patients who received placebo in 12-week double-blind, placebo-controlled trials in Social Anxiety Disorder.

The mean change from baseline in corrected QT interval (QTc) for patients treated with venlafaxine hydrochloride extended-release capsules in major depressive disorder studies was increased relative to that for placebo-treated patients (increase of 4.7 msec for venlafaxine hydrochloride extended-release capsules and decrease of 1.9 msec for placebo).

The mean change from baseline in QTc for patients treated with venlafaxine hydrochloride extended-release capsules in the Social Anxiety Disorder studies was increased relative to that for placebo-treated patients (increase of 2.8 msec for venlafaxine hydrochloride extended-release capsules and decrease of 2.0 msec for placebo).

In these same trials, the mean change from baseline in heart rate for patients treated with venlafaxine hydrochloride extended-release capsules in the major depressive disorder studies was significantly higher than that for placebo (a mean increase of 4 beats per minute for venlafaxine hydrochloride extended-release capsules and 1 beat per minute for placebo).

The mean change from baseline in heart rate for patients treated with venlafaxine hydrochloride extended-release capsules in the Social Anxiety Disorder studies was significantly higher than that for placebo (a mean increase of 5 beats per minute for venlafaxine hydrochloride extended-release capsules and no change for placebo).

In a flexible-dose study, with doses of venlafaxine hydrochloride immediate-release tablets in the range of 200 to 375 mg/day and mean dose greater than 300 mg/day, patients treated with venlafaxine hydrochloride immediate-release tablets had a mean increase in heart rate of 8.5 beats per minute compared with 1.7 beats per minute in the placebo group.

As increases in heart rate were observed, caution should be exercised in patients whose underlying medical conditions might be compromised by increases in heart rate (e.g., patients with hyperthyroidism, heart failure, or recent myocardial infarction).

Evaluation of the electrocardiograms for 769 patients who received venlafaxine hydrochloride immediate-release tablets in 4- to 6-week double-blind, placebo-controlled trials showed that the incidence of trial-emergent conduction abnormalities did not differ from that with placebo.

5.17 Laboratory Tests There are no specific laboratory tests recommended.

INFORMATION FOR PATIENTS

17 PATIENT COUNSELING INFORMATION See FDA-approved Medication Guide (17.9) Prescribers or other health professionals should inform patients, their families, and their caregivers about the benefits and risks associated with treatment with Venlafaxine Extended Release Tablets and should counsel them in its appropriate use.

A patient Medication Guide about “Antidepressant Medicines, Depression and Other Serious Mental Illness, and Suicidal Thoughts or Actions” is available for Venlafaxine Extended Release Tablets.

The prescriber or health professional should instruct patients, their families, and their caregivers to read the Medication Guide and should assist them in understanding its contents.

Patients should be given the opportunity to discuss the contents of the Medication Guide and to obtain answers to any questions they may have.

The complete text of the Medication Guide is reprinted at the end of this document.

Patients should be advised of the following issues and asked to alert their prescriber if these occur while taking Venlafaxine Extended Release Tablets.

17.1 Clinical Worsening and Suicide Risk Patients, their families, and their caregivers should be encouraged to be alert to the emergence of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia (psychomotor restlessness), hypomania, mania, other unusual changes in behavior, worsening of depression, and suicidal ideation, especially early during antidepressant treatment and when the dose is adjusted up or down.

Families and caregivers of patients should be advised to look for the emergence of such symptoms on a day-to-day basis, since changes may be abrupt.

Such symptoms should be reported to the patient’s prescriber or health professional, especially if they are severe, abrupt in onset, or were not part of the patient’s presenting symptoms.

Symptoms such as these may be associated with an increased risk for suicidal thinking and behavior and indicate a need for very close monitoring and possibly changes in the medication.

17.2 Interference with Cognitive and Motor Performance Clinical studies were performed to examine the effects of venlafaxine on behavioral performance of healthy individuals.

The results revealed no clinically significant impairment of psychomotor, cognitive, or complex behavior performance.

However, since any psychoactive drug may impair judgment, thinking, or motor skills, patients should be cautioned about operating hazardous machinery, including automobiles, until they are reasonably certain that venlafaxine therapy does not adversely affect their ability to engage in such activities.

17.3 Concomitant Medication Patients should be advised to inform their physicians if they are taking, or plan to take, any prescription or over-the-counter drugs, including herbal preparations and nutritional supplements, since there is a potential for interactions.

Patients should be cautioned about the risk of serotonin syndrome with the concomitant use of Venlafaxine Extended Release Tablets and triptans, tramadol, tryptophan supplements or other serotonergic agents [ see Warnings and Precautions (5.2) and Drug Interactions (7.10) ].

Patients should be cautioned about the concomitant use of Venlafaxine Extended Release Tablets and NSAID’s, aspirin, warfarin, or other drugs that affect coagulation since combined use of psychotropic drugs that interfere with serotonin reuptake and these agents has been associated with an increased risk of bleeding [ see Warnings and Precautions (5.13) and Drug Interactions (7.11) ].

