Pharmacodynamics<unk>  binds directly to the androgen receptor (AR) and estrogen receptor (ER), where it acts as an agonist and antagonist, respectively. It is described as potent in its activity as an antiestrogen and comparatively weak as an AAS. In any case, in terms of AAS potency,<unk>  has been found to have 11 times the anabolic activity and approximately equal androgenic activity relative to that of the reference AAS methyltestosterone. The mechanism of action of<unk>  in breast cancer is multimodal; it directly suppresses tumor growth through activation of the AR and inhibition of the ER, and, in premenopausal women, it additionally acts as an antigonadotropin and reducing systemic estrogen levels via AR activation and consequent suppression of the hypothalamic-pituitary-gonadal axis.<unk>  is unique among AAS in acting as an antagonist of the ER. Pharmacokinetics Similarly to the case of testosterone,<unk>  shows poor bioavailability and weak therapeutic efficacy when taken orally due to extensive first-pass metabolism. As such, it must instead be administered via intramuscular injection.
Epitiostanol
Oprelvekin
Vosoritide
Elinogrel
Eptifibatide
Tafamidis
Pentoxifylline
Mepitiostane