Prostate cancer is an androgen-dependent tumor. Since it was first reported in 1941, endocrine therapy for prostate cancer has been widely used in clinical practice. The aim is to reduce the concentration of androgens in the body, inhibit the synthesis of adrenal-derived androgens, inhibit the conversion of testosterone to dihydrotestosterone or block the binding of androgens to their receptors in order to inhibit or control the growth of prostate cancer cells. Endocrine therapy includes debulking and anti-androgen therapy. Debulking includes surgical debulking and pharmacological debulking. Surgical debulking refers to the removal of both testes, which causes a rapid and sustained decline in testosterone to debulking levels. Pharmacologic depot refers to the use of luteinizing hormone-releasing hormone analogs. By inhibiting the release of gonadotropins from the pituitary gland, the production of testosterone is inhibited, resulting in “depotting”. The other major part of endocrine therapy is anti-androgen therapy, the mechanism of action of which is to bind to androgen receptors in prostate cancer cells, affecting the activation of the receptors by testosterone and dihydrotestosterone. The commonly used anti-androgens are: flutamide and bicalutamide, which bind only to the androgen receptor and are therefore also called pure anti-androgens.