17.4 Alcohol Although venlafaxine has not been shown to increase the impairment of mental and motor skills caused by alcohol, patients should be advised to avoid alcohol while taking venlafaxine.

17.5 Allergic Reactions Patients should be advised to notify their physician if they develop a rash, hives, or a related allergic phenomenon.

17.6 Pregnancy Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during therapy.

17.7 Nursing Patients should be advised to notify their physician if they are breast-feeding an infant.

17.8 Angle Closure Glaucoma Patients should be advised that taking Venlafaxine can cause mild pupillary dilation, which in susceptible individuals, can lead to an episode of angle closure glaucoma.

Pre-existing glaucoma is almost always open-angle glaucoma because angle closure glaucoma, when diagnosed, can be treated definitively with iridectomy.

Open-angle glaucoma is not a risk factor for angle closure glaucoma.

Patients may wish to be examined to determine whether they are susceptible to angle closure, and have a prophylactic procedure (e.g., iridectomy), if they are susceptible.

[see Warnings and Precautions (5.4) ] 17.9 FDA-Approved Medication Guide

DOSAGE AND ADMINISTRATION

2 Venlafaxine Extended Release Tablets should be administered in a single dose with food either in the morning or in the evening at approximately the same time each day.

Each tablet should be swallowed whole with fluid and not divided, crushed, chewed, or placed in water.

Initial Treatment ( 2.1 ) Indication Starting Dose Dose Increase Maximum Dose Major Depressive Disorder 75 mg/day (in some patients, 37.5 mg/day for 4-7 days) 75 mg/day increments at intervals of 4 days or longer 225 mg/day Social Anxiety Disorder 75 mg/day No benefit at higher doses 75 mg/day Venlafaxine extended-release tablets should be taken as a single daily dose with food in either the morning or evening at the same time each day.

( 2 ) Discontinuation: Gradual; individualized as necessary.

( 2.4 ) 2.1 Initial Treatment Major Depressive Disorder For most patients, the recommended starting dose for Venlafaxine Extended Release Tablets is 75 mg/day, administered in a single dose.

In the clinical trials establishing the efficacy of venlafaxine hydrochloride extended-release capsules in moderately depressed outpatients, the initial dose of venlafaxine was 75 mg/day.

For some patients, it may be desirable to start at 37.5 mg/day for 4 to 7 days, to allow new patients to adjust to the medication before increasing to 75 mg/day.

While the relationship between dose and antidepressant response for venlafaxine hydrochloride extended-release capsules has not been adequately explored, patients not responding to the initial 75 mg/day dose may benefit from dose increases to a maximum of approximately 225 mg/day.

Dose increases should be in increments of up to 75 mg/day, as needed, and should be made at intervals of not less than 4 days, since steady state plasma levels of venlafaxine and its major metabolites are achieved in most patients by day 4.

In the clinical trials establishing efficacy, upward titration was permitted at intervals of 2 weeks or more; the average doses were about 140 to 180 mg/day [ see Clinical Studies (14) ].

It should be noted that, while the maximum recommended dose for moderately depressed outpatients is also 225 mg/day for venlafaxine hydrochloride immediate-release tablets, more severely depressed inpatients in one study of the development program for that product responded to a mean dose of 350 mg/day (range of 150 to 375 mg/day).

Whether or not higher doses of Venlafaxine Extended Release Tablets are needed for more severely depressed patients is unknown; however, the experience with venlafaxine hydrochloride extended-release capsule doses higher than 225 mg/day is very limited.

[ See Warnings and Precautions (5.17) ] Social Anxiety Disorder (Social Phobia) The recommended dose is 75 mg/day, administered in a single dose.

There was no evidence that higher doses confer any additional benefit.

[ See Warnings and Precautions (5.17) ] 2.2 Maintenance Treatment There is no body of evidence available from controlled trials to indicate how long patients with major depressive disorder should be treated with Venlafaxine Extended Release Tablets.

It is generally agreed that acute episodes of major depressive disorder require several months or longer of sustained pharmacological therapy beyond response to the acute episode.

In one study, in which patients responding during 8 weeks of acute treatment with venlafaxine hydrochloride extended-release capsules were assigned randomly to placebo or to the same dose of venlafaxine hydrochloride extended-release capsules (75, 150, or 225 mg/day, qAM) during 26 weeks of maintenance treatment as they had received during the acute stabilization phase, longer-term efficacy was demonstrated.

A second longer-term study has demonstrated the efficacy of venlafaxine hydrochloride immediate-release tablets in maintaining a response in patients with recurrent major depressive disorder who had responded and continued to be improved during an initial 26 weeks of treatment and were then randomly assigned to placebo or venlafaxine hydrochloride immediate-release tablets for periods of up to 52 weeks on the same dose (100 to 200 mg/day, on a b.i.d.

schedule)[ see Clinical Studies (14) ].

Based on these limited data, it is not known whether or not the dose of Venlafaxine Extended Release Tablets needed for maintenance treatment is identical to the dose needed to achieve an initial response.

