Pharmacodynamics<unk>  belongs to a class of drugs called 5α-reductase inhibitors, which block the action of the 5α-reductase enzymes that convert testosterone into DHT. It inhibits all three forms of 5α-reductase, and can decrease DHT levels in the blood by up to 98%. Specifically it is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III ( values are 3.9 nM for type I and 1.8 nM for type II). This is in contrast to finasteride, which is similarly an irreversible inhibitor of 5α-reductase but only inhibits the type II and III isoenzymes. As a result of this difference,<unk>  is able to achieve a reduction in circulating DHT levels of up to 98%, whereas finasteride is able to achieve a reduction of only 65 to 70%. In spite of the differential reduction in circulating DHT levels, the two drugs decrease levels of DHT to a similar extent of approximately 85 to 90% in the prostate gland, where the type II isoform of 5α-reductase predominates. Since 5α-reductases degrade testosterone to DHT, the inhibition of them could cause an increase in testosterone. However, a 2018 review found that initiation of 5α-reductase inhibitors did not result in a consistent increase in testosterone levels, with some studies showing increases and others showing no change. There was no statistically significant change in testosterone levels from 5α-reductase inhibitors in the overall meta-analysis, though men with lower baseline testosterone levels may show a rise in testosterone levels. In addition to inhibition of DHT production, 5α-reductase inhibitors like<unk>  are also neurosteroidogenesis inhibitors, preventing the 5α-reductase-mediated biosynthesis of various neurosteroids including allopregnanolone (from progesterone), (from deoxycorticosterone), and 3α-androstanediol (from testosterone). These neurosteroids are potent positive allosteric modulators of the GABAA receptor and have been found to possess antidepressant, anxiolytic, and pro-sexual effects in animal research. For this reason, prevention of neurosteroid formation may be involved in the sexual dysfunction and depression that has been associated with 5α-reductase inhibitors like<unk> . Pharmacokinetics The oral bioavailability of<unk>  is approximately 60%. Food does not adversely affect the absorption of<unk> . Peak plasma levels occur 2 to 3 hours after administration. Levels of<unk>  in semen have been found to be 3 ng/mL, with no significant effects on DHT levels in sexual partners. The drug is extensively metabolized in the liver by CYP3A4. It has three major metabolites, including 6'-hydroxydutasteride, 4'-hydroxydutasteride, and 1,2-dihydrodutasteride; the former two are formed by CYP3A4, while the latter is not. All three metabolites are active; 6'-hydroxydutasteride has similar potency as a 5α-reductase inhibitor to<unk> , while the other two are less potent.<unk>  has an extremely long terminal or elimination half-life of about 4 or 5 weeks. The elimination half-life of<unk>  is increased in the elderly (170 hours for men age 20–49 years, 300 hours for men age >70 years). No dosage adjustment is necessary in the elderly nor in renal impairment. Because of its long elimination half-life,<unk>  requires 5 or 6 months to reach steady state concentrations. It also remains in the body for a long time after discontinuation and can be detected for up to 4 to 6 months. In contrast to<unk> , finasteride has a short terminal half-life of only 5 to 8 hours.<unk>  is eliminated mainly in the feces (40%) as metabolites. A small portion (5%) is eliminated unchanged in the urine.
Dutasteride
Finasteride
Tadalafil
Ingenol mebutate
Tamsulosin
Cyproterone acetate
Alclometasone
Vardenafil