FINCAR Tablets (Finasteride)

Table of Content

Composition

Each film-coated tablet contains:

Finasteride ..………………. 5 mg

Dosage Form

Tablet

Pharmacology

Mechanism of Action

The development and enlargement of the prostate gland is dependent on the potent androgen, 5α-dihydrotestosterone (DHT). Type II 5 α-reductase metabolizes testosterone to DHT in the prostate gland, liver and skin. DHT induces androgenic effects by binding to androgen receptors in the cell nuclei of these organs.

Finasteride is a synthetic 4-azasteroid compound. Finasteride is a competitive and specific inhibitor of Type II 5 alpha-reductase with which it slowly forms a stable enzyme complex. Turnover from this complex is extremely slow (t½ ~ 30 days). This has been demonstrated both in vivo and in vitro. Finasteride has no affinity for the androgen receptor. In man, the 5α-reduced steroid metabolites in blood and urine are decreased after administration of finasteride.

Pharmacodynamics

In man, a single 5 mg oral dose of finasteride produces a rapid reduction in serum DHT concentration, with the maximum effect observed 8 hours after the first dose. The suppression of DHT is maintained throughout the 24-hour dosing interval and with continued treatment. Daily dosing of finasteride at 5 mg/day for up to 4 years has been shown to reduce the serum DHT concentration by approximately 70%. The median circulating level of testosterone increased by approximately 10–20%,but remained within the physiologic range. In a separate study in healthy men treated with finasteride 1 mg per day (n=82) or placebo (n=69), mean circulating levels of testosterone and estradiol were increased by approximately 15% as compared to baseline, but these remained within the physiologic range.

In patients receiving finasteride 5 mg/day, increases of about 10% were observed in luteinizing hormone (LH) and follicle-stimulating hormone (FSH), but levels remained within the normal range. In healthy volunteers, treatment with finasteride did not alter the response of LH and FSH to gonadotropin-releasing hormone indicating that the hypothalamic-pituitary-testicular axis was not affected.

In patients with BPH, finasteride has no effect on circulating levels of cortisol, prolactin, thyroid-stimulating hormone, or thyroxine. No clinically meaningful effect was observed on the plasma lipid profile (i.e., total cholesterol, low density lipoproteins, high density lipoproteins and triglycerides) or bone mineral density.

Adult males with genetically inherited Type II 5 alpha-reductase deficiency also have decreased levels of DHT. Except for the associated urogenital defects present at birth, no other clinical abnormalities related to Type II 5 alpha-reductase deficiency have been observed in these individuals. These individuals have a small prostate gland throughout life and do not develop BPH.

In patients with benign prostatic hyperplasia (BPH) treated with finasteride (1–100 mg/day) for 7–10 days prior to prostatectomy, an approximate 80% lower DHT content was measured in prostatic tissue removed at surgery, compared to placebo; testosterone tissue concentration was increased up to 10 times over pre-treatment levels, relative to placebo. Intraprostatic content of the prostate-specific antigen (PSA) was also decreased.

In healthy male volunteers treated with finasteride for 14 days, discontinuation of therapy resulted in a return of DHT levels to pre-treatment levels in approximately 2 weeks. In patients treated for 3 months, prostate volume, which declined by approximately 20%, returned to close to baseline value after approximately 3 months of discontinuation of therapy.

Pharmacokinetics

Absorption

In a study of 15 healthy young subjects, the mean bioavailability of finasteride 5 mg tablets was 63% (range: 34% to 108%), based on the ratio of area under the curve (AUC) relative to an intravenous (I.V.) reference dose. Maximum finasteride plasma concentration averaged 37 ng/mL (range: 27 to 49 ng/mL) and was reached 1–2 hours postdose. Bioavailability of finasteride was not affected by food.

