Finasteride 1 MG Oral Tablet
Generic Name: FINASTERIDE
Brand Name: Finasteride
- Substance Name(s):
- FINASTERIDE
DRUG INTERACTIONS
7 7.1 Cytochrome P450-Linked Drug Metabolizing Enzyme System No drug interactions of clinical importance have been identified.
Finasteride does not appear to affect the cytochrome P450-linked drug-metabolizing enzyme system.
Compounds that have been tested in man include antipyrine, digoxin, propranolol, theophylline, and warfarin and no clinically meaningful interactions were found.
7.2 Other Concomitant Therapy Although specific interaction studies were not performed, finasteride doses of 1 mg or more were concomitantly used in clinical studies with acetaminophen, acetylsalicylic acid, α-blockers, analgesics, angiotensin-converting enzyme (ACE) inhibitors, anticonvulsants, benzodiazepines, beta blockers, calcium-channel blockers, cardiac nitrates, diuretics, H2 antagonists, HMG-CoA reductase inhibitors, prostaglandin synthetase inhibitors (also referred to as NSAIDs), and quinolone anti-infectives without evidence of clinically significant adverse interactions.
OVERDOSAGE
10 In clinical studies, single doses of finasteride up to 400 mg and multiple doses of finasteride up to 80 mg/day for three months did not result in adverse reactions.
Until further experience is obtained, no specific treatment for an overdose with finasteride can be recommended.
Significant lethality was observed in male and female mice at single oral doses of 1500 mg/m2 (500 mg/kg)and in female and male rats at single oral doses of 2360 mg/m2 (400 mg/kg)and 5900 mg/m2(1000 mg/kg), respectively.
DESCRIPTION
11 Finasteride tablets USP, 1 mg contains finasteride as the active ingredient.
Finasteride USP, a synthetic 4-azasteroid compound, is a specific inhibitor of steroid Type II 5α-reductase, an intracellular enzyme that converts the androgen testosterone in to 5α-dihydrotestosterone (DHT).
Finasteride is 4-azaandrost-1-ene-17-carboxamide, N-(1,1-dimethylethyl)-3-oxo-, (5α, 17β)-.
The empirical formula of finasteride is C23H36N2O2 and its molecular weight is 372.55.
Its structural formula is: Finasteride is a white crystalline powder with a melting point near 250° C.
It is freely soluble in chloroform and in lower alcohol solvents but is practically insoluble in water.
Finasteride tablets USP for oral administration are film-coated tablets that contain 1 mg of finasteride and the following inactive ingredients: lactose monohydrate, microcrystalline cellulose, pregelatinized starch, sodium starch glycolate, docusate sodium, magnesium stearate and opadry brown (hypromellose, iron oxide red, talc, titanium dioxide, yellow iron oxide).
structure6
CLINICAL STUDIES
14 14.1 Studies in Men The efficacy of finasteride tablets USP was demonstrated in men (88% Caucasian)with mild to moderate androgenetic alopecia (male pattern hair loss) between 18 and 41 years of age.
In order to prevent seborrheic dermatitis which might confound the assessment of hair growth in these studies, all men, whether treated with finasteride or placebo, were instructed to use a specified, medicated, tar-based shampoo (Neutrogena T/Gel® Shampoo)during the first 2 years of the studies.
There were three double-blind, randomized, placebo-controlled studies of 12-month duration.
The two primary endpoints were hair count and patient self-assessment; the two secondary endpoints were investigator assessment and ratings of photographs.
In addition, information was collected regarding sexual function (based on a self-administered questionnaire) and non-scalp body hair growth.
The three studies were conducted in 1879 men with mild to moderate, but not complete, hair loss.
Two of the studies enrolled men with predominantly mild to moderate vertex hair loss (n=1553).
The third enrolled men having mild to moderate hair loss in the anterior mid-scalp area with or without vertex balding (n=326).
Studies in Men with Vertex Baldness Of the men who completed the first 12 months of the two vertex baldness trials, 1215 elected to continue in double-blind, placebo-controlled, 12-month extension studies.
There were 547 men receiving finasteride tablets USP, 1 mg for both the initial study and first extension periods (up to 2 years of treatment) and 60 men receiving placebo for the same periods.
The extension studies were continued for 3 additional years, with 323 men on finasteride tablets USP, 1 mg and 23 on placebo entering the fifth year of the study.
In order to evaluate the effect of discontinuation of therapy, there were 65 men who received finasteride tablets USP for the initial 12 months followed by placebo in the first 12-month extension period.
