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finasteride 5 mg tablet (generic proscar)

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Uses

Benign Prostatic Hyperplasia

Finasteride is used to reduce prostatic size, urinary obstruction and associated manifestations (e.g., urinary hesitancy and/or urgency, nocturia), the risk of acute urinary retention, and the risk of the need for surgery (including transurethral resection of the prostate [TURP] and prostatectomy) in patients with symptomatic benign prostatic hyperplasia (BPH, benign prostatic hypertrophy). Finasteride also is used concomitantly with an α1-adrenergic blocking agent (e.g., doxazosin) to decrease the risk of symptomatic progression of BPH.

BPH, an abnormal enlargement of the prostate gland that occurs in most men 55 years of age or older, produces manifestations such as a weak urinary stream, difficulty in initiating urination, and urinary frequency and urgency. Urinary flow obstruction secondary to BPH historically has been treated with surgical correction of the hyperplasia (e.g.,via TURP). However, medical therapy with a 5α-reductase inhibitor (e.g., finasteride, dutasteride) and/or other drugs (e.g., α1-adrenergic blocking agents such as alfuzosin, doxazosin, tamsulosin, or terazosin) may be a useful alternative to surgery in patients who are awaiting or are unwilling to undergo surgical correction of the hyperplasia or who are at increased risk from or are not candidates for such surgery. Although drug therapy usually is not as effective as surgical therapy, it may provide adequate symptomatic relief with fewer and less serious adverse effects compared with surgery.

Therapy with either a 5α-reductase inhibitor (e.g., finasteride) or an α1-adrenergic blocker is effective in partially relieving lower urinary tract symptoms, although therapy with an α1-adrenergic blocker appears to result in greater symptomatic improvement. Finasteride also has been shown to decrease the risk of acute urinary retention and the need for BPH-related surgery.

Most experts currently consider therapy with a 5α-reductase inhibitor to be an appropriate option for treatment of bothersome lower urinary tract symptoms in patients with BPH who have evidence of prostatic enlargement. Therapy with a 5α-reductase inhibitor is ineffective in patients who do not have evidence of prostatic enlargement. Most experts state that therapy with a 5α-reductase inhibitor also may be considered in patients who have symptomatic prostatic enlargement but whose symptoms are not bothersome (i.e., do not interfere with activities of daily living) in order to prevent progression of the disease. However, the disadvantages of this therapeutic approach (e.g., adverse effects including sexual dysfunction, the need for long-term daily therapy) should be discussed with the patient relative to that individual's risk for acute urinary retention and potential risks associated with BPH-related surgery so that an informed decision can be made.

Results of a long-term (4-year) controlled clinical study in patients with moderate to severe symptoms of BPH indicate that finasteride (5 mg daily) reduces symptoms of BPH, reduces prostatic size and increases urinary flow rate, and reduces the risk of acute urinary retention and the need for surgery. In this study, treatment with finasteride or placebo for 4 years reduced symptom scores by a mean of 3.3 or 1.3 points, respectively, from an average baseline score of 15 (as measured on a scale of 0-34, with the total score equal to the sum of the scores for 7 measures of obstructive or irritative symptoms). A difference in symptom scores between treatment groups was evident within the first year of treatment and continued throughout the 4-year study. In general, at least 6 months of therapy was required to determine whether a beneficial reduction in symptoms had been achieved, although some patients experienced earlier improvement. Prostatic volume decreased during the first year of the study in patients receiving finasteride and then remained stable during years 2-4, whereas values in the placebo group increased steadily over the 4 years of the study. Acute urinary retention requiring catheterization of the bladder occurred in 2.8 or 6.6% of patients receiving finasteride or placebo, respectively, and 4.6 or 10.1% of patients receiving finasteride or placebo, respectively, underwent surgery for BPH.

Results of a meta-analysis of 1 year of data from 7 similarly designed controlled studies indicate that improvements in symptoms and maximum urinary flow rates associated with finasteride therapy are greater in patients with prostatic enlargement at baseline.

