The pharmacology of<unk><unk>  inhibition is complex, but involves the binding of NADPH to the enzyme followed by the substrate. Specific substrates include testosterone, progesterone, androstenedione, epitestosterone, cortisol, aldosterone, and deoxycorticosterone. The entire physiologic effect of their reduction is unknown, but likely related to their excretion or is itself physiologic.<unk><unk>  reduces the steroid Δ4,5 double bond in testosterone to its more active form DHT. Thus, inhibition results in decreased amounts of DHT. Because of this, slight elevations in testosterone and estradiol levels occur. The<unk><unk>  reaction is a rate-limiting step in the testosterone reduction and involves the binding of NADPH to the enzyme followed by the substrate. ::: Substrate + NADPH + H+ →<unk> -substrate + NADP+ Beyond being a catalyst in the rate-limiting step in testosterone reduction,<unk><unk>  isoforms I and II reduce progesterone to<unk> -dihydroprogesterone <unk> -DHP) and deoxycorticosterone to dihydrodeoxycorticosterone (DHDOC). In vitro and animal models suggest subsequent 3α-reduction of DHT,<unk> -DHP and DHDOC lead to neurosteroid metabolites with effect on cerebral function. These neurosteroids, which include allopregnanolone, tetrahydrodeoxycorticosterone (THDOC), and 3α-androstanediol, act as potent positive allosteric modulators of GABAA receptors, and have antidepressant, anxiolytic, prosexual, and anticonvulsant effects.<unk> -Dihydrocortisol is present in the aqueous humor of the eye, is synthesized in the lens, and might help make the aqueous humor itself.<unk> -Dihydroaldosterone is a potent antinatriuretic agent, although different from aldosterone. Its formation in the kidney is enhanced by restriction of dietary salt, suggesting it may help retain sodium.<unk> -DHP is a major hormone in circulation of normal cycling and pregnant women. Other enzymes compensate to a degree for the absent conversion of<unk><unk> , specifically with local expression at the skin of reductive 17β-hydroxysteroid dehydrogenase, and oxidative 3α-hydroxysteroid dehydrogenase and 3β-hydroxysteroid dehydrogenase enzymes. In BPH, DHT acts as a potent cellular androgen and promotes prostate growth; therefore, it inhibits and alleviates symptoms of BPH. In alopecia, male and female-pattern baldness is an effect of androgenic receptor activation, so reducing levels of DHT also reduces hair loss.
5α-Reductase inhibitor
Aromatase inhibitor
Antiandrogen
Steroidogenesis inhibitor
N-Terminal domain antiandrogen
Reuptake inhibitor
COX-2 inhibitor
Selective androgen receptor modulator