Some of these men continued in additional extension studies and were switched back to treatment with finasteride tablets USP, with 32 men entering the fifth year of the study.
Lastly, there were 543 men who received placebo for the initial 12 months followed by finasteride tablets USP in the first 12-month extension period.
Some of these men continued in additional extension studies receiving finasteride tablets USP, with 290 men entering the fifth year of the study (see Figure 1 below).
Hair counts were assessed by photographic enlargements of a representative area of active hair loss.
In these two studies in men with vertex baldness, significant increases in hair count were demonstrated at 6 and 12 months in men treated with finasteride tablets USP, while significant hair loss from baseline was demonstrated in those treated with placebo.
At 12 months there was a 107-hair difference from placebo (p<0.001, finasteride tablets USP [n=679] vs placebo [n=672]) within a 1-inch diameter circle (5.1 cm2).
Hair count was maintained in those men taking finasteride tablets USP for up to 2 years, resulting in a 138-hair difference between treatment groups (p<0.001, finasteride tablets USP [n=433] vs placebo [n=47]) within the same area.
In men treated with finasteride tablets USP, the maximum improvement in hair count compared to baseline was achieved during the first 2 years.
Although the initial improvement was followed by a slow decline, hair count was maintained above baseline throughout the 5 years of the studies.
Furthermore, because the decline in the placebo group was more rapid, the difference between treatment groups also continued to increase throughout the studies, resulting in a 277-hair difference (p<0.001, finasteride tablets USP [n=219] vs placebo [n=15]) at 5 years (see Figure 1 below).
Patients who switched from placebo to finasteride tablets USP (n=425) had a decrease in hair count at the end of the initial 12-month placebo period, followed by an increase in hair count after 1 year of treatment with finasteride tablets USP.
This increase in hair count was less (56 hairs above original baseline) than the increase (91 hairs above original baseline) observed after 1 year of treatment in men initially randomized to finasteride tablets USP.
Although the increase in hair count, relative to when therapy was initiated, was comparable between these two groups, a higher absolute hair count was achieved in patients who were started on treatment with finasteride tablets USP in the initial study.
This advantage was maintained through the remaining 3 years of the studies.
A change of treatment from finasteride tablets USP to placebo (n=48) at the end of the initial 12 months resulted in reversal of the increase in hair count 12 months later, at 24 months (see Figure 1 below).
At 12 months, 58% of men in the placebo group had further hair loss (defined as any decrease in hair count from baseline), compared with 14% of men treated with finasteride tablets USP.
In men treated for up to 2 years, 72% of men in the placebo group demonstrated hair loss, compared with 17% of men treated with finasteride tablets USP.
At 5 years, 100% of men in the placebo group demonstrated hair loss, compared with 35% of men treated with finasteride tablets USP.
Figure 1 Patient self-assessment was obtained at each clinic visit from a self-administered questionnaire, which included questions on their perception of hair growth, hair loss, and appearance.
This self-assessment demonstrated an increase in amount of hair, a decrease in hair loss, and improvement in appearance in men treated with finasteride tablets USP.
Overall improvement compared with placebo was seen as early as 3 months (p<0.05), with improvement maintained over 5 years.
Investigator assessment was based on a 7-point scale evaluating increases or decreases in scalp hair at each patient visit.
This assessment showed significantly greater increases in hair growth in men treated with finasteride tablets USP compared with placebo as early as 3 months (p<0.001).
At 12 months, the investigators rated 65% of men treated with finasteride tablets USP as having increased hair growth compared with 37% in the placebo group.
At 2 years, the investigators rated 80% of men treated with finasteride tablets USP as having increased hair growth compared with 47% of men treated with placebo.
At 5 years, the investigators rated 77% of men treated with finasteride tablets USP as having increased hair growth, compared with 15% of men treated with placebo.
An independent panel rated standardized photographs of the head in a blinded fashion based on increases or decreases in scalp hair using the same 7-point scale as the investigator assessment.
At 12 months, 48% of men treated with finasteride tablets USP had an increase as compared with 7% of men treated with placebo.
At 2 years, an increase in hair growth was demonstrated in 66% of men treated with finasteride tablets USP, compared with 7% of men treated with placebo.
At 5 years, 48% of men treated with finasteride tablets USP demonstrated an increase in hair growth, 42% were rated as having no change (no further visible progression of hair loss from baseline) and 10% were rated as having lost hair when compared to baseline.
