Not to be confused with quingestanol.
Clinical data
Trade names Enol-Luteovis
Routes of
ATC code G03A (WHO)
Legal status
Legal status
  • ℞ (Prescription only)
Synonyms W-3399; Progesterone 3-cyclopentyl enol ether; 3-Cyclopentyloxypregna-3,5-dien-20-one
CAS Number 67-95-8
PubChem (CID) 9929903
ChemSpider 8105534
KEGG D05680
Chemical and physical data
Formula C26H38O2
Molar mass 382.57872 g/mol
3D model (Jmol) Interactive image

Quingestrone (INN, USAN) (brand name Enol-Luteovis; former developmental code name W-3399), also known as progesterone 3-cyclopentyl enol ether (PCPE) or as 3-cyclopentyloxypregna-3,5-dien-20-one, is a semisynthetic, steroidal, pure progestin that was developed by Vister and introduced in Italy as an oral contraceptive (in combination with ethinyl estradiol or mestranol)[1][2] in 1962.[3][4][5][6][7] It is closely related to progesterone, being the 3-cyclopentyl enol ether of the progestogen sex hormone.[6]


Along with the retroprogesterone derivative dydrogesterone, quingestrone is described as a "true" progesterone derivative due to its close similarity to natural progesterone.[8] Similarly to progesterone, dydrogesterone, and hydroxyprogesterone caproate, quingestrone is a pure progestogen and lacks any androgenic effects.[9] As such, it poses no risk of androgenic side effects or virilizing teratogenic effects on female fetuses.[9] Accordingly, the drug was studied in the clinical prevention of miscarriage during pregnancy; however, insufficient efficacy was observed at the dosage assessed (100 mg/day orally).[10][11][12][13] 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 or very weak glucocorticoid properties similarly to progesterone.[14][15]


Quingestrone has been suggested to act as a prodrug of progesterone via slow hydrolysis in the body.[10][16] Indeed, it produces similar metabolites (e.g., pregnanediols and allopregnanediols) to progesterone,[10][17] although with differing ratios,[18][5] and notably is the only progestin that is known to produce pregnanediol as a metabolite.[19] Subsequent research has cast doubt on the notion that quingestrone is a prodrug of progesterone however, and indicates that it instead is directly metabolized into pregnanediols without intermediate conversion into progesterone.[20]

Relative to progesterone, quingestrone shows improved pharmacokinetics, including higher potency,[21] oral activity,[22] and a longer half-life and hence duration of action.[16] This is considered to be due to its higher lipophilicity,[16] being stored into and slowly released from fat.[6][10] Quingestrone also shows slower metabolism and more stable blood levels, with a longer time to peak concentrations and a less intense peak compared to progesterone.[23]

The bioavailability of quingestrone 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)).[17]