Finasteride therapy in BPH appears to be suppressive rather than curative, and eventual return of the hyperplasia likely will occur if the drug is withdrawn.

Combination Therapy

Finasteride may be used concomitantly with an α1-adrenergic blocking agent (e.g., doxazosin, alfuzosin, terazosin) to decrease the risk of symptomatic progression of BPH (i.e., an increase from baseline of at least 4 on the American Urological Association [AUA] symptom score). Although studies of up to 1 year in duration generally have found combination therapy with a 5α-reductase inhibitor (e.g., finasteride) and an α1-adrenergic blocker to be no more effective than α1-adrenergic blocker monotherapy in providing symptomatic relief of BPH, a long-term (mean follow-up: 4.5 years), double-blind study (Medical Therapy of Prostatic Symptoms [MTOPS]) found that combined therapy with finasteride (5 mg daily) and doxazosin (4-8 mg daily) was more effective than therapy with either drug alone in preventing symptom progression (defined as an increase from baseline of at least 4 points in the AUA symptom score, acute urinary retention, urinary incontinence, renal insufficiency, or recurrent urinary tract infection). The percent reduction in the risk of symptom progression (generally manifested as an increase in AUA symptom score) relative to placebo was 34% with finasteride, 39% with doxazosin, and 67% with combination therapy. The risks of long-term acute urinary retention and the need for invasive therapy were reduced by combination therapy and by finasteride monotherapy but not by doxazosin monotherapy. Combination therapy or doxazosin or finasteride monotherapy each were effective in providing improvement in symptom scores, with combination therapy providing greater improvement than either drug alone.

Most experts state that combined therapy with a 5α-reductase inhibitor and an α1-adrenergic blocker can be considered for men with bothersome moderate to severe BPH and demonstrable prostatic enlargement, weighing the benefit of preventing progression of BPH with the risks and cost of the combination. Men at risk for BPH progression are most likely to benefit from combination therapy. Although the benefit of combination therapy was not as substantial in men with low baseline prostate-specific antigen (PSA) levels compared with those with high baseline values in the MTOPS study, the potential benefit appears to be greatest in those in whom baseline risk of progression generally is high rather than specifically in those with larger prostates or higher PSA levels at baseline.

Adverse effects associated with combined 5α-reductase inhibitor and α1-adrenergic blocker therapy generally reflect the combined toxicity profile of each drug alone, although certain adverse effects (e.g., effects on sexual function and libido, postural hypotension, peripheral edema, dizziness, asthenia, rhinitis) may be more common with combined therapy.(See Cautions.)

For further information on the treatment of BPH, .

Alopecia

For use in the management of alopecia,

Dosage and Administration

Administration

Finasteride is administered orally without regard to meals.

Dosage

Finasteride is recommended for use in adult men. The manufacturer states that the drug is not indicated for use in children or in women.

For the treatment of symptomatic benign prostatic hyperplasia (BPH), the usual dosage of finasteride, administered alone or concomitantly with an α1-adrenergic blocking agent (e.g., doxazosin), is 5 mg once daily. While early symptomatic improvement may occur, 6 months or more of therapy with finasteride may be necessary to determine whether therapy with the drug is of clinical benefit. Periodic follow-up evaluations should be performed to monitor the patient's clinical response to therapy.

Although the elimination rate of finasteride is decreased in geriatric individuals, the manufacturer states that dosage adjustment is not necessary in this age group. The manufacturer also states that dosage adjustment is not necessary in patients with renal impairment; the pharmacokinetics of finasteride following a single dose in patients with chronic renal impairment (i.e., creatinine clearance of 9-55 mL/minute) was similar to that observed in healthy individuals, although the proportion of the dose excreted as metabolites in feces versus urine was increased in those with renal impairment. Because finasteride is metabolized extensively in the liver, the drug should be used with caution in patients with hepatic impairment.

