Quingestrone

Quingestrone, also known as progesterone 3-cyclopentyl enol ether (PCPE) and sold under the brand name Enol-Luteovis, is a progestin medication which was previously used in birth control pills in Italy but is now no longer marketed. It is taken by mouth. Quingestrone is a progestin, or a synthetic progestogen, and hence is an agonist of the progesterone receptor, the biological target of progestogens like progesterone. It has weak glucocorticoid activity. Quingestrone was introduced for medical use by 1962. It is no longer available. Quingestrone was formerly used in combination with ethinylestradiol or mestranol in combined birth control pills in Italy. The medication was studied in the clinical prevention of miscarriage during pregnancy, but insufficient efficacy was observed at the dosage assessed (100 mg/day orally). Progesterone (medication)#Side effects and Progestin#Side effects Along with the retroprogesterone derivative dydrogesterone, quingestrone 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, quingestrone 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. Quingestrone 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. Quingestrone 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 quingestrone of 10 to 20 times those of subcutaneous progesterone were insufficient to maintain pregnancy in animals, and oral or intraperitoneal doses of quingestrone 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).