Finasteride effects on 5α-reductase ferment. This ferment turns testosterone into a more androgen-active dihydrotestosterone (DHT) form. Finasteride is a 5α-reductase inhibitor, in particular, type II and III, and therefore an antiandrogen. It decreases the production of dihydrotestosterone, including in the prostate gland and the scalp. Inhibits the effect of dihydrotestosterone on the development of prostate adenoma. Finasteride decreases the enlargement of the gland, improves urinary flow, and reduces symptoms associated with benign prostatic hypertrophy. It may take several months of treatment to reduce the clinical symptoms of the disease.
Mechanism of action
By inhibiting 5-reductase, finasteride prevents the conversion of testosterone to dihydrotestosterone (DHT). Type II and III isoenzymes lead to a decrease in serum DHT levels by about 65-70%, and in the prostate, DHT levels decrease up to 85-90%, where the Type II isoenzyme presented mostly. Unlike triple inhibitors of all three 5a-reductase isoenzymes, such as dutasteride, which can reduce whole-body DHT levels by more than 99%, finasteride does not completely inhibit DHT production because it lacks a significant inhibitory effect on the 5a-reductase type I isoenzyme.
By blocking the production of DHT, finasteride reduces androgen a