Cautions

Finasteride generally is well tolerated, and adverse effects are infrequent and usually mild and transient. In controlled clinical trials, adverse effects related to sexual function (e.g., impotence, decreased libido, decreased volume of ejaculate, ejaculation disorder or abnormal ejaculation) were the most frequently reported adverse effects. In one 4-year study, 3.7% of men receiving finasteride discontinued the drug because of an adverse sexual effect compared with 2.1% of those receiving placebo. Finasteride-associated adverse sexual effects appear to be most likely to occur during the first 9 months of therapy with the drug. The manufacturer states that there currently is no evidence of increased adverse sexual effects associated with increased duration of finasteride use.

Genitourinary Effects

Impotence, decreased volume of ejaculate, and abnormal ejaculation are the most common adverse genitourinary effects of finasteride. Impotence or decreased volume of ejaculate was reported in 3.7-8.1 or 2.8-3.7%, respectively, of patients receiving the drug for 12 months in controlled clinical trials. In a long-term (4-6 years) controlled clinical trial, impotence, abnormal ejaculation, or abnormal sexual function was reported in 18.5, 7.2, or 2.5%, respectively, of patients receiving finasteride monotherapy; when finasteride was given in conjunction with doxazosin, the frequencies of impotence, abnormal ejaculation, and abnormal sexual function (22.6, 14.1, and 3.1%, respectively) exceeded those with either finasteride (18.5, 7.2, and 2.5%, respectively) or doxazosin (14.4, 4.5, and 2%, respectively) alone. An additive effect on the frequency of abnormal ejaculation was observed with combined finasteride and doxazosin therapy.

New reports of finasteride-related adverse sexual effects appear to decrease with prolonged duration of therapy. During the first year of a large controlled clinical trial, impotence occurred more frequently in men receiving finasteride than in those receiving placebo (8.1 versus 3.7%), but there was no substantial difference in the frequency of impotence between treatment groups during years 2-4 of the study (5.1% with either finasteride or placebo). Decreased volume of ejaculate was reported in 3.7 or 0.8% of men receiving finasteride or placebo, respectively, during the first year of the study and in 1.5 or 0.5%, respectively, during years 2-4 of the study. Ejaculation disorder was reported in less than 1% of men receiving finasteride or placebo; ejaculation disorder was reported more frequently with finasteride than with placebo during the first year of the study but at approximately the same frequencies with finasteride and placebo during years 2-4 of the study.

Continued impotence following discontinuance of the drug has been reported during postmarketing surveillance.

Decreased volume of ejaculate does not appear to interfere with normal sexual function. The total number of sperm per ejaculate, sperm motility, and sperm structure as well as standard biochemical sperm markers generally are unaffected by finasteride. In a study of healthy men receiving finasteride for 24 weeks, a mean decrease of 0.6 mL (22.1%) in ejaculate volume and a reduction in total number of sperm per ejaculate were reported, but these values remained within the normal range; there were no clinically important effects on semen pH or sperm concentration, mobility, or morphology, and the decreases were reversible, returning to baseline values within an average of 84 weeks after discontinuance of the drug.

In long-term controlled clinical trials, breast enlargement or gynecomastia has been reported in up to 1.8 or 2.2%, respectively, of men receiving finasteride. Breast pain or tenderness, pelvic or testicular pain, dysuria, and orgasm dysfunction each have been reported in less than 1% of men receiving finasteride in controlled clinical trials.

Breast neoplasm has been reported in men receiving finasteride during long-term clinical trials. In a 4- to 6-year clinical trial in 3047 men, breast cancer was reported in 3 men receiving finasteride monotherapy and 1 man receiving combined therapy with finasteride and doxazosin but in no men receiving placebo or doxazosin alone; however, in a clinical trial in 18,882 men receiving finasteride or placebo for up to 7 years, breast neoplasm was reported in 1 patient receiving finasteride and 1 patient receiving placebo. In another clinical trial in 3040 men receiving finasteride or placebo for up to 4 years, breast cancer occurred in 2 patients receiving placebo and in none of those receiving finasteride. Whether a causal relationship exists between long-term finasteride use and breast neoplasia in men has not been established.

