Pharmacodynamics<unk>  is described as a pure progestogen similar in profile to progesterone. In contrast to progesterone however,<unk>  is more potent and is orally active. There is reportedly no information available on the receptor binding of<unk>  at the various steroid hormone receptors. However, based on animal research (e.g., the Clauberg test and other assays),<unk>  appears to be a potent progestogen, devoid of androgenic, estrogenic, and glucocorticoid activity, but with weak antiandrogenic and very weak antimineralocorticoid activity. Accordingly, no evidence of androgenic or glucocorticoid activity, including effects on the estrogen-induced increase in triglycerides and HDL cholesterol and adrenal suppression, were observed in clinical studies. However, in a very high-dosage (100 mg/day for 6 months) study of<unk>  for benign prostatic hyperplasia, a hyperglycemic effect and changes in plasma cortisol levels were observed and considered likely to be secondary to glucocorticoid activity, and decreased sodium levels were also observed and attributed to antimineralocorticoid activity. In any case, under normal circumstances (i.e., at typical clinical dosages),<unk>  is described as a progestogen and antigonadotropin and weak antiandrogen in humans without other clinically relevant activity.<unk>  has been found to be an inhibitor of 3β-hydroxysteroid dehydrogenase/Δ5-4 isomerase in vitro, preventing conversion of pregnenolone to progesterone and 17α-hydroxypregnenolone to 17α-hydroxyprogesterone in rat testis preparations, and inhibits the biosynthesis of testosterone in vivo in rats. In addition, similarly to progesterone,<unk>  can inhibit 5α-reductase in vitro in microsomal preparations of skin and prostate. Although their clinical relevance is uncertain, these actions of<unk>  could contribute to its weak antiandrogen activity. Pharmacokinetics Upon oral administration,<unk>  is rapidly absorbed, and the bioavailability is nearly 100%. After ingestion of a 10 mg dose of<unk> , peak circulating concentrations (Cmax) of 10–15 ng/mL are achieved. The distribution and elimination half-lives of<unk>  are 4 hours and 35–36 hours, respectively. The drug is largely bound (90%) to albumin, and to only small extents to corticosteroid-binding globulin (3%) and sex hormone-binding globulin (2%). The metabolism of<unk>  is most importantly by hydroxylation.
Medrogestone
Oxogestone
Phospho soda
Hermaphrodite 
Anagestone acetate
Medi-Cal
Diatrizoate
Lithotrite