See also


  1. Larrey D, Geneve J, Pessayre D, Machayekhi JP, Degott C, Benhamou JP (1987). "Prolonged cholestasis after cyproheptadine-induced acute hepatitis". J. Clin. Gastroenterol. 9 (1): 102–4. doi:10.1097/00004836-198702000-00026. ISSN 0192-0790. PMID 3559100.
  2. International Planned Parenthood Federation. Medical Committee. Oral Advisory Group (1965). Handbook on oral contraception. Little, Brown. p. 18. OCLC 2717593.
  3. J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. p. 163. doi:10.1007/978-1-4757-2085-3. ISBN 978-1-4757-2085-3. OCLC 898564124.
  4. Pei-Show Juo (21 December 2001). Concise Dictionary of Biomedicine and Molecular Biology. CRC Press. pp. 922–. ISBN 978-1-4200-4130-9. LCCN 2001043892. OCLC 48057162.
  5. 1 2 Denis Frank Hawkins (1974). Obstetric therapeutics: clinical pharmacology and therapeutics in obstetric practice. Baillière Tindall. pp. 129, 138, 145. ISBN 978-0-7020-0471-1.
  6. 1 2 3 P. J. Bentley (1980). Endocrine Pharmacology: Physiological Basis and Therapeutic Applications. CUP Archive. pp. 274–. ISBN 978-0-521-22673-8.
  7. Watts, GeorgeT. (1962). "EMERGENCY TREATMENT OF POISONING". The Lancet. 279 (7228): 533–534. doi:10.1016/S0140-6736(62)91504-0. ISSN 0140-6736.
  8. Erica G. Wachtel (1969). Exfoliative cytology in gynaecological practice. Appleton-Century-Crofts. p. 134. LCCN 77008744.
  9. 1 2 Dugald Baird; John Martin Munro Kerr (1969). Combined textbook of obstetrics and gynæcology for students and practitioners. E. & S. Livingstone. LCCN 70360656.
  10. 1 2 3 4 Burton, Eunice R.; Wachtel, Erica G. (1967). "A CLINICAL TRIAL AND CYTOLOGICAL ASSESSMENT OF ENOL LUTEOVIS IN THE TREATMENT OF THREATENED AND RECURRENT ABORTION". BJOG: An International Journal of Obstetrics and Gynaecology. 74 (4): 533–536. doi:10.1111/j.1471-0528.1967.tb03986.x. ISSN 1470-0328. PMID 5340429.
  11. Vitamins and Hormones. Academic Press. 9 February 1973. pp. 332–. ISBN 978-0-08-086627-7.
  12. Ian S. Fraser (1998). Estrogens and Progestogens in Clinical Practice. Churchill Livingstone. ISBN 978-0-443-04706-0.
  13. Goldstein, Peter; Berrier, Jayne; Rosen, Scott; Sacks, Henry S.; Chalmers, Thomas C. (1989). "A meta-analysis of randomized control trials of progestational agents in pregnancy". BJOG: An International Journal of Obstetrics and Gynaecology. 96 (3): 265–274. doi:10.1111/j.1471-0528.1989.tb02385.x. ISSN 1470-0328. PMID 2653414.
  14. Luciano Martini (1966). Neuroendocrinology. Academic Press. p. 331. LCCN 66026256.
  15. Steinetz, B.G.; Beach, V.L.; DiPasquale, G.; Battista, J.V. (1965). "Effects of different gestagenic steroid types on plasma-free corticosteroid levels in ACTH-treated rats". Steroids. 5 (1): 93–108. doi:10.1016/0039-128X(65)90134-0. ISSN 0039-128X.
  16. 1 2 3 Charman, William N.; Porter, Christopher J.H. (1996). "Lipophilic prodrugs designed for intestinal lymphatic transport". Advanced Drug Delivery Reviews. 19 (2): 149–169. doi:10.1016/0169-409X(95)00105-G. ISSN 0169-409X.
  17. 1 2 Fatouros DG, Karpf DM, Nielsen FS, Mullertz A (2007). "Clinical studies with oral lipid based formulations of poorly soluble compounds". Ther Clin Risk Manag. 3 (4): 591–604. PMC 2374933Freely accessible. PMID 18472981.
  18. http://www.popline.org/node/474452
  19. Current Medicine and Drugs. 1962. ISSN 0590-4048. Enol Luteovis (3 cyclo-pentyl enol ether of progesterone) is the only oral progestin producing pregnanediol as a metabolite. It is not very potent and probably carries very little risk of producing virilizing effects on a female foetus. Thus it is more closely related to progesterone than the other synthetic progestins.
  20. Meli, A.; Wolff, A.; Lucker, W. E.; Steinetz, B. G. (1965). "The Biological Profile of Progesterone 3-Cyclopentyl Enol Ether as Compared with That of Progesterone". Experimental Biology and Medicine. 118 (3): 714–717. doi:10.3181/00379727-118-29947. ISSN 1535-3702.
  21. http://www.popline.org/node/474452
  22. Joseph Bolivar De Lee (1965). The ... Year Book of Obstetrics and Gynecology. Year Book Publishers. p. 150. ISSN 0084-3911. LCCN cdr38000020.
  23. Caie, E.; Klopper, A. (1964). "THE URINARY EXCRETION OF PREGNANEDIOL AFTER THE ADMINISTRATION OF AN ORAL GESTAGEN (PROGESTERONE CYCLOPENTYL ENOL ETHER)". Journal of Endocrinology. 28 (2): 221–222. doi:10.1677/joe.0.0280221. ISSN 0022-0795. PMID 14112260.

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