5α-Reductase inhibitors may increase the risk of development of high-grade prostate cancer. The efficacy of finasteride for prevention of prostate cancer occurrence was evaluated in a 7-year placebo-controlled trial (Prostate Cancer Prevention Trial; PCPT) in men 55 years of age or older with baseline serum prostate-specific antigen (PSA) concentrations of 3 ng/mL or less and normal digital rectal examinations. Although results showed that finasteride (5 mg daily) was associated with an overall reduction in prostate cancer occurrence (which reflected a reduction in lower-grade [Gleason score of 6 or less] tumors), high-grade tumors (Gleason score of 8-10) were detected more frequently in men receiving finasteride (1.8%) than in those receiving placebo (1.1%). Similar results were reported for a 4-year placebo-controlled trial (Reduction by Dutasteride of Prostate Cancer Events; REDUCE) evaluating preventive therapy with the 5α-reductase inhibitor dutasteride; in this trial, high-grade prostate cancer occurred in 1% of men receiving dutasteride compared with 0.5% of those receiving placebo, and the reduction in risk of prostate cancer was limited to tumors with a Gleason score of 6 or less. It is not known whether detection bias (e.g., 5α-reductase inhibitors potentially could increase the number of biopsy-detected tumors by reducing prostate volume, since this would result in a greater proportion of the prostate being sampled) or study-related factors influenced the results of these studies. Finasteride is not labeled by the US Food and Drug Administration (FDA) for prevention of prostate cancer.

Nervous System Effects

Decreased libido has been reported in 3.3-6.4% of men receiving finasteride for 12 months in controlled clinical trials. In one long-term clinical trial, reports of decreased libido in men receiving finasteride decreased from 6.4% during the first year of the trial to 2.6% during years 2-4; in patients receiving placebo, reports of decreased libido decreased from 3.4% to 2.6% over the same time period. In another long-term (4-6 years) controlled clinical trial, decreased libido was reported in 10% of men receiving finasteride monotherapy; when finasteride was given in conjunction with doxazosin, the frequency of decreased libido (11.6%) exceeded that with either finasteride (10%) or doxazosin (7%) alone.

Dizziness, asthenia, or headache has been reported in less than 1% of men receiving finasteride in controlled clinical trials for 12 months. In a long-term (4-6 years) controlled clinical trial, dizziness, asthenia, headache, and somnolence were reported in 7.4, 5.3, 2, and 1.7%, respectively, of men receiving finasteride monotherapy; when finasteride was given in conjunction with doxazosin, the frequencies of dizziness and asthenia (23.2 and 16.8%, respectively) exceeded those with either finasteride (7.4 and 5.3%, respectively) or doxazosin (17.7 and 15.7%, respectively) alone. Depression has been reported during postmarketing surveillance.

GI Effects

Abdominal pain, diarrhea, flatulence, and nausea each have been reported in less than 1% of men receiving finasteride in controlled clinical trials for 12 months.

Ocular and Otic Effects

Lens changes or opacities have been reported in about 1% or less of men receiving finasteride in controlled clinical trials for 12 months, although there was no clinically important change in visual acuity. There was no evidence of adverse otic effects in men receiving finasteride in controlled clinical trials for 12 months.

Dermatologic and Sensitivity Reactions

Rash has been reported in less than 1% of men receiving finasteride in controlled clinical trials; allergic reaction also has been reported during controlled clinical trials. Hypersensitivity reactions (e.g., pruritus, urticaria, swelling of the lips and face) have been reported during postmarketing surveillance.

Cardiovascular Effects

In a long-term (4-6 years) controlled clinical trial, postural hypotension, peripheral edema, and hypotension were reported in 9.1, 1.3, and 1.2%, respectively, of men receiving finasteride monotherapy; when finasteride was given in conjunction with doxazosin, the frequencies of postural hypotension and peripheral edema (17.8 and 3.3%, respectively) exceeded those with either finasteride (9.1 and 1.3%, respectively) or doxazosin (16.7 and 2.6%, respectively) alone.