In comparison, 6% of men treated with placebo demonstrated an increase in hair growth, 19% were rated as having no change and 75% were rated as having lost hair when compared to baseline.
A 48-week, placebo-controlled study designed to assess by phototrichogram the effect of finasteride tablets USP on total and actively growing (anagen) scalp hairs in vertex baldness enrolled 212 men with androgenetic alopecia.
At baseline and 48 weeks, total and anagen hair counts were obtained in a 1-cm2 target area of the scalp.
Men treated with finasteride tablets USP showed increases from baseline in total and anagen hair counts of 7 hairs and 18 hairs, respectively, whereas men treated with placebo had decreases of 10 hairs and 9 hairs, respectively.
These changes in hair counts resulted in a between-group difference of 17 hairs in total hair count (p<0.001) and 27 hairs in anagen hair count (p<0.001), and an improvement in the proportion of anagen hairs from 62% at baseline to 68% for men treated with finasteride tablets USP.
Other Results in Vertex Baldness Studies A sexual function questionnaire was self-administered by patients participating in the two vertex baldness trials to detect more subtle changes in sexual function.
At Month 12, statistically significant differences in favor of placebo were found in 3 of 4 domains (sexual interest, erections, and perception of sexual problems).
However, no significant difference was seen in the question on overall satisfaction with sex life.
In one of the two vertex baldness studies, patients were questioned on non-scalp body hair growth.
Finasteride tablets USP did not appear to affect non-scalp body hair.
Study in Men with Hair Loss in the Anterior Mid-Scalp Area A study of 12-month duration, designed to assess the efficacy of finasteride tablets USP in men with hair loss in the anterior mid-scalp area, also demonstrated significant increases in hair count compared with placebo.
Increases in hair count were accompanied by improvements in patient self-assessment, investigator assessment, and ratings based on standardized photographs.
Hair counts were obtained in the anterior mid-scalp area, and did not include the area of bitemporal recession or the anterior hairline.
Summary of Clinical Studies in Men Clinical studies were conducted in men aged 18 to 41 with mild to moderate degrees of androgenetic alopecia.
All men treated with finasteride tablets USP or placebo received a tar-based shampoo (Neutrogena T/Gel® Shampoo) during the first 2 years of the studies.
Clinical improvement was seen as early as 3 months in the patients treated with finasteride tablets USP and led to a net increase in scalp hair count and hair regrowth.
In clinical studies for up to 5 years, treatment with finasteride tablets USP slowed the further progression of hair loss observed in the placebo group.
In general, the difference between treatment groups continued to increase throughout the 5 years of the studies.
Ethnic Analysis of Clinical Data from Men In a combined analysis of the two studies on vertex baldness, mean hair count changes from baseline were 91 vs -19 hairs (Finasteride tablets USP vs placebo) among Caucasians (n=1185), 49 vs -27 hairs among Blacks (n=84), 53 vs -38 hairs among Asians (n=17), 67 vs 5 hairs among Hispanics (n=45) and 67 vs -15 hairs among other ethnic groups (n=20).
Patient self-assessment showed improvement across racial groups with finasteride tablets USP treatment, except for satisfaction of the frontal hairline and vertex in Black men, who were satisfied overall.
structure7 14.2 Studies in Women In a study involving 137 postmenopausal women with androgenetic alopecia who were treated with finasteride tablets USP (n=67) or placebo (n=70) for 12 months, effectiveness could not be demonstrated.
There was no improvement in hair counts, patient self-assessment, investigator assessment, or ratings of standardized photographs in the women treated with finasteride tablets USP when compared with the placebo group [ see Indications and Usage (1) ].
HOW SUPPLIED
16 /STORAGE AND HANDLING Finasteride tab le t s USP, 1 mg, is brown color, round film coated tablets, debossed with ‘H’ on one side and ‘36’ on other side.
They are supp lied as f o llo w s: NDC 31722-526-30 bottles of 30 NDC 31722-526-90 bottles of 90 NDC 31722-526-10 bottles of 1000 Storage and Handling Store at 20° to 25° C (68° to 77° F) [see USP Controlled Room Temperature].
Keep container closed and protect from moisture.
Women should not handle crushed or broken finasteride tablets USP tablets when they are pregnant or may potentially be pregnant because of the possibility of absorption of finasteride and the subsequent potential risk to a male fetus.
finasteride tablets USP are coated and will prevent contact with the active ingredient during normal handling, provided that the tablets are not broken or crushed [ see Warnings and Precautions (5.1) , Use in Specific Populations (8.1) and Patient Counseling Information (17.1) ].
