Brands, Medical Use, Clinical Data
- Anti-baldness Agents
- Antihyperplasia Agents
- Skin and Mucous Membrane Agents (84:92.00)
Brands / Synonyms
Chibro-Proscar; Finasterida [Inn-Spanish]; Finasteride and Its Intermediates; Finasteride [Usan:Ban:Inn]; Finasteridum [Inn-Latin]; Finastid; Finpecia; Propecia; Proscar; Prostide
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 prostat.
Finasteride is indicated for the treatment of male pattern hair loss (androgenetic alopecia) in men only. Finasteride is a competitive and specific inhibitor of Type II 5a-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 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.
Mechanism of Action
The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5a-reductase, an intracellular enzyme that converts the androgen testosterone into DHT. Inhibition of Type II 5a-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations.
Biotrnasformation / Drug Metabolism
PROPECIA is contraindicated in the following:
Pregnancy. Finasteride use is contraindicated in women when they are or may potentially be pregnant. Because of
the ability of Type II 5-reductase inhibitors to inhibit the conversion of testosterone to DHT, finasteride
may cause abnormalities of the external genitalia of a male fetus 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 fetus. In female rats, low doses of finasteride administered during
pregnancy have produced abnormalities of the external genitalia in male offspring.
Hypersensitivity to any component of this medication.
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.
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, a-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.
Drug/Laboratory Test Interactions
Finasteride had no effect on circulating levels of cortisol, thyroid-stimulating hormone, or thyroxine, nor did it
affect the plasma lipid profile (e.g., total cholesterol, low-density lipoproteins, high-density lipoproteins and
triglycerides) or bone mineral density. In studies with finasteride, no clinically meaningful changes in luteinizing
hormone (LH), follicle-stimulating hormone (FSH) or prolactin were detected. 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 clinical studies with PROPECIA (finasteride, 1 mg) in men 18-41 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 PROSCAR (finasteride, 5 mg) when used in older men who have benign prostatic hyperplasia (BPH), PSA
levels are decreased by approximately 50%. These findings should be taken into account for proper interpretation of
serum PSA when evaluating men treated with finasteride.