Respiratory Effects

In a long-term (4-6 years) controlled clinical trial, dyspnea and rhinitis each were reported in 1% or less of men receiving finasteride monotherapy; when finasteride was given in conjunction with doxazosin, the frequency of rhinitis (2.4%) exceeded that with either finasteride (1%) or doxazosin (1.3%) alone.

Precautions and Contraindications

Candidates for finasteride therapy should be evaluated for conditions that might mimic benign prostatic hyperplasia (BPH), such as infection, prostate cancer, stricture disease, hypotonic bladder, and other neurogenic disorders, prior to initiating therapy with the drug. Digital rectal examinations, as well as other screening tests for prostate cancer, also should be performed before initiating finasteride therapy and periodically thereafter. To allow assessment of potentially cancer-related changes in prostate specific antigen (PSA) values, a new baseline PSA concentration should be established at least 6 months after initiation of treatment with finasteride, and PSA concentrations should be monitored periodically thereafter.

The possibility that finasteride could interfere with interpretation of serum PSA determinations should be considered. Serum concentrations of PSA--a serine protease secreted exclusively by prostatic epithelial cells--may be elevated in patients with BPH, prostate cancer, or other prostatic disease. Finasteride causes a decrease in serum PSA concentrations of approximately 50% in patients with BPH; decreases in PSA can occur even in those with prostate cancer. However, the effect of finasteride on serum PSA concentrations has not been demonstrated to provide clinical benefit in patients with prostate cancer and should not be interpreted as a therapeutic effect of the drug on the disease. The effect of finasteride on serum PSA concentrations is predictable over the entire range of PSA values, although there is evidence of interindividual variation. For clinical interpretation of PSA values in men who have been receiving finasteride for 6 months or longer, the reported PSA value should be doubled for comparison with normal values in men not receiving the drug. This adjustment will preserve the utility of the serum PSA assay and maintain its usefulness in the detection of prostate cancer. Finasteride does not substantially alter the ratio of free to total PSA (percentage of free PSA). If clinicians elect to use this ratio in the detection of prostate cancer, no adjustment of the reported value of the ratio appears to be necessary. Any confirmed increase in serum PSA concentration during finasteride therapy should be evaluated carefully, even if PSA values are within the normal range for men not receiving 5α-reductase inhibitor therapy. Noncompliance with finasteride may affect PSA concentrations and should be considered when evaluating test results. Patients should be informed that finasteride decreases serum PSA concentrations and should be advised of the importance of appropriate medical evaluation of any increase in PSA concentration. If a PSA test is performed, the patient should inform the clinician that he is taking a 5α-reductase inhibitor.

Since not all patients exhibit a response to finasteride, patients with a large residual urinary volume and/or severely diminished urinary flow should be monitored carefully for obstructive uropathy; such patients may not be candidates for therapy with the drug.

Because of the potential for absorption of finasteride and the subsequent potential risk to a male fetus, pregnant women or women who potentially may be pregnant should avoid direct contact with broken (e.g., crushed) tablets of the drug. Intact tablets are coated and the coating will prevent contact with finasteride during normal handling. A pregnant woman who has come into contact with finasteride should inform her clinician and should wash the affected area immediately with soap and water.(See Cautions: Pregnancy, Fertility, and Lactation.) In female rats, low doses of finasteride administered during pregnancy produced abnormalities of the external genitalia in male offspring.

Patients should be informed that finasteride therapy may result in a decreased volume of ejaculate that does not appear to interfere with normal sexual function; however, impotence and/or decreased libido also may occur. Because breast changes (e.g., enlargement, tenderness, neoplasia) have been reported in men receiving finasteride, patients receiving the drug should be instructed to promptly report any changes in their breasts (e.g., lumps, pain, nipple discharge) to their clinician; whether a causal relationship exists between long-term finasteride use and breast neoplasia in men has not been established.

