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E2-3G; 17β-Estradiol 3-(β-D-glucuronide); 17β-Hydroxyestra-1,3,5(10)-trien-3-yl β-D-glucopyranosiduronic acid;
3D model (JSmol)
CompTox Dashboard (EPA)
|Molar mass||448.512 g/mol|
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Estradiol 3-glucuronide (E2-3G), also known as 17β-estradiol 3-(β-D-glucuronide), is a naturally occurring and endogenous estrogen conjugate. It is specifically the C3 glucuronide conjugate of estradiol, the major estrogen in the body. It is formed from estradiol in the liver by UDP-glucuronosyltransferase via attachment of glucuronic acid and is eventually excreted in urine and bile. Similarly to estrogen sulfates like estrone sulfate, estrogen glucuronides have much higher water solubility than do unconjugated estrogens like estradiol.
Estrogen glucuronides can be deconjugated into the corresponding free estrogens by β-glucuronidase in tissues that express this enzyme, such as the mammary gland. As a result, estrogen glucuronides have estrogenic activity via conversion into estrogens.
|Estrogen||Other names||RBA (%)a||REP (%)b|
|Estradiol 3-sulfate||E2S; E2-3S||?||0.02||0.04|
|Estradiol benzoate||EB; Estradiol 3-benzoate||10||1.1||0.52|
|Estradiol diacetate||EDA; Estradiol 3,17β-diacetate||?||0.79||?|
|Estradiol propionate||EP; Estradiol 17β-propionate||19–26||2.6||?|
|Estradiol valerate||EV; Estradiol 17β-valerate||2–11||0.04–21||?|
|Estradiol cypionate||EC; Estradiol 17β-cypionate||?c||4.0||?|
|Estradiol palmitate||Estradiol 17β-palmitate||0||?||?|
|Estradiol stearate||Estradiol 17β-stearate||0||?||?|
|Estrone sulfate||E1S; Estrone 3-sulfate||2||0.004||0.002|
|Estrone glucuronide||E1G; Estrone 3-glucuronide||?||<0.001||0.0006|
|Mestranol||EE 3-methyl ether||1||1.3–8.2||0.16|
|Quinestrol||EE 3-cyclopentyl ether||?||0.37||?|
|Footnotes: a = Relative binding affinities (RBAs) were determined via in-vitro displacement of labeled estradiol from estrogen receptors (ERs) generally of rodent uterine cytosol. Estrogen esters are variably hydrolyzed into estrogens in these systems (shorter ester chain length -> greater rate of hydrolysis) and the ER RBAs of the esters decrease strongly when hydrolysis is prevented. b = Relative estrogenic potencies (REPs) were calculated from half-maximal effective concentrations (EC50) that were determined via in-vitro β‐galactosidase (β-gal) and green fluorescent protein (GFP) expression assays in yeast expressing human ERα and human ERβ. Both mammalian cells and yeast have the capacity to hydrolyze estrogen esters. c = The affinities of estradiol cypionate for the ERs are similar to those of estradiol valerate and estradiol benzoate (figure). Sources: See template page.|
- Zhu BT, Conney AH (January 1998). "Functional role of estrogen metabolism in target cells: review and perspectives". Carcinogenesis. 19 (1): 1–27. doi:10.1093/carcin/19.1.1. PMID 9472688.
- 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.
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