GERIATRIC USE
8.5 Geriatric Use Clinical efficacy studies with finasteride tablets USP did not include subjects aged 65 and over.
Based on the pharmacokinetics of finasteride 5 mg, no dosage adjustment is necessary in the elderly for finasteride tablets USP [ see Clinical Pharmacology (12.3) ].
However the efficacy of finasteride tablets USP in the elderly has not been established.
DOSAGE FORMS AND STRENGTHS
3 DOSAGE FORMS & STRENGTHS Finasteride tablets USP, 1 mg is brown color, round film coated tablets, debossed with ‘H’ on one side and ’36’ on other side.
1 mg tablets (3).
MECHANISM OF ACTION
12.1 Mechanism of Action Finasteride is a competitive and specific inhibitor of Type II 5α-reductase, an intracellular enzyme that converts the androgen testosterone into DHT.
Two distinct isozymes are found in mice, rats, monkeys, and humans: Type I and II.
Each of these isozymes is differentially expressed in tissues and developmental stages.
In humans, Type I 5α-reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and liver.
Type I 5α-reductase is responsible for approximately one-third of circulating DHT.
The Type II 5α-reductase isozyme is primarily found in prostate, seminal vesicles, epididymides, and hair follicles as well as liver, and is responsible for two-thirds of circulating DHT.
In humans, the mechanism of action of finasteride is based on its preferential inhibition of the Type II isozyme.
Using native tissues (scalp and prostate), in vitro binding studies examining the potential of finasteride to inhibit either isozyme revealed a 100-fold selectivity for the human Type II 5α-reductase over Type I isozyme (IC 50=500 and 4.2 nM for Type I and II, respectively).
For both isozymes, the inhibition by finasteride is accompanied by reduction of the inhibitor to dihydrofinasteride and adduct formation with NADP+.
The turnover for the enzyme complex is slow (t1/2 approximately 30 days for the Type II enzyme complex and 14 days for the Type I complex).
Inhibition of Type II 5α-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations.
In men with male pattern hair loss (androgenetic alopecia), the balding scalp contains miniaturized hair follicles and increased amounts of DHT compared with hairy scalp.
Administration of finasteride decreases scalp and serum DHT concentrations in these men.
The relative contributions of these reductions to the treatment effect of finasteride have not been defined.
By this mechanism, finasteride appears to interrupt a key factor in the development of androgenetic alopecia in those patients genetically predisposed.
INDICATIONS AND USAGE
1 INDICATIONS & USAGE Finasteride tablets USP are indicated for the treatment of male pattern hair loss (androgenetic alopecia) in MEN ONLY.
Efficacy in bitemporal recession has not been established.
Finasteride tablets USP are not indicated for use in women.
• Finasteride tablets USP are 5α-reductase inhibitors indicated for the treatment of male pattern hair loss (androgenetic alopecia) in MEN ONLY (1).
• Finasteride tablets USP are not indicated for use in women (1, 4, 5.1).
PEDIATRIC USE
8.4 Pediatric Use Finasteride tablets USP are not indicated for use in pediatric patients.
Safety and effectiveness in pediatric patients have not been established.
PREGNANCY
8.1 Pregnancy Teratogenic Effects : Pregnancy Category X [ see Contraindications (4) ].
Finasteride tablets USP is contraindicated for use in women who are or may become pregnant.
Finasteride tablets USP are Type II 5α-reductase inhibitor that prevents conversion of testosterone to 5α-dihydrotestosterone (DHT), a hormone necessary for normal development of male genitalia.
In animal studies, finasteride caused abnormal development of external genitalia in male fetuses.
If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the male fetus.
Abnormal male genital development is an expected consequence when conversion of testosterone to 5α-dihydrotestosterone (DHT) is inhibited by 5α-reductase inhibitors.
These outcomes are similar to those reported in male infants with genetic 5α-reductase deficiency.
Women could be exposed to finasteride through contact with crushed or broken finasteride tablets or semen from a male partner taking finasteride tablets USP.
With regard to finasteride exposure through the skin, finasteride tablets USP are coated and will prevent skin contact with finasteride during normal handling if the tablets have not been crushed or broken.
Women who are pregnant or may become pregnant should not handle crushed or broken finasteride tablets USP because of possible exposure of a male fetus.
If a pregnant woman comes in contact with crushed or broken finasteride tablets , the contact area should be washed immediately with soap and water.