Distribution

Mean steady-state volume of distribution was 76 litres (range: 44 to 96 litres). Approximately 90% of circulating finasteride is bound to plasma proteins. There is a slow accumulation phase for finasteride after multiple dosing. After dosing with 5 mg/day of finasteride for 17 days, plasma concentrations of finasteride were 47% and 54% higher than after the first dose in males aged 45 to 60 years (n=12) and 70 years and older (n=12), respectively. Mean trough concentrations after 17 days of dosing were 6.2 ng/mL (range: 2.4 to 9.8 ng/mL) and 8.1 ng/mL (range: 1.8 to 19.7 ng/mL), respectively, in the two age groups. Although the steady state was not reached in this study, mean trough plasma concentration in another study in patients with BPH (mean age: 65 years) receiving 5 mg/day was 9.4 ng/mL (range: 7.1 to 13.3 ng/mL; n=22) after over a year of dosing.

Finasteride has been shown to cross the blood–brain barrier but does not appear to distribute preferentially to the cerebrospinal fluid (CSF).

In two studies of healthy subjects (n=69) receiving finasteride 5 mg/day for 6–24 weeks, finasteride concentrations in semen ranged from undetectable (<0.1 ng/mL) to 10.54 ng/mL. In an earlier study using a less sensitive assay, finasteride concentrations in the semen of 16 subjects receiving finasteride 5 mg/day ranged from undetectable (<1.0 ng/mL) to 21 ng/mL. Thus, based on a 5 mL ejaculate volume, the amount of finasteride in semen was estimated to be 50- to 100-fold less than the dose of finasteride (5 µg) that had no effect on circulating DHT levels in men.

Metabolism

Finasteride is extensively metabolized in the liver, primarily via the cytochrome P450 3A4 enzyme subfamily. Two metabolites, the t-butyl side chain monohydroxylated and monocarboxylic acid metabolites, have been identified that possess no more than 20% of the 5 -reductase inhibitory activity of finasteride.

Excretion

In healthy young subjects (n=15), mean plasma clearance of finasteride was 165 mL/min (range: 70 to 279 mL/min) and mean elimination half-life in plasma was 6 hours (range: 3 to 16 hours). Following an oral dose of 14C-finasteride in man (n=6), a mean of 39% (range: 32% to 46%) of the dose was excreted in the urine in the form of metabolites; 57% (range: 51% to 64%) was excreted in the faeces.

The mean terminal half-life of finasteride in subjects >70 years of age was approximately 8 hours (range: 6 to 15 hours; n=12), compared with 6 hours (range: 4 to 12 hours; n=12) in subjects 45 to 60 years of age. As a result, the mean AUC(0–24 hours) after 17 days of dosing was 15% higher in subjects > 70 years of age than in subjects 45 to 60 years of age (p=0.02).

Table 1: Mean (SD) Pharmacokinetic Parameters in Healthy Young Subjects (n=15)

 

Mean (SD)

Bioavailability

63% (34-108%)*

Clearance (mL/min)

165 (55)

Volume of Distribution (L)

76 (14)

Half-Life (hours)

6.2 (2.1)

 

 

 

*Range

Pharmacokinetics in special populations

Pediatric: Finasteride pharmacokinetics have not been investigated in patients <18 years of age. Finasteride is not indicated for use in pediatric patients

Gender: Finasteride is not indicated for use in women

Geriatric: No dosage adjustment is necessary in the elderly. Although the elimination rate of finasteride is decreased in the elderly, these findings are of no clinical significance.

Table 2: Mean (SD) Noncompartmental Pharmacokinetic Parameters After Multiple Doses of 5 mg/day in Older Men

 

Mean ( + SD)

45-60 years old (n=12)

>70 years old (n=12)

AUC (ng hr/mL)

389 (98)

463 (186)

Peak Concentration (ng/mL)

46.2 (8.7)

48.4 (14.7)

Time to Peak (hours)

1.8 (0.7)

1.8 (0.6)

Half-Life (hours)*

6.0 (1.5)

8.2 (2.5)

*First-dose values; all other parameters are last-dose values

Race: The effect of race on finasteride pharmacokinetics has not been studied.

Hepatic Impairment: The effect of hepatic impairment on finasteride pharmacokinetics has not been studied. Caution should be exercised in the administration of finasteride in those patients with liver function abnormalities, as finasteride is metabolized extensively in the liver.

