An orally active testosterone 5-alpha-reductase inhibitor. It is used as a surgical alternative for treatment of benign prostatic hyperplasia.
For the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to: Improve symptoms, reduce the risk of acute urinary retention, reduce the risk of the need for surgery including transurethral resection of the prostate.
Also used for the stimulation of regrowth of hair in men with mild to moderate androgenetic alopecia (male pattern alopecia, hereditary alopecia, common male baldness).
Finasteride is a synthetic 4-azasteroid compound. This drug is a competitive and specific inhibitor of Type II 5a-reductase, an intracellular enzyme that converts the androgen testosterone into 5α-dihydrotestosterone (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 5a-reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and liver.
Type I 5a-reductase is responsible for approximately one-third of circulating DHT. The Type II 5a-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. Although finasteride is 100-fold more selective for type II 5a-reductase than for the type I isoenzyme, chronic treatment with this drug may have some effect on type I 5a-reductase.
The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5a-reductase through the formation of a stable complex with the enzyme. Inhibition of Type II 5a-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations, minimal to moderate increase in serum testosterone concentrations, and substantial increases in prostatic testosterone concetrations.
As DHT appears to be the principal androgen responsible for stimulation of prostatic growth, a decrease in DHT concentrations will result in a decrease in prostatic volume (approximately 20-30% after 6-24 months of continued therapy).
In men with androgenic alopecia, the mechanism of action has not been fully determined, but finasteride has shown to decrease scalp DHT concentration to the levels found in hairy scalp, reduce serum DHT, increase hair regrowth, and slow hair loss.
Metabolism: Drug is extensively metabolized, primarily in the liver via CYP3A4. Two metabolites have been identified with ≤20% of the activity of finasteride.
Route of elimination: 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 feces. Urinary excretion of metabolites was decreased in patients with renal impairment. This decrease was associated with an increase in fecal excretion of metabolites.
Half life: 4.5 hours (range 3.3-13.4 hours)
All medicines may cause side effects, but many people have no, or minor, side effects.Some medical conditions may interact with Finasteride.
Tell your doctor or pharmacist if you have any medical conditions.
Common side effects may include: loss of interest in sex, impotence, trouble having an orgasm or abnormal ejaculation.
The sexual side effects of finasteride may continue after you stop taking finasteride. Talk to your doctor if you have concerns about these side effects.
This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider.