Pharmacodynamics Along with the retroprogesterone derivative dydrogesterone,<unk>  has been described as a "true" progesterone derivative or progestogen due to its close similarity to natural progesterone. Similarly to progesterone, dydrogesterone, and hydroxyprogesterone caproate,<unk>  is a pure progestogen and lacks any androgenic effects. As such, it poses no risk of androgenic side effects or virilizing teratogenic effects on female fetuses.<unk>  is said to influence the hypothalamic–pituitary–adrenal axis similarly to progesterone and medroxyprogesterone acetate, producing adrenal suppression at sufficiently high doses, and this suggests that it possesses weak glucocorticoid activity similarly to progesterone.<unk>  is a very weak progestogen. When administered orally or intraperitoneally in animals, the medication showed 1/80 and 1/20 the potency of subcutaneously injected progesterone, respectively. Similarly, oral doses of<unk>  of 10 to 20 times those of subcutaneous progesterone were insufficient to maintain pregnancy in animals, and oral or intraperitoneal doses of<unk>  20 to 40 times those of oral or intraperitoneal progesterone were unable to potentiate hexobarbital-induced anesthesia in animals (which progesterone does and is thought to do by inhibiting the hepatic metabolism of barbiturates). With oral administration of equal doses of progesterone and<unk>  in animals, 3 to 4 times less pregnanediol was recovered from urine with<unk> . The fact that<unk>  is more potent by intraperitoneal than oral administration in animals suggests that it is transformed into a less active metabolite in the intestines. The effective dosage of<unk>  in the menstrual delay test has been studied.<unk>  has no anesthetic effect in animals, in contrast to progesterone. Pharmacokinetics<unk>  has been suggested to act as a prodrug of progesterone via slow hydrolysis in the body. Indeed, it produces similar metabolites (e.g., pregnanediols and allopregnanediols) as progesterone, although with differing ratios, and notably is the only progestin that is known to produce pregnanediol as a metabolite. Subsequent research has cast doubt on the notion that<unk>  is a prodrug of progesterone however, and indicates that it instead is directly metabolized into pregnanediols without intermediate conversion into progesterone. Based on its chemical structure,<unk>  may be transformed into 3α-dihydroprogesterone and/or 3β-dihydroprogesterone and then further metabolized into pregnanolones and pregnanediols. 3β-Dihydroprogesterone has been reported to possess about the same progestogenic potency as progesterone in the Clauberg test, whereas 3α-dihydroprogesterone was not assessed. Relative to progesterone,<unk>  shows improved pharmacokinetics, including higher potency, oral activity, and a longer terminal half-life and hence duration of action. This is considered to be due to its higher lipophilicity, being stored into and slowly released from fat.<unk>  also shows slower metabolism and more stable blood levels, with a longer time to peak concentrations and a less intense peak compared to progesterone. The bioavailability of<unk>  is highest when it is given as a sesame seed oil solution (compared to an oil suspension (~2-fold less) or micronization (~7-fold less)). The C3 enol ethers of progesterone are less suited for use via depot injection relative to progestogen esters like hydroxyprogesterone caproate due to their susceptibility to oxidative metabolism. The pharmacokinetics of<unk>  have been reviewed.
Quingestrone
Gestodene
Hexestrol
Estradiol dienantate
Doisynoestrol
Dienestrol
Estradiol enantate
Benzestrol