Renal Impairment: No dosage adjustment is necessary in patients with renal impairment. In patients with chronic renal impairment, with creatinine clearances ranging from 9.0 to 55 mL/min, AUC, maximum plasma concentration, half-life, and protein binding after a single dose of 14C-finasteride were similar to values obtained in healthy volunteers. Urinary excretion of metabolites was decreased in patients with renal impairment. This decrease was associated with an increase in fecal excretion of metabolites. Plasma concentrations of metabolites were significantly higher in patients with renal impairment (based on a 60% increase in total radioactivity AUC). However, finasteride has been well tolerated in BPH patients with normal renal function receiving up to 80 mg/day for 12 weeks, where exposure of these patients to metabolites would presumably be much greater.

Indications

Benign prostatic hypertrophy only.

Limitation of Use

Finasteride is not approved for the prevention of prostate cancer.

Dosage and Administration

FINCAR may be administered with or without meals.

Monotherapy

The recommended dose of FINCAR is one tablet (5 mg) once a day, with or without meals.

Combination with Alpha-Blocker

The recommended dose of FINCAR tablet is one tablet (5 mg) taken once a day in combination with the alpha-blocker doxazosin.

Contraindications

FINCAR tablets are contraindicated in the following:

  • Hypersensitivity to any component of this medication.
  • Pregnancy: Finasteride use is contraindicated in women when they are or may potentially be pregnant. Because of the ability of Type II 5 alpha-reductase inhibitors to inhibit the conversion of testosterone to 5 alpha-dihydrotestosterone (DHT), finasteride may cause abnormalities of the external genitalia of a male foetus of a pregnant woman who receives finasteride. If this drug is used during pregnancy, or if pregnancy occurs while taking this drug, the pregnant woman should be apprised of the potential hazard to the male foetus. In female rats, low doses of finasteride administered during pregnancy have produced abnormalities of the external genitalia in male offspring.

Warnings and Precautions

Drug Interactions

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 have included antipyrine, digoxin, propranolol, theophylline, and warfarin and no clinically meaningful interactions were found. 

Other Concomitant Therapy

Although specific interaction studies were not performed, finasteride was concomitantly used in clinical studies with acetaminophen, acetylsalicylic acid, alpha-blockers, angiotensin-converting enzyme (ACE) inhibitors, analgesics, anti-convulsants, beta-adrenergic blocking agents, diuretics, calcium channel blockers, cardiac nitrates, HMG-CoA reductase inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), benzodiazepines, H2 antagonists and quinolone anti-infectives without evidence of clinically significant adverse interactions.

Renal Impairment

No dosage adjustment is necessary in patients with renal impairment

Hepatic Impairment

Caution should be used in the administration of finasteride in those patients with liver function abnormalities, as finasteride is metabolized extensively in the liver.

Pregnancy

Pregnancy Category X

FINCAR is contraindicated for use in women who are or may become pregnant. Finasteride is a 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. With regard to finasteride exposure through the skin, finasteride tablets 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 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, two studies have been conducted in men receiving finasteride 5 mg/day that measured finasteride concentrations in semen.

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 0.1 to 86 times the maximum recommended human dose (MRHD) of 5 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 is a critical period in male fetal rats for differentiation of the external genitalia. At oral maternal doses approximately 0.03 times the MRHD (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 0.003 times the MRHD (based on AUC at animal dose of 0.003 mg/kg/day). No abnormalities were observed in female offspring at any maternal dose of finasteride.

No developmental abnormalities were observed in the offspring of untreated females mated with finasteride treated male rats that received approximately 61 times the MRHD (based on AUC at animal dose of 80 mg/kg/day). Slightly decreased fertility was observed in male offspring after administration of about 3 times the MRHD (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 6-18) at maternal oral 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 20-100), 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 143 times the highest estimated exposure of pregnant women to finasteride from semen of men taking 5 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 18,000 times the highest estimated blood levels of finasteride from semen of men taking 5 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.

Lactation

Finasteride is not indicated for use in women. It is not known whether finasteride is excreted in human milk.

Paediatric Use

Finasteride is not indicated for use in paediatric patients. Safety and effectiveness in paediatric patients have not been established.

