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Clinical data
Trade names Ginecosid, Ginecoside, Mediol, Renodiol
Synonyms NSC-52245; 17α-Methylestradiol; 17α-ME; 17α-Methylestra-1,3,5(10)-triene-3,17β-diol
Routes of
By mouth[1]
Drug class Estrogen
CAS Number
PubChem CID
Chemical and physical data
Formula C19H26O2
Molar mass 286.409 g/mol
3D model (JSmol)

Methylestradiol, sold under the brand names Ginecosid, Ginecoside, Mediol, and Renodiol, is an estrogen medication which is used in the treatment of menopausal symptoms.[2][3][4] It is formulated in combination with normethandrone, a progestin and androgen/anabolic steroid medication.[3][4] Methylestradiol is taken by mouth.[1]

Side effects of methylestradiol include nausea, breast tension, edema, and breakthrough bleeding among others.[5] It is an estrogen, or an agonist of the estrogen receptors, the biological target of estrogens like estradiol.[6]

Methylestradiol is or has been marketed in Brazil, Venezuela, and Indonesia;[3] in addition to its use as a medication, methylestradiol has been studied for use as a radiopharmaceutical for the estrogen receptor.[7]

Medical uses[edit]

Methylestradiol is used in combination with the progestin and androgen/anabolic steroid normethandrone (methylestrenolone) in the treatment of menopausal symptoms.[3][4]

Side effects[edit]

Side effects of methylestradiol include nausea, breast tension, edema, and breakthrough bleeding.[5]



Methylestradiol is an estrogen, or an agonist of the estrogen receptor,[6] it shows somewhat lower affinity for the estrogen receptor than estradiol or ethinylestradiol.[6]

Methylestradiol is an active metabolite of the androgens/anabolic steroids methyltestosterone (17α-methyltestosterone), metandienone (17α-methyl-δ1-testosterone), and normethandrone (17α-methyl-19-nortestosterone), and is responsible for their estrogenic side effects, such as gynecomastia and fluid retention.[8][9][10]


Due to the presence of its C17α methyl group, methylestradiol cannot be deactivated by oxidation of the C17β hydroxyl group, resulting in improved metabolic stability and potency relative to estradiol.[8] This is analogous to the case of ethinylestradiol and its C17α ethynyl group.[8]


Methylestradiol, or 17α-methylestradiol (17α-ME), also known as 17α-methylestra-1,3,5(10)-triene-3,17β-diol, is a synthetic estrane steroid and a derivative of estradiol.[2][3] It is specifically the derivative of estradiol with a methyl group at the C17α positions.[2][3] Closely related steroids include ethinylestradiol (17α-ethynylestradiol) and ethylestradiol (17α-ethylestradiol),[2] the C3 cyclopentyl ether of methylestradiol has been studied and shows greater oral potency than methylestradiol in animals, similarly to quinestrol (ethinylestradiol 3-cyclopentyl ether) and quinestradol (estriol 3-cyclopentyl ether).[14]

Society and culture[edit]

Generic names[edit]

Methylestradiol has not been assigned an INN or other formal name designations.[2][3] Its generic name in English and German is methylestradiol, in French is méthylestradiol, and in Spanish is metilestadiol.[3] It is also known as 17α-methylestradiol.[3]

Brand names[edit]

Methylestradiol is or has been marketed under the brand names Ginecosid, Ginecoside, Mediol, and Renodiol, all in combination with normethandrone.[3][2]


Methylestradiol is or has been marketed in Brazil, Venezuela, and Indonesia.[3]


  1. ^ a b HEGEMANN O (May 1959). "[Oral hormonal treatment with methylestrene-olone & methylestradiol as early pregnancy tests]". Medizinische (in German). 4 (21): 1032–3. PMID 13673847. 
  2. ^ a b c d e f J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 898–. ISBN 978-1-4757-2085-3. 
  3. ^ a b c d e f g h i j k "Methylestradiol". Retrieved 2 January 2016. 
  4. ^ a b c IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; World Health Organization; International Agency for Research on Cancer (2007). Combined Estrogen-progestogen Contraceptives and Combined Estrogen-progestogen Menopausal Therapy. World Health Organization. pp. 389–. ISBN 978-92-832-1291-1. 
  5. ^ a b Wittlinger, H. (1980). "Clinical Effects of Estrogens": 67–71. doi:10.1007/978-3-642-67568-3_10. 
  6. ^ a b c d Ojasoo T, Raynaud JP (November 1978). "Unique steroid congeners for receptor studies". Cancer Res. 38 (11 Pt 2): 4186–98. PMID 359134. 
  7. ^ Feenstra A, Vaalburg W, Nolten GM, Reiffers S, Talma AG, Wiegman T, van der Molen HD, Woldring MG (1983). "Estrogen receptor binding radiopharmaceuticals: II. Tissue distribution of 17 alpha-methylestradiol in normal and tumor-bearing rats". J. Nucl. Med. 24 (6): 522–8. PMID 6406650. 
  8. ^ a b c Detlef Thieme; Peter Hemmersbach (18 December 2009). Doping in Sports. Springer Science & Business Media. pp. 470–. ISBN 978-3-540-79088-4. 
  9. ^ William Llewellyn (2011). Anabolics. Molecular Nutrition Llc. pp. 533–. ISBN 978-0-9828280-1-4. 
  10. ^ Friedl KE (1990). "Reappraisal of the health risks associated with the use of high doses of oral and injectable androgenic steroids". NIDA Res. Monogr. 102: 142–77. PMID 1964199. 
  11. ^ Raynaud, J.P.; Ojasoo, T.; Bouton, M.M.; Philibert, D. (1979). "Receptor Binding as a Tool in the Development of New Bioactive Steroids": 169–214. doi:10.1016/B978-0-12-060308-4.50010-X. 
  12. ^ Ojasoo T, Delettré J, Mornon JP, Turpin-VanDycke C, Raynaud JP (1987). "Towards the mapping of the progesterone and androgen receptors". J. Steroid Biochem. 27 (1-3): 255–69. doi:10.1016/0022-4731(87)90317-7. PMID 3695484. 
  13. ^ Raynaud JP, Bouton MM, Moguilewsky M, Ojasoo T, Philibert D, Beck G, Labrie F, Mornon JP (January 1980). "Steroid hormone receptors and pharmacology". J. Steroid Biochem. 12: 143–57. doi:10.1016/0022-4731(80)90264-2. PMID 7421203. 
  14. ^ Falconi, G., Rossi, G. L., & Ercoli, A. (1970). Quinestrol and other cyclopentyl ethers of estrogenic steroids: different rates of storage in body fat.