17β-Dihydroequilin

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17β-Dihydroequilin
17β-Dihydroequilin.svg
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[edit]

Pharmacodynamics[edit]

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
Estrogen Type HF FSH HDL-C SHBG CBG AGT Ratio
Estradiol Bioidentical 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Estriol Bioidentical 0.3 0.3 0.2 ND ND ND 0.67
Estrone sulfate Bioidentical ND 0.9 0.5 0.9 0.7 1.5 0.56–1.7
Conjugated estrogens Natural 1.2 1.1 1.5 3.0 1.5 5.0 1.3–4.5
Equilin sulfate Natural ND ND 6.0 7.5 6.0 7.5 ND
Ethinylestradiol Synthetic 120 120 400 500 600 350 2.9–5.0
Diethylstilbestrol Synthetic ND 3.4 ND 25.6 24.5 19.5 5.7–7.5
HF = clinical relief of hot flashes. FSH = suppression of FSH 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 FSH suppression. 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. ND = no data. Sources:[1][3][4][5]

Pharmacokinetics[edit]

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[edit]

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[edit]

  1. ^ a b c d e f g h i j k l m n o p 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. ^ 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. 
  4. ^ 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. 
  5. ^ 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.