Geriatric Use

Of the total number of subjects included in 4-Year Placebo-Controlled Study (PLESS), 1480 and 105 subjects were 65 and over and 75 and over, respectively. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients.  No dosage adjustment is necessary in the elderly

Effects on Prostate Specific Antigen (PSA) and the Use of PSA in Prostate Cancer Detection

In clinical studies, finasteride reduced serum PSA concentration by approximately 50% within six months of treatment. This decrease is predictable over the entire range of PSA values in patients with symptomatic BPH, although it may vary in individuals.

For interpretation of serial PSAs in men taking finasteride, a new PSA baseline should be established at least six months after starting treatment and PSA monitored periodically thereafter. Any confirmed increase from the lowest PSA value while on finasteride 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 with finasteride therapy may also affect PSA test results. To interpret an isolated PSA value in patients treated with finasteride for six months or more, PSA values should be doubled for comparison with normal ranges in untreated men. These adjustments preserve the utility of PSA to detect prostate cancer in men treated with finasteride.

Finasteride may also cause decreases in serum PSA in the presence of prostate cancer.

The ratio of free to total PSA (percent free PSA) remains constant even under the influence of finasteride. If clinicians elect to use percent free PSA as an aid in the detection of prostate cancer in men undergoing finasteride therapy, no adjustment to its value appears necessary.

Increased Risk of High-Grade Prostate Cancer

Men aged 55 and over with a normal digital rectal examination and PSA ≤3.0 ng/mL at baseline taking finasteride 5 mg/day in the 7-year Prostate Cancer Prevention Trial (PCPT) had an increased risk of Gleason score 8-10 prostate cancer (finasteride 1.8% vs placebo 1.1%). Similar results were observed in a 4-year placebo-controlled clinical trial with another 5α-reductase inhibitor (dutasteride) (1% dutasteride vs 0.5% placebo). 5αreductase 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.

Exposure of Women – Risk to Male Foetus

Women should not handle crushed or broken FINCAR tablets when they are pregnant or may potentially be pregnant because of the possibility of absorption of finasteride and the subsequent potential risk to the male foetus. FINCAR tablets are coated and will prevent contact with the active ingredient during normal handling, provided that the tablets have not been broken or crushed.

Pediatric Patients and Women

FINCAR is not indicated for use in pediatric patients or women.

Effect on Semen Characteristics

Treatment with finasteride for 24 weeks to evaluate semen parameters in healthy male volunteers revealed no clinically meaningful effects on sperm concentration, mobility, morphology or pH. A 0.6 mL (22.1%) median decrease in ejaculate volume, with a concomitant reduction in total sperm per ejaculate, was observed. These parameters remained within the normal range and were reversible upon discontinuation of therapy with an average time to return to baseline of 84 weeks.

Consideration of Other Urological Conditions

Prior to initiating treatment with finasteride, consideration should be given to other urological conditions that may cause similar symptoms. In addition, prostate cancer and BPH may coexist. Patients with large residual urinary volume and/or severely diminished urinary flow should be carefully monitored for obstructive uropathy. These patients may not be candidates for finasteride therapy.

Undesirable Effects

Clinical Trials Experience

Finasteride is generally well tolerated; adverse reactions usually have been mild and transient.

4-Year Placebo-Controlled Study (PLESS)

In PLESS, 1,524 patients treated with finasteride and 1,516 patients treated with placebo were evaluated for safety over a period of 4 years. The most frequently reported adverse reactions were related to sexual function. 3.7% (57 patients) treated with finasteride and 2.1% (32 patients) treated with placebo discontinued therapy as a result of adverse reactions related to sexual function, which are the most frequently reported adverse reactions.

Table 3 presents the only clinical adverse reactions considered possibly, probably or definitely drug-related by the investigator, for which the incidence on finasteride was ≥1% and greater than placebo over the 4 years of the study. In years 2–4 of the study, there was no significant difference between treatment groups in the incidences of impotence, decreased libido and ejaculation disorder.