Patients should be informed that the incidence of high-grade prostate cancer was increased in men receiving 5α-reductase inhibitors (including finasteride) in clinical trials evaluating efficacy of these drugs for prostate cancer prevention.(See Cautions: Genitourinary Effects.)

Patients should be instructed to read the patient information provided by the manufacturer prior to initiation of finasteride therapy and to reread it each time the prescription is refilled, since the information may have been revised.

Since finasteride is metabolized extensively in the liver, the drug should be used with caution in patients with liver function abnormalities.

Finasteride is contraindicated in patients with hypersensitivity to the drug or any ingredient in the formulation. The drug also is contraindicated in women who are or may potentially be pregnant.(See Cautions: Pregnancy, Fertility, and Lactation.)

Pediatric Precautions

Safety and efficacy of finasteride in children have not been established, but the drug is not indicated for use in children.

Geriatric Precautions

Because BPH occurs mainly in men 55 years of age or older, efficacy and safety of finasteride in this age group have been established, although only limited data are available on use of the drug in men older than 80 years of age. Of the 3040 patients enrolled in a long-term (4 years) controlled clinical trial of the drug, 1480 (49%) were 65 years of age or older and 105 (3.5%) were 75 years of age or older. No overall differences in efficacy or safety were observed in this trial between geriatric and younger patients, and other clinical experience has revealed no evidence of age-related differences. Generally, finasteride is well tolerated in geriatric men.

The elimination rate of the drug is decreased in geriatric individuals, but dosage adjustment is not necessary. The mean terminal half-life of finasteride in individuals 70 years of age or older was approximately 8 hours (range: 6-15 hours) compared with 6 hours (range: 4-12 hours) in individuals 45-60 years of age; consequently, the mean daily area under the plasma concentration-time curve after 17 days of dosing was 15% higher in the individuals 70 years of age or older.

Mutagenicity and Carcinogenicity

No evidence of mutagenicity was observed in an in vitro bacterial mutagenesis assay, a mammalian cell mutagenesis assay, or an in vitro alkaline elution assay. There was a slight increase in chromosome aberrations in Chinese hamster ovary cells at high finasteride concentrations corresponding to 4000-5000 times the peak plasma finasteride concentrations that would result in humans with a 5-mg dose; such concentrations are not achievable in a biologic system. In an in vivo assay in mice, no treatment-related increase in chromosome aberration was observed with finasteride at the maximum tolerated dose of 250 mg/kg daily (228 times the human exposure) as determined in carcinogenicity studies.

No evidence of a tumorigenic effect was observed in male rats receiving finasteride dosages up to 160 mg/kg daily or female rats receiving up to 320 mg/kg daily for 24 months (111 and 274 times, respectively, the systemic exposure observed in humans receiving a recommended finasteride dosage of 5 mg daily). In another 19-month study in CD-1 mice, a substantial increase in the incidence of testicular Leydig-cell adenomas was observed at a finasteride dosage of 250 mg/kg daily (228 times the human exposure). In mice receiving 25 mg/kg daily (estimated 23 times the human exposure) and in rats receiving 40 or more mg/kg daily (39 times the human exposure), an increase in the incidence of Leydig-cell hyperplasia was observed. A positive correlation between the proliferative changes in Leydig cells and an increase in serum LH concentrations (twofold to threefold above control concentrations) was demonstrated in both rodent species receiving high doses of finasteride. No drug-related Leydig-cell changes were seen in rats or dogs receiving finasteride for 1 year at dosages of 20 and 45 mg/kg daily, respectively (30 and 350 times, respectively, the human exposure), or in mice receiving 2.5 mg/kg daily (estimated 2.3 times the human exposure) for 19 months.

