17α-Epiestriol

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17α-Epiestriol
17α-Epiestriol.svg
Names
IUPAC name
(1S,10R,11S,13R,14S,15S)-15-methyltetracyclo[8.7.0.0²,⁷.0¹¹,¹⁵]heptadeca-2,4,6-triene-5,13,14-triol
Other names
17-Epiestriol; 16α-Hydroxy-17α-estradiol; Estra-1,3,5(10)-triene-3,16α,17α-triol; 3,16α,17α-Trihydroxy-1,3,5(10)-estratriene
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
UNII
Properties
C18H24O3
Molar mass 288.38136 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

17α-Epiestriol, or simply 17-epiestriol, also known as 16α-hydroxy-17α-estradiol or estra-1,3,5(10)-triene-3,16α,17α-triol, is a minor and weak endogenous estrogen, and the 17α-epimer of estriol (which is 16α-hydroxy-17β-estradiol).[1][2][3] It is formed from 16α-hydroxyestrone;[4][5] in contrast to other endogenous estrogens like estradiol, 17α-epiestriol is a selective agonist of the ERβ.[6] It is described as a relatively weak estrogen, which is in accordance with its relatively low affinity for the ERα.[7] 17α-Epiestriol has been found to be approximately 400-fold more potent than estradiol in inhibiting tumor necrosis factor α (TNFα)-induced vascular cell adhesion molecule 1 (VCAM-1) expression in vitro.[8]

See also[edit]

References[edit]

  1. ^ Ashutosh K Tewari (5 April 2013). Prostate Cancer: A Comprehensive Perspective. Springer Science & Business Media. pp. 373–. ISBN 978-1-4471-2864-9. 
  2. ^ A. Labhart (6 December 2012). Clinical Endocrinology: Theory and Practice. Springer Science & Business Media. pp. 522–. ISBN 978-3-642-96158-8. 
  3. ^ N. S. Assali (3 September 2013). The Maternal Organism. Elsevier. pp. 341–. ISBN 978-1-4832-6380-9. 
  4. ^ U.S. Von Euler (2 December 2012). Comparative Endocrinology. Elsevier Science. pp. 135–. ISBN 978-0-323-14609-8. 
  5. ^ Norbert W. Tietz (1 August 1976). Fundamentals of clinical chemistry. Saunders. p. 773. ISBN 978-0-7216-8866-4. 
  6. ^ Gajanan V. Sherbet (26 July 2013). Therapeutic Strategies in Cancer Biology and Pathology. Elsevier. pp. 83–. ISBN 978-0-12-416590-8. 
  7. ^ Ralph I. Dorfman (22 October 2013). Steroidal Activity in Experimental Animals and Man. Elsevier Science. pp. 13–. ISBN 978-1-4832-7299-3. 
  8. ^ Mukherjee, T. K.; Nathan, L.; Dinh, H.; Reddy, S. T.; Chaudhuri, G. (2003). "17-Epiestriol, an Estrogen Metabolite, Is More Potent Than Estradiol in Inhibiting Vascular Cell Adhesion Molecule 1 (VCAM-1) mRNA Expression". Journal of Biological Chemistry. 278 (14): 11746–11752. doi:10.1074/jbc.M207800200. ISSN 0021-9258. PMID 12547825. 
  9. ^ 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. 
  10. ^ Ojasoo T, Raynaud JP (November 1978). "Unique steroid congeners for receptor studies". Cancer Res. 38 (11 Pt 2): 4186–98. PMID 359134. 
  11. ^ 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. 
  12. ^ 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.