With regard to potential finasteride exposure through semen, a study has been conducted in men receiving finasteride tablets USP 1 mg/day that measured finasteride concentrations in semen [ see Clinical Pharmacology (12.3) ].
In an embryo-fetal development study, pregnant rats received finasteride during the period of major organogenesis (gestation days 6 to 17).
At maternal doses of oral finasteride approximately 1 to 684 times the recommended human dose ( RHD ) of 1 mg/day (based on AUC at animal doses of 0.1 to 100 mg/kg/day) there was a dose-dependent increase in hypospadias that occurred in 3.6 to 100% of male offspring.
Exposure multiples were estimated using data from nonpregnant rats.
Days 16 to 17 of gestation are a critical period in male fetal rats for differentiation of the external genitalia.
At oral maternal doses approximately 0.2 times the RHD (based on AUC at animal dose of 0.03 mg/kg/day), male offspring had decreased prostatic and seminal vesicular weights, delayed preputial separation and transient nipple development.
Decreased anogenital distance occurred in male offspring of pregnant rats that received approximately 0.02 times the RHD (based on AUC at animal dose of 0.003 mg/kg/day).
No abnormalities were observed in female offspring exposed to any dose of finasteride in utero.
No developmental abnormalities were observed in the offspring of untreated females mated with finasteride-treated male rats that received approximately 488 times the RHD (based on AUC at animal dose of 80 mg/kg/day).
Slightly decreased fertility was observed in male offspring after administration of about 20 times the RHD (based on AUC at animal dose of 3 mg/kg/day) to female rats during late gestation and lactation.
No effects on fertility were seen in female offspring under these conditions.
No evidence of male external genital malformations or other abnormalities were observed in rabbit fetuses exposed to finasteride during the period of major organogenesis (gestation days 6 to 18) at maternal doses up to 100 mg/kg/day (finasteride exposure levels were not measured in rabbits).
However, this study may not have included the critical period for finasteride effects on development of male external genitalia in the rabbit.
The fetal effects of maternal finasteride exposure during the period of embryonic and fetal development were evaluated in the rhesus monkey (gestation days 20 to 100), in a species and development period more predictive of specific effects in humans than the studies in rats and rabbits.
Intravenous administration of finasteride to pregnant monkeys at doses as high as 800 ng/day (estimated maximal blood concentration of 1.86 ng/mL or about 930 times the highest estimated exposure of pregnant women to finasteride from semen of men taking 1 mg/day) resulted in no abnormalities in male fetuses.
In confirmation of the relevance of the rhesus model for human fetal development, oral administration of a dose of finasteride (2 mg/kg/day or approximately 120,000 times the highest estimated blood levels of finasteride from semen of men taking 1 mg/day) to pregnant monkeys resulted in external genital abnormalities in male fetuses.
No other abnormalities were observed in male fetuses and no finasteride-related abnormalities were observed in female fetuses at any dose.
NUSRING MOTHERS
8.3 Nursing Mothers Finasteride tablets USP are not indicated for use in women.
It is not known whether finasteride is excreted in human milk.
WARNING AND CAUTIONS
5 WARNINGS AND PRECAUTIONS Finasteride tablets USP are not indicated for use in women or pediatric patients (5.1, 5.4).
• Women should not handle crushed or broken finasteride tablets USP when they are pregnant or may potentially be pregnant due to potential risk to a male fetus (5.1, 8.1,16).
• Finasteride tablets USP causes a decrease in serum PSA levels.
Any confirmed increase in PSA while on finasteride tablets USP may signal the presence of prostate cancer and should be evaluated, even if those values are still within the normal range for men not taking a 5α-reductase inhibitor (5.2).
• 5α-reductase inhibitors may increase the risk of high-grade prostate cancer (5.3, 6.1).
5.1 Exposure of Women – Risk to Male Fetus Finasteride tablets USP are not indicated for use in women.
Women should not handle crushed or broken finasteride tablets USP, when they are pregnant or may potentially be pregnant because of the possibility of absorption of finasteride and the subsequent potential risk to a male fetus.
Finasteride tablets USP are coated and will prevent contact with the active ingredient during normal handling, provided that the tablets have not been broken or crushed.
[See Indications and Usage (1), Contraindications (4), Use in Specific Populations (8.1), How Supplied/Storage and Handling (16) and Patient Counseling Information (17.1).] 5.2 Effects on Prostate Specific Antigen (PSA) In clinical studies with finasteride tablets USP in men 18 to 41 years of age, the mean value of serum prostate specific antigen (PSA) decreased from 0.7 ng/mL at baseline to 0.5 ng/mL at Month 12.
