Epristeride

5α-reductase but is of relatively low efficacy and can decrease DHT levels in the blood only by about 25 to 54%.^[8]

isoform of the enzyme similarly to finasteride and turosteride but unlike dutasteride.^[8]

NADPH.^[8][9] 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 epristeride.^[8][9] However, subsequent clinical data have not supported this hypothesis.^[8] Moreover, in spite of the fact that epristeride 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.^[8] For this reason, relative to other 5α-reductase inhibitors like finasteride and dutasteride, the degree of DHT suppression with epristeride falls short of that desirable for full clinical benefit.^[8]

elimination half-life of 26 hours.^[2]

synthetic androstane steroid

GlaxoSmithKline) in the 1990s and reached phase III clinical trials in the United States, United Kingdom, and Japan,^[6] but ultimately was never marketed in these countries.^[4] Instead, epristeride was developed by Ono Pharmaceutical and introduced for the treatment of BPH in China in 2000.^[4]

INNTooltip International Nonproprietary Name, USANTooltip United States Adopted Name, BANTooltip British Approved Name, and JANTooltip Japanese Accepted Name.^[5]