The<unk>  (CPA), concerns the pharmacology (pharmacodynamics, pharmacokinetics, and routes of administration) of the steroidal antiandrogen and progestin medication<unk><unk> . CPA blocks the effects of androgens like testosterone in the body, which it does by preventing them from interacting with their biological target, the androgen receptor (AR), and by reducing their production by the gonads and hence their concentrations in the body. In addition, it has progesterone-like effects by activating the progesterone receptor (PR). By activating the PR, CPA has antigonadotropic effects and can inhibit fertility and suppress sex hormone production in both men and women. CPA can also produce weak and partial cortisol-like effects at very high doses under certain circumstances by activating the glucocorticoid receptor (GR). CPA can be taken by mouth or by injection into muscle. It has near-complete oral bioavailability, is highly and exclusively bound to albumin in terms of plasma protein binding, is metabolized in the liver by hydroxylation and conjugation, has 15β-hydroxycyproterone<unk>  (15β-OH-CPA) as a single major active metabolite, has a long elimination half-life of about 2 to 4 days regardless of route of administration, and is excreted in feces primarily and to a lesser extent in urine.
Pharmacology of cyproterone acetate
Pharmacology of bicalutamide
Pharmacokinetics of testosterone
Pharmacokinetics of estradiol
Prolactin modulator
Steroidal antiandrogen
Feminizing hormone therapy
Masculinizing hormone therapy