Pharmacodynamics Steroidogenesis.<unk>  inhibits 3β-HSD.<unk>  is a steroidogenesis inhibitor. It is specifically an inhibitor of 3β-hydroxysteroid dehydrogenase (3β-HSD). As a result of this action,<unk>  blocks the conversion of Δ5-3β-hydroxysteroids, including pregnenolone, 17α-hydroxypregnenolone, dehydroepiandrosterone (DHEA), and androstenediol, into Δ4-3-ketosteroids, including progesterone, 17α-hydroxyprogesterone, androstenedione, and testosterone, respectively. Consequently,<unk>  inhibits the production of all classes of steroid hormones, including androgens, estrogens, progestogens, glucocorticoids, and mineralocorticoids. The mechanism of action of<unk>  in Cushing's syndrome and Conn's syndrome is by inhibiting the production of corticosteroids such as cortisol and aldosterone in the adrenal glands.<unk>  has also been used as an abortifacient due to its inhibition of progesterone synthesis.<unk>  is not an aromatase inhibitor and hence does not inhibit the conversion of androgens like androstenedione and testosterone into estrogens like estrone and estradiol. However,<unk>  may nonetheless inhibit estrogen synthesis by inhibiting androgen synthesis. In addition to steroidogenesis inhibition,<unk>  has been found to act as a noncompetitive antiestrogen, via direct and presumably allosteric interactions with the estrogen receptor. The effectiveness of<unk>  in postmenopausal breast cancer may relate this apparent antiestrogenic activity.<unk>  has also been found to act as an agonist of the androgen receptor. As such, its use in men with prostate cancer may warrant caution. Pharmacokinetics<unk>  is metabolized in the liver. The major metabolite of<unk>  is 17-ketotrilostane. The conversion of<unk>  into 17-ketotrilostane is reversible, suggesting that<unk>  and 17-ketotrilostane undergo interconversion in the body. 17-Ketotrilostane circulates at 3-fold higher levels than<unk>  and is more active than<unk>  as a 3β-HSD inhibitor. The elimination half-lives of<unk>  and 17-ketotrilostane are both 1.2 hours, with both compounds cleared from the blood within 6 to 8 hours of a dose of<unk> . 17-Ketotrilostane is excreted by the kidneys.
Trilostane
Mepitiostane
Oprelvekin
Epitiostanol
Ganirelix
Triptorelin
Vosoritide
Atosiban