Table 3: Drug-related adverse experiences

 

Year 1
(%)

Years 2, 3 and 4*
(%)

Finasteride

Placebo

Finasteride

Placebo

Impotence

8.1

3.7

5.1

5.1

Decreased  libido

6.4

3.4

2.6

2.6

Decreased volume of
ejaculate

3.7

0.8

1.5

0.5

Ejaculation disorder

0.8

0.1

0.2

0.1

Breast enlargement

0.5

0.1

1.8

1.1

Breast tenderness

0.4

0.1

0.7

0.3

Rash

0.5

0.2

0.5

0.1

 

*Combined years 2–4

  N=1,524 and 1,516, finasteride vs placebo, respectively

Phase III Studies and 5-Year Open Extensions

The adverse experience profile in the 1-year, placebo-controlled, Phase III studies, the 5-year open extensions, and 4-year PLESS were similar.

Medical Therapy of Prostatic Symptoms (MTOPS) study

In the MTOPS study, 3047 men with symptomatic BPH were randomized to receive finasteride 5 mg/day (n=768), doxazosin 4 or 8 mg/day (n=756), the combination of finasteride 5 mg/day and doxazosin 4 or 8 mg/day (n=786), or placebo (n=737) for 4 to 6 years. The incidence rates of drug-related adverse experiences reported by ≥2% of patients in any treatment group in the MTOPS Study are listed in Table 4.

The individual adverse effects which occurred more frequently in the combination group compared to either drug alone were: asthenia, postural hypotension, peripheral edema, dizziness, decreased libido, rhinitis, abnormal ejaculation, impotence and abnormal sexual function (see Table 4). Of these, the incidence of abnormal ejaculation in patients receiving combination therapy was comparable to the sum of the incidences of this adverse experience reported for the two monotherapies.

Combination therapy with finasteride and doxazosin was associated with no new clinical adverse experience.

Four patients in MTOPS reported the adverse experience breast cancer. Three of these patients were on finasteride only and one was on combination therapy. The MTOPS Study was not specifically designed to make statistical comparisons between groups for reported adverse experiences. In addition, direct comparisons of safety data between the MTOPS study and previous studies of the single agents may not be appropriate based upon differences in patient population, dosage or dose regimen, and other procedural and study design elements.

Table 4: Incidence ≥2% in One or More Treatment Groups Drug-Related Clinical Adverse Experiences in MTOPS

Adverse Experience

Placebo (N=737) (%)

Doxazosin 4 mg or 8 mg* (N=756) (%)

Finasteride (N=768) (%)

Combination (N=786) (%)

Body as a whole

 

 

 

 

Asthenia

7.1

15.7

5.3

16.8

Headache

2.3

4.1

2.0

2.3

Cardiovascular

 

 

 

 

Hypotension

0.7

3.4

1.2

1.5

Postural Hypotension

8.0

16.7

9.1

17.8

Metabolic and Nutritional

 

 

 

 

Peripheral Edema

0.9

2.6

1.3

3.3

Nervous

 

 

 

 

Dizziness

8.1

17.7

7.4

23.2

Libido Decreased

5.7

7.0

10.0

11.6

Somnolence

1.5

3.7

1.7

3.1

Respiratory

 

 

 

 

Dyspnea

0.7

2.1

0.7

1.9

Rhinitis

0.5

1.3

1.0

2.4

Urogenital

 

 

 

 

Abnormal Ejaculation

2.3

4.5

7.2

14.1

Gynecomastia

0.7

1.1

2.2

1.5

Impotence

12.2

14.4

18.5

22.6

Sexual Function Abnormal

0.9

2.0

2.5

3.1

Doxazosin dose was achieved by weekly titration (1 to 2 to 4 to 8 mg). The final tolerated dose (4 mg or 8 mg) was administered at end-Week 4. Only those patients tolerating at least 4 mg were kept on doxazosin. The majority of patients received the 8-mg dose over the duration of the study.

