Antiandrogens are useful in the treatment of prostate cancer, benign prostate hyperplasia, precocious puberty, and male pattern baldness, as well as hirsutism in females and acne in both sexes. Antiandrogens used for therapeutic purposes ( Table ) are either AR antagonists, such as the steroidal progesterone derivative cyproterone acetate; nonsteroidal antagonists, such as hydroxyflutamide and bicalutamide; or inhibitors of testosterone or DHT synthesis, such as the steroidal CYP17 inhibitor abiraterone  and the SRD5A inhibitors finasteride and dutasteride  . Inappropriate exposure to antiandrogens during critical periods of human development such as pregnancy may result in pseudohermaphroditism in male offspring; exposure during puberty will delay male virilization  . AR antagonists block the action of endogenous androgens by competing for the AR ligand-binding site. AR agonists, once bound, induce a number of conformational changes that protect ARs against protein degradation and allow them to accumulate in the cytoplasm  , homodimerize, recruit coregulators, and translocate to the nucleus. One mechanism of action of AR antagonists is to prevent this agonist-mediated conformational protection against degradation [42,43] , resulting in downregulation of the receptor or an inability of the AR to shed its HSPs, thus preventing homodimerization; or modifying the conformational change such that binding of coregulators is no longer possible or preferential binding of corepressors occurs  . A modified conformational change may also result in increased access of the AR to phosphatases that would prevent AR phosphorylation and transactivation  .
Unlike NSAAs, most SAAs show off-target hormonal activity such as progestogenic , glucocorticoid , or antimineralocorticoid activity, possess antigonadotropic effects, and are weak partial agonists of the AR with some capacity to activate the receptor.  Due to their antigonadotropic effects, SAAs lower androgen levels in addition to directly blocking the actions of androgens at the AR; at sufficiently high dosages, they are able to lower circulating testosterone levels by up to 70 to 80% in men, to just above the castrate range.    However, due to their other hormonal effects, suppression of estrogen levels alongside testosterone levels, and AR activation, SAAs have increased side effects and show lower efficacy in the treatment of prostate cancer relative to NSAAs.