Patients should be periodically reassessed to determine the need for maintenance treatment and the appropriate dose for such treatment.

2.3 Special Populations Treatment of Pregnant Women During the Third Trimester Neonates exposed to venlafaxine hydrochloride extended-release capsules, other SNRIs, or SSRIs, late in the third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding [ see Use in Specific Populations (8.1) ].

When treating pregnant women with Venlafaxine Extended Release Tablets during the third trimester, the physician should carefully consider the potential risks and benefits of treatment.

Patients with Hepatic Impairment Given the decrease in clearance and increase in elimination half-life for both venlafaxine and ODV that is observed in patients with hepatic cirrhosis and mild and moderate hepatic impairment compared with normal subjects [ see Use in Specific Populations (8.6) and Clinical Pharmacology (12.3) ], it is recommended that the total daily dose be reduced by 50% in patients with mild to moderate hepatic impairment.

Since there was much individual variability in clearance between patients with cirrhosis, it may be necessary to reduce the dose even more than 50%, and individualization of dosing may be desirable in some patients.

Patients with Renal Impairment Given the decrease in clearance for venlafaxine and the increase in elimination half-life for both venlafaxine and ODV that is observed in patients with renal impairment (GFR = 10 to 70 mL/min) compared with normal subjects [ see Use in Specific Populations (8.7) and Clinical Pharmacology (12.3) ], it is recommended that the total daily dose be reduced by 25% to 50%.

In patients undergoing hemodialysis, it is recommended that the total daily dose be reduced by 50% .

Because there was much individual variability in clearance between patients with renal impairment, individualization of dosage may be desirable in some patients.

Elderly Patients No dose adjustment is recommended for elderly patients solely on the basis of age.

As with any drug for the treatment of major depressive disorder or Social Anxiety Disorder, however, caution should be exercised in treating the elderly.

When individualizing the dosage, extra care should be taken when increasing the dose.

2.4 Discontinuing Venlafaxine Extended Release Tablets Symptoms associated with discontinuation of venlafaxine hydrochloride extended-release capsules, other SNRI’s, and SSRI’s have been reported [ see Warnings and Precautions (5.5) ].

Patients should be monitored for these symptoms when discontinuing treatment.

A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible.

If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered.

Subsequently, the physician may continue decreasing the dose but at a more gradual rate.

In clinical trials with venlafaxine hydrochloride extended-release capsules, tapering was achieved by reducing the daily dose by 75 mg at 1 week intervals.

Individualization of tapering may be necessary.

2.5 Switching Patients from Venlafaxine Hydrochloride Immediate-Release Tablets Depressed patients who are currently being treated at a therapeutic dose with venlafaxine hydrochloride immediate-release tablets may be switched to Venlafaxine Extended Release Tablets at the nearest equivalent dose (mg/day), e.g., 37.5 mg venlafaxine two-times-a-day to 75 mg Venlafaxine Extended Release Tablets once daily.

However, individual dosage adjustments may be necessary.

2.6 Switching a Patient To or From a Monoamine Oxidase Inhibitor (MAOI) Intended to Treat Psychiatric Disorders At least 14 days should elapse between discontinuation of an MAOI intended to treat psychiatric disorders and initiation of therapy with Venlafaxine Extended Release Tablets.

Conversely, at least 7 days should be allowed after stopping Venlafaxine Extended Release Tablets before starting an MAOI intended to treat psychiatric disorders [ see Contraindications (4.1) ].

2.7 Use of Venlafaxine Extended Release Tablets with Other MAOIs, Such as Linezolid or Methylene Blue Do not start Venlafaxine Extended Release Tablets in a patient who is being treated with linezolid or intravenous methylene blue because there is increased risk of serotonin syndrome.

In a patient who requires more urgent treatment of a psychiatric condition, other interventions, including hospitalization, should be considered [ see CONTRAINDICATIONS (4.1) ].

In some cases, a patient already receiving Venlafaxine Extended Release Tablets therapy may require urgent treatment with linezolid or intravenous methylene blue.

If acceptable alternatives to linezolid or intravenous methylene blue treatment are not available and the potential benefits of linezolid or intravenous methylene blue treatment are judged to outweigh the risks of serotonin syndrome in a particular patient, Venlafaxine Extended Release Tablets should be stopped promptly, and linezolid or intravenous methylene blue can be administered.

The patient should be monitored for symptoms of serotonin syndrome for 7 days or until 24 hours after the last dose of linezolid or intravenous methylene blue, whichever comes first.

Therapy with Venlafaxine Extended Release Tablets may be resumed 24 hours after the last dose of linezolid or intravenous methylene blue [ see WARNINGS AND PRECAUTIONS (5.2) ].

The risk of administering methylene blue by non-intravenous routes (such as oral tablets or by local injection) or in intravenous doses much lower than 1 mg/kg with Venlafaxine Extended Release Tablets is unclear.

The clinician should, nevertheless, be aware of the possibility of emergent symptoms of serotonin syndrome with such use [ see WARNINGS AND PRECAUTIONS (5.2) ].