17β-Dihydroequilin

17β-Dihydroequilin
Clinical data
Synonyms β-Dihydroequilin; Δ7-17β-Estradiol; 7-Dehydro-17β-estradiol; Estra-1,3,5(10),7-tetraen-3,17β-diol; NSC-12170
Routes of
administration		 By mouth
Drug class Estrogen
Identifiers
CAS Number
PubChem CID
ChemSpider
UNII
ChEBI
ChEMBL
Chemical and physical data
Formula C18H22O22
Molar mass 270.366 g/mol
3D model (JSmol)

17β-Dihydroequilin is a naturally occurring estrogen sex hormone found in horses as well as a medication.[1][2] As the C3 sulfate ester sodium salt, it is a minor constituent (1.7%) of conjugated estrogens (CEEs; brand name Premarin).[1] However, as equilin, with equilin sulfate being a major component of CEEs, is transformed into 17β-dihydroequilin in the body, analogously to the conversion of estrone into estradiol, 17β-dihydroequilin is, along with estradiol, the most important estrogen responsible for the effects of CEEs.[1]

Pharmacology

Pharmacodynamics

17β-Dihydroequilin is an estrogen, or an agonist of the estrogen receptors (ERs), the ERα and ERβ.[1] In terms of relative binding affinity for the ERs, 17β-dihydroequilin has about 113% and 108% of that of estradiol for the ERα and ERβ, respectively.[1] 17β-Dihydroequilin has about 83% of the relative potency of CEEs in the vagina and 200% of the relative potency of CEEs in the uterus.[1] Of the equine estrogens, it shows the highest estrogenic activity and greatest estrogenic potency.[1]

Like CEEs as a whole, 17β-dihydroequilin has disproportionate effects in certain tissues such as the liver and uterus.[1] Equilin, the second major component of conjugated estrogens after estrone, is reversibly transformed into 17β-dihydroequilin analogously to the transformation of estrone into estradiol.[1] However, whereas the balance of mutual interconversion of estrone and estradiol is largely shifted in the direction of estrone, it is nearly equal in the case of equilin and 17β-dihydroequilin.[1] As such, although 17β-dihydroequilin is only a minor constituent of CEEs, it is, along with estradiol, the most important estrogen relevant to the estrogenic activity of the medication.[1]

Relative oral potencies of estrogens
EstrogenTypeHFVEUCaFSHLHHDL-CSHBGCBGAGTRatio
EstradiolBioidentical1.01.01.01.01.01.01.01.01.01.0
EstroneBioidenticalNDNDND0.30.3NDNDNDNDND
EstriolBioidentical0.30.30.10.3ND0.2NDNDND0.67
Estrone sulfateBioidenticalND0.90.90.90.90.50.90.71.50.56–1.7
Conjugated estrogensNatural1.21.52.01.11.01.53.01.55.01.3–4.5
Equilin sulfateNaturalNDNDNDNDND6.07.56.07.5ND
EthinylestradiolSynthetic120150401201004005006003502.9–5.0
DiethylstilbestrolSyntheticNDNDND3.4NDND25.624.519.55.7–7.5
Notes: Values are ratios, with estradiol as standard (i.e., 1.0). Abbreviations: HF = Clinical relief of hot flashes. VE = Increased proliferation of vaginal epithelium. UCa = Decrease in UCa. FSH = Suppression of FSH levels. LH = Suppression of LH levels. HDL-C, SHBG, CBG, and AGT = Increase in the serum levels of these hepatic proteins. Ratio = Ratio of liver protein effects to hot flashes relief and gonadotropin suppression. ND = No data. Type: Bioidentical = Identical to those found in humans. Natural = Naturally occurring but not identical to those found in humans (e.g., estrogens of other species). Synthetic = Man-made, does not naturally occur in animals or in the environment. Miscellaneous: Direct link to table. Sources: [1][3][4][5][6][7]

Pharmacokinetics

17β-Dihydroequilin has about 30% of the relative binding affinity of testosterone for sex hormone-binding globulin (SHBG), relative to 50% for estradiol.[1] The metabolic clearance rate of 17β-dihydroequilin is 1,250 L/day/m2, relative to 580 L/day/m2 for estradiol.[1]

Chemistry

17β-Dihydroequilin, or simply β-dihydroequilin, also known as δ7-17β-estradiol or as 7-dehydro-17β-estradiol, as well as estra-1,3,5(10),7-tetraen-3,17β-diol, is a naturally occurring estrane steroid and an analogue of estradiol.[1] In terms of chemical structure and pharmacology, equilin (δ7-estrone) is to 17β-dihydroequilin as estrone is to estradiol.[1]

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Kuhl H (2005). "Pharmacology of estrogens and progestogens: influence of different routes of administration" (PDF). Climacteric. 8 Suppl 1: 3–63. doi:10.1080/13697130500148875. PMID 16112947.
  2. ↑ Marc A. Fritz; Leon Speroff (28 March 2012). Clinical Gynecologic Endocrinology and Infertility. Lippincott Williams & Wilkins. pp. 751–. ISBN 978-1-4511-4847-3.
  3. ↑ Alfred S. Wolf; H.P.G. Schneider (12 March 2013). Östrogene in Diagnostik und Therapie. Springer-Verlag. pp. 78–. ISBN 978-3-642-75101-1.
  4. ↑ Manfred Kaufmann; Serban-Dan Costa; Anton Scharl (27 November 2013). Die Gynäkologie. Springer-Verlag. pp. 105–. ISBN 978-3-662-11496-4.
  5. ↑ Mashchak CA, Lobo RA, Dozono-Takano R, Eggena P, Nakamura RM, Brenner PF, Mishell DR (November 1982). "Comparison of pharmacodynamic properties of various estrogen formulations". Am. J. Obstet. Gynecol. 144 (5): 511–8. doi:10.1016/0002-9378(82)90218-6. PMID 6291391.
  6. ↑ Helgason S (1982). "Estrogen replacement therapy after the menopause. Estrogenicity and metabolic effects". Acta Obstet Gynecol Scand Suppl. 107: 1–29. doi:10.3109/00016348209155333. PMID 6282033.
  7. ↑ Lobo RA, Nguyen HN, Eggena P, Brenner PF (February 1988). "Biologic effects of equilin sulfate in postmenopausal women". Fertil. Steril. 49 (2): 234–8. doi:10.1016/S0015-0282(16)59708-8. PMID 3338581.


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