Finasteride is a synthetic 4-azasteroid compound, a competitive and specific inhibitor of type II isoenzyme-type steroid 5-α-reductase, which converts testosterone in the active androgen 5-α-dihydrotestosterone (DHT). Finasteride inhibits the stimulating effect of testosterone on tumor development; inhibition of the formation of dihydrogenase is accompanied by a decrease in the volume of the prostate gland, an increase in the maximum rate of urinary outflow and a decrease in symptoms of obstruction of the urinary tract. With constant admission, a statistically significant effect is recorded after 3 months (decrease in the volume of the gland) and 7 months, (a decrease in the severity of symptoms associated with prostatic hyperplasia).
In the human body there are 2 types of 5-α-reductase: I and II. Their distribution in tissues is not the same: isoenzyme II is found in the prostate, testicles and their appendages, glans penis, scrotum, seminal vesicles, liver and in the chest; I type occurs mainly in the skin of the head, back and chest, sebaceous glands, in the liver, adrenal glands and kidneys. Finasteride oppresses primarily isoenzyme type II, responsible for most of the DHT in the blood.
A single dose of finasteride quickly and significantly changes the level of DHT in plasma. A single dose of 5 mg of finasteride reduces the level of DHT in plasma by 75%, which reaches its minimum by 24 hours, then returns to the initial level within 7 days.
With multiple reception finasteride keeps efficiency. Finasteride reduces the level of DHT in the prostate itself by ≤15% and provides a corresponding increase in testosterone levels in the prostate. Compared with surgical or chemical castration, treatment with finasteride is accompanied by a significantly greater decrease in the level of DHT in the prostate.
Prostate-specific antigen (PSA) is a sensitive and specific androgen-dependent marker of prostate carcinoma. In most cases, after several months of treatment with finasteride, there is a rapid decrease in PSA level, and then setting on new baseline marks.
After 1 year of taking 5 mg doses of finasteride, the average PSA concentration is reduced by 50%.
Finasteride does not show an affinity for androgen receptors and does not have a different hormonal effect.Following the discovery of 5-α-reductase and the description of the 5-α-reductase deficiency syndrome of type II (hermaphroditism of the male type), the role of androgens in benign prostatic hyperplasia was reconsidered. The development of the prostate depends on DHT, strong androgen. When 5-α-reductase is deficient against a background of normal or high testosterone levels, adult atrophy of the prostate is observed.
DHT activates androgen receptors, forming after the addition of dimers to them, which, when linked to DNA, directly or indirectly contribute to the proliferation of cells by changing the expression of genes responsible for proliferation and apoptosis. In the intact prostate, the processes of apoptosis and proliferation are in balance. Despite the fact that factors that provoke prostate hyperplasia at the molecular level are not known, the role of DHT in this is very likely. Specific inhibitors of 5-a-reductase type II can reduce the level of DHT in the prostate and promote the reverse development of hyperplastic prostate. There was a significant mortality in mice and rats of both sexes when fed with a first single dose of finasteride equal to 1500 mg / m2 (500 mg / kg), and the second - 2360 mg / m2 (400 mg / kg for females) and 5900 mg / m2 (1000 mg / kg for males). Small doses of the drug, fed to pregnant rats, caused malformations of the genitals in male offspring.