Long-Term Data

High-Grade Prostate Cancer

The PCPT trial was a 7-year randomized, double-blind, placebo-controlled trial 18,882 men> 55 years with a normal digital rectal examination and a PSA ≤3.0 ng/mL were enrolled. The men received either finasteride 5 mg or placebo daily. Patients were evaluated annually with PSA and digital rectal exams. Biopsies were performed for elevated PSA, an abnormal digital rectal exam, or the end of study. The incidence of Gleason score 8–10 prostate cancer was higher in men treated with finasteride (1.8%) than in those treated with placebo (1.1%). In a 4-year placebo-controlled clinical trial with another 5 alpha-reductase inhibitor (dutasteride), similar results for Gleason score 8–10 prostate cancer were observed (1% dutasteride vs 0.5% placebo).

No clinical benefit has been demonstrated in patients with prostate cancer treated with finasteride.

Breast Cancer

During the 4- to 6-year placebo- and comparator-controlled study that enrolled 3,047 men, there were four cases of breast cancer in men treated with finasteride but no cases in men not treated with finasteride. During the 4-year placebo-controlled study that enrolled 3,040 men, there were two cases of breast cancer in placebo-treated men, but no cases were reported in men treated with finasteride. During the 7-year placebo-controlled Prostate Cancer Prevention Trial (PCPT) that enrolled 18,882 men, there was 1 case of breast cancer in men treated with finasteride, and 1 case of breast cancer in men treated with placebo. The relationship between long-term use of finasteride and male breast neoplasia is currently unknown.

Sexual Function

There is no evidence of increased sexual adverse experiences with increased duration of treatment with finasteride. New reports of drug-related sexual adverse experiences decreased with duration of therapy.

Postmarketing Experience

The following additional adverse events have been reported in post-marketing experience with finasteride. Because these events are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure:

- hypersensitivity reactions such as pruritus, urticaria, and angioedema (including) swelling of the lips, tongue, throat, and face

- testicular pain

- sexual dysfunction that continued after discontinuation of treatment including erectile dysfunction, decreased libido and ejaculation disorders (e.g. reduced ejaculate volume). These events were reported rarely in men taking finasteride for the treatment of BPH. Most men were older and were taking concomitant medications and/or had co-morbid conditions. The independent role of finasteride in these events is unknown.

-male infertility and/or poor seminal quality have been reported rarely in men taking finasteride for the treatment of BPH. Normalization or improvement of seminal quality has been reported after discontinuation of finasteride. The independent role of finasteride in these events is unknown.

- depression

- male breast cancer.

The following additional adverse event related to sexual dysfunction that continued after discontinuation of treatment has been reported in postmarketing experience with finasteride at lower doses used to treat male pattern baldness. Because the event is reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate its frequency or establish a causal relationship to drug exposure:

- orgasm disorders

If you experience any side effects, talk to your doctor or pharmacist or write to drugsafety@cipla.com. You can also report side effects directly via the national pharmacovigilance program of India by calling on 1800 180 3024. 

By reporting side effects you can help provide more information on the safety of this product.

Overdosage

Patients have received single doses of finasteride up to 400 mg and multiple doses of finasteride up to 80 mg/day for 3 months without adverse effects. 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.

Storage and Handling Instructions

Store at a room temperature below 30°C. Protect from light and keep container tightly closed. Women should not handle crushed or broken finasteride 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.

Packaging Information

FINCAR: Blister pack of 10 tablets

Information for Patients

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 5 alpha-reductase inhibitors indicated for BPH treatment, including finasteride, compared to those treated with placebo in studies looking at the use of these drugs to prevent prostate cancer.

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 FINCAR tablets because of the possibility of absorption of finasteride and the subsequent potential risk to the male foetus. FINCAR tablets 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 FINCAR tablets, the contact area should be washed immediately with soap and water.

Additional Instructions

Physicians should inform patients that the volume of ejaculate may be decreased in some patients during treatment with FINCAR tablets. This decrease does not appear to interfere with normal sexual function. However, impotence and decreased libido may occur in patients treated with FINCAR tablets.

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.

Physicians should instruct their patients to read the patient package insert before starting therapy with FINACR tablets and to reread it each time the prescription is renewed so that they are aware of current information for patients regarding FINACR tablets.

Last updated: December 2018

Last reviewed: January 2019