Further, in clinical studies with finasteride tablets USP 5 mg when used in older men who have benign prostatic hyperplasia (BPH), PSA levels are decreased by approximately 50%.
Other studies with finasteride tablets USP 5 mg showed it may also cause decreases in serum PSA in the presence of prostate cancer.
These findings should be taken into account for proper interpretation of serum PSA when evaluating men treated with finasteride.
Any confirmed increase from the lowest PSA value while on finasteride tablets USP may signal the presence of prostate cancer and should be evaluated, even if PSA levels are still within the normal range for men not taking a 5α-reductase inhibitor.
Non-compliance to therapy with finasteride tablets USP may also affect PSA test results.
5.3 Increased Risk of High-Grade Prostate Cancer with 5-Reductase Inhibitors Men aged 55 and over with a normal digital rectal examination and PSA ≤3 ng/mL at baseline taking finasteride 5 mg/day (5 times the dose of finasteride tablets USP 1 mg) in the 7-year Prostate Cancer Prevention Trial (PCPT) had an increased risk of Gleason score 8 to 10 prostate cancer (finasteride 1.8% vs placebo 1.1%).
[See Adverse Reactions (6.1).] Similar results were observed in a 4-year placebo-controlled clinical trial with another 5α-reductase inhibitor (dutasteride, AVODART)(1% dutasteride vs 0.5% placebo).
5α-reductase inhibitors may increase the risk of development of high-grade prostate cancer.
Whether the effect of 5α-reductase inhibitors to reduce prostate volume, or study-related factors, impacted the results of these studies has not been established.
5.4 Pediatric Patients Finasteride tablets USP are not indicated for use in pediatric patients [ see Use in Specific Populations (8.4) ].
INFORMATION FOR PATIENTS
17 PATIENT COUNSELING INFORMATION See FDA-approved patient labeling (Patient Information) 17.1 Exposure of Women-Risk to Male Fetus Physicians should inform patients that women who are pregnant or may potentially be pregnant should not handle crushed or broken finasteride tablets USP because of the possibility of absorption of finasteride and the subsequent potential risk to a male fetus.
Finasteride tablets USP are coated and will prevent contact with the active ingredient during normal handling, provided that the tablets have not been broken or crushed.
If a woman who is pregnant or may potentially be pregnant comes in contact with crushed or broken finasteride tablets USP, the contact area should be washed immediately with soap and water [see Contraindications (4), Warnings and Precautions (5.1), Use in Specific Populations (8.1) and How Supplied/Storage and Handling (16)].
17.2 Increased Risk of High-Grade Prostate Cancer Patients should be informed that there was an increase in high-grade prostate cancer in men treated with 5α-reductase inhibitors indicated for BPH treatment, compared to those treated with placebo in studies looking at the use of these drugs to prevent prostate cancer [see Warnings and Precautions (5.3) and Adverse Reactions (6.1)].
17.3 Additional Instructions Physicians should instruct their patients to promptly report any changes in their breasts such as lumps, pain or nipple discharge.
Breast changes including breast enlargement, tenderness and neoplasm have been reported [ see Adverse Reactions (6.1) ].
Physicians should instruct their patients to read the patient package insert before starting therapy with finasteride tablets USP and to read it again each time the prescription is renewed so that they are aware of current information for patients regarding finasteride tablets USP.
Manufactured for: Camber Pharmaceuticals, Inc.
Piscataway, NJ 08854 Manufactured by: HETEROTM Hetero Labs Limited Jeedimetla, Hyderabad-500 055, India.
or Manufactured by: HETEROTM Hetero Labs Limited Unit V, Polepally, Jadcherla, Mahaboob Nagar-509 301, India.
structure9
DOSAGE AND ADMINISTRATION
2 DOSAGE & ADMINISTRATION Finasteride tablets USP may be administered with or without meals.
The recommended dose of finasteride tablets USP is one tablet (1 mg) taken once daily.
In general, daily use for three months or more is necessary before benefit is observed.
Continued use is recommended to sustain benefit, which should be re-evaluated periodically.
Withdrawal of treatment leads to reversal of effect within 12 months.
• Finasteride tablets USP may be administered with or without meals (2).
• One tablet (1 mg) taken once daily (2).
• In general, daily use for three months or more is necessary before benefit is observed (2).