Pharmacodynamics<unk>  is a selective, transition-state, non-competitive or uncompetitive, irreversible inhibitor of 5α-reductase, and is specific to the type II isoform of the enzyme similarly to finasteride and turosteride but unlike dutasteride.<unk>  is unique in its mechanism of action relative to finasteride and dutasteride in that it binds irreversibly to 5α-reductase and results in the formation of an unproductive complex of the 5α-reductase enzyme, the substrate testosterone, and the cofactor NADPH. For this reason, testosterone is caught in a trap, and it was initially speculated that the reciprocal increase in intraprostatic levels of testosterone seen with finasteride and dutasteride should not happen with<unk> . However, subsequent clinical data have not supported this hypothesis. Moreover, in spite of the fact that<unk>  is a very potent inhibitor of 5α-reductase type II (0.18–2 nM), it has been found to reduce circulating levels of dihydrotestosterone (DHT) by only 25 to 54% following 8 days of therapy over a dosage range of 0.4 to 160 mg/day. For this reason, relative to other 5α-reductase inhibitors like finasteride and dutasteride, the degree of DHT suppression with<unk>  falls short of that desirable for full clinical benefit. Pharmacokinetics The oral bioavailability of<unk>  is 93%. It has an elimination half-life of 26 hours.
Epristeride
Lapisteride
Amitriptylinoxide
Metenolone acetate
Iomeprol
Gestodene
Trestolone
Hydrastinine