Pregnancy, Fertility, and Lactation

Pregnancy

Finasteride is not indicated for use in women and is contraindicated in women who are pregnant or may potentially be pregnant. Because of the ability of 5α-reductase inhibitors to inhibit the conversion of testosterone to DHT, finasteride may cause abnormalities of the external genitalia of male fetuses exposed to the drug during pregnancy. Studies have shown that low doses of finasteride administered to female rats during pregnancy can produce abnormalities of the external genitalia in male offspring. If finasteride is administered during pregnancy, the pregnant woman should be apprised of the potential fetal hazard. In addition, because of the possibility of absorption and subsequent risk to a male fetus, women who are pregnant or who potentially may be pregnant should not handle broken (e.g., crushed) finasteride tablets; if such contact occurs, the affected area should be washed immediately with soap and water and the woman should inform her clinician. Intact finasteride tablets are coated, and the coating will prevent contact with finasteride during normal handling.

Reproduction studies in pregnant rats receiving finasteride dosages ranging from 100 mcg/kg daily to 100 mg/kg daily (1-1000 times the recommended human dosage of 5 mg daily) resulted in dose-dependent development of hypospadias in 3.6-100% of male offspring. Pregnant rats produced male offspring with decreased prostatic and seminal vesicular weights, delayed preputial separation, and transient nipple development when given dosages of 30 or more mcg/kg daily (0.3 or more times the recommended human dosage of 5 mg daily) and decreased anogenital distance when given dosages of 3 or more mcg/kg daily (0.03 or more times the recommended human dosage of 5 mg daily). The critical period during which these effects can be induced in male rats has been determined to be days 16-17 of gestation. These effects are expected pharmacologic effects of 5α-reductase inhibitors and are similar to those reported in male infants with a genetic deficiency of 5α-reductase. No abnormalities were observed in female offspring exposed to any finasteride dosage in utero.

No developmental abnormalities were observed in first filial generation (F1) male or female offspring resulting from mating of male rats receiving finasteride 80 mg/kg daily (61 times the human exposure) with untreated females. Administration of the drug at a dosage of 3 mg/kg daily (30 times the recommended human dosage of 5 mg daily) during the late gestation and lactation period resulted in slightly decreased fertility in F1 male offspring. No effects were seen in female offspring. No evidence of malformations was observed in rabbit fetuses exposed to finasteride in utero from days 6-18 of gestation at dosages up to 100 mg/kg daily (1000 times the recommended human dosage of 5 mg daily); however, effects on male genitalia would not be expected, since the rabbits were not exposed during the critical period of genital system development.

No abnormalities were observed in male fetuses when pregnant rhesus monkeys were given finasteride IV at dosages up to 800 ng daily (60-120 times the highest estimated exposure of a pregnant woman to finasteride via the semen of a sexual partner receiving finasteride 5 mg daily) during days 20-100 of gestation; however, external genital abnormalities were observed in male rhesus monkey fetuses in studies using an oral finasteride dosage of 2 mg/kg daily (20 times the recommended human dosage of 5 mg daily or 1 million to 2 million times the highest estimated exposure of a pregnant woman to finasteride via the semen of a sexual partner receiving 5 mg daily). No other abnormalities were observed in male fetuses, and no abnormalities were observed in female fetuses exposed to finasteride at any dosage in utero.

Fertility

In sexually mature male rabbits treated with a finasteride dosage of 80 mg/kg daily (543 times the human exposure) for up to 12 weeks, no effect on fertility, sperm count, or ejaculate volume was seen. In sexually mature male rats receiving 80 mg/kg daily (61 times the human exposure), there were no substantial effects on fertility after 6 or 12 weeks of treatment; however, when treatment was continued for up to 24 or 30 weeks, there was an apparent decrease in fertility, fecundity, and an associated substantial decrease in the weights of the seminal vesicles and prostate. All of these effects were reversible within 6 weeks of discontinuance of finasteride. No drug-related effect on testes or on mating performance was seen in rats or rabbits. The decrease in fertility in finasteride-treated rats is secondary to its effect on accessory sex organs (prostate and seminal vesicles), resulting in failure to form a seminal plug. The seminal plug is essential for normal fertility in rats and is not relevant in humans.

Lactation

It is not known whether finasteride is distributed into human milk, but the drug is not indicated for use in women.

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