Androgen deprivation therapy has been the standard of care in advanced prostate cancer for over 50 years. Although castration is initially effective, most patients eventually develop progressive disease despite low levels of testosterone. The term castration-resistant prostate cancer (CRPC), however, is a misnomer, as the disease is still dependent on continued activation of the androgen receptor (AR). New secondary hormonal therapies seek to prolong suppression of the AR and thus delay the development of truly hormone-"refractory" prostate cancer. Extra-gonadal androgens, and specifically adrenal androgens, represent a means for continued AR-mediated growth in CRPC and have thus become a therapeutic target. Abiraterone acetate (CB-7630) is an orally administered, specific inhibitor of CYP17A1, a rate-limiting enzyme in androgen biosynthesis. Preliminary data from phase I and II trials suggest that prostate-specific antigen declines occur in a large proportion of patients and that the toxicity profile is acceptable. Two large phase III clinical trials are currently open to accrual, and if abiraterone acetate is proven to be efficacious, it will result in widespread use of a drug specifically developed to suppress adrenal androgens.