<unk> agonists act as agonists of the<unk> receptor, the biological target of gonadotropin-releasing hormone <unk> . These drugs can be both peptides and small-molecules. They are modeled after the hypothalamic neurohormone<unk>  which interacts with the<unk> receptor to elicit its biologic response, the release of the pituitary hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH). However, after the initial "flare" response, continued stimulation with<unk> agonists desensitizes the pituitary gland (by causing<unk> receptor downregulation) to<unk>  Pituitary desensitization reduces the secretion of LH and FSH and thus induces a state of hypogonadotropic hypogonadal anovulation, sometimes referred to as "pseudomenopause" or "medical oophorectomy."<unk> agonists are able to completely shutdown gonadal testosterone production and thereby suppress circulating testosterone levels by 95% or into the castrate/female range in men. Agonists do not quickly dissociate from the<unk> receptor. As a result, initially there is an increase in FSH and LH secretion (so-called "flare effect"). Levels of LH may increase by up to 10-fold, while levels of testosterone generally increase to 140 to 200% of baseline values. However, after continuous administration, a profound hypogonadal effect (i.e. decrease in FSH and LH) is achieved through receptor downregulation by internalization of receptors. Generally this induced and reversible hypogonadism is the therapeutic goal. During the flare, peak levels of testosterone occur after 2 to 4 days, baseline testosterone levels are returned to by 7 to 8 days, and castrate levels of testosterone are achieved by 2 to 4 weeks. Following cessation of exogenous<unk> agonist it takes 5 to 8 days before normal gonadotropin secretion is completely restored. Various medications can be used to prevent the testosterone flare and/or its effects at the initiation of<unk> agonist therapy. These include antigonadotropins such as progestogens like cyproterone acetate and chlormadinone acetate and estrogens like diethylstilbestrol, fosfestrol (diethylstilbestrol diphosphate), and estramustine phosphate; antiandrogens such as nonsteroidal antiandrogens like flutamide, nilutamide, and bicalutamide; and androgen synthesis inhibitors such as ketoconazole and abiraterone acetate.
Gonadotropin-releasing hormone agonist
Gonadotropin-releasing hormone antagonist
Gonadotropin-releasing hormone modulator
Prolactin modulator
Antiandrogen
Thyroid blocker
17α-Alkylated anabolic steroid
Steroidal antiandrogen