Prostate cancer is the second leading cause of cancer death in men in the US and 
Europe. The treatment of advanced-stage prostate cancer has been androgen 
deprivation. Medical castration leads to decreased production of testosterone 
and dihydrotestosterone by the testes, but adrenal glands and even prostate 
cancer tissue continue to produce androgens, which eventually leads to continued 
prostate cancer growth despite castrate level of androgens. This stage is known 
as castrate-resistant prostate cancer (CRPC), which continues to be a challenge 
to treat. Addition of androgen antagonists to hormonal deprivation has been 
successful in lowering the prostate-specific antigen levels further, but has not 
actually translated into life-prolonging options. The results of several 
contemporary studies have continued to demonstrate activation of the androgen 
receptor as being the key factor in the continued growth of prostate cancer. 
Blockade of androgen production by nongonadal sources has led to clinical 
benefit in this setting. One such agent is abiraterone acetate, which 
significantly reduces androgen production by blocking the enzyme, cytochrome 
P450 17 alpha-hydroxylase (CYP17). This has provided physicians with another 
treatment option for patients with CRPC. The landscape for prostate cancer 
treatment has changed with the approval of cabazitaxel, sipuleucel-T and 
abiraterone. Here we provide an overview of abiraterone acetate, its mechanism 
of action, and its potential place for therapy in CRPC.