Template:Affinities and estrogenic potencies of estrogen esters and ethers at the estrogen receptors
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| Estrogen | Other names | RBA (%)a | REP (%)b | |||
|---|---|---|---|---|---|---|
| ER | ERα | ERβ | ||||
| Estradiol | E2 | 100 | 100 | 100 | ||
| Estradiol 3-sulfate | E2S; E2-3S | ? | 0.02 | 0.04 | ||
| Estradiol 3-glucuronide | E2-3G | ? | 0.02 | 0.09 | ||
| Estradiol 17β-glucuronide | E2-17G | ? | 0.002 | 0.0002 | ||
| Estradiol benzoate | EB; Estradiol 3-benzoate | 10 | 1.1 | 0.52 | ||
| Estradiol 17β-acetate | E2-17A | 31–45 | 24 | ? | ||
| 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 | E1; 17-Ketoestradiol | 11 | 5.3–38 | 14 | ||
| Estrone sulfate | E1S; Estrone 3-sulfate | 2 | 0.004 | 0.002 | ||
| Estrone glucuronide | E1G; Estrone 3-glucuronide | ? | <0.001 | 0.0006 | ||
| Ethinylestradiol | EE; 17α-Ethynylestradiol | 100 | 17–150 | 129 | ||
| 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.[1][2] 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) production assays in yeast expressing human ERα and human ERβ. Both mammalian cells and yeast have the capacity to hydrolyze estrogen esters.[3] c = The affinities of estradiol cypionate for the ERs are similar to those of estradiol valerate and estradiol benzoate (figure).[4] Sources: Affinities: [1][2][5][6][7] Estrogenic potencies: [8][9][10][11] Additional: [4][3][12] | ||||||
Template documentationSee also
- Template:Affinities of estrogen receptor ligands for the ERα and ERβ
- Template:Relative affinities of estrogens for steroid hormone receptors and blood proteins
- Template:Selected biological properties of endogenous estrogens in rats
References
- ^ a b Janocko L, Larner JM, Hochberg RB (April 1984). "The interaction of C-17 esters of estradiol with the estrogen receptor". Endocrinology. 114 (4): 1180–6. doi:10.1210/endo-114-4-1180. PMID 6705734.
- ^ a b Abul-Hajj YJ, Nurieddin A (October 1983). "Significance of lipoidal estradiol in human mammary tumors". Steroids. 42 (4): 417–26. doi:10.1016/0039-128x(83)90140-x. PMID 6679946.
- ^ a b Hoogenboom LA, de Haan L, Hooijerink D, Bor G, Murk AJ, Brouwer A (February 2001). "Estrogenic activity of estradiol and its metabolites in the ER-CALUX assay with human T47D breast cells". APMIS. 109 (2): 101–7. doi:10.1034/j.1600-0463.2001.d01-110.x. PMID 11398990.
- ^ a b Dubey RK, Jackson EK, Gillespie DG, Zacharia LC, Imthurn B, Keller PJ (April 2000). "Clinically used estrogens differentially inhibit human aortic smooth muscle cell growth and mitogen-activated protein kinase activity". Arterioscler. Thromb. Vasc. Biol. 20 (4): 964–72. doi:10.1161/01.atv.20.4.964. PMID 10764660.
- ^ Kuhl H (September 1990). "Pharmacokinetics of oestrogens and progestogens". Maturitas. 12 (3): 171–97. doi:10.1016/0378-5122(90)90003-o. PMID 2170822.
- ^ Kuhl, Herbert; Taubert, Hans-Dieter (1987). Das Klimakterium – Pathophysiologie, Klinik, Therapie [The Climacteric – Pathophysiology, Clinic, Therapy] (in German). Stuttgart, Germany: Thieme Verlag. p. 122. ISBN 978-3137008019.
- ^ Matthews J, Celius T, Halgren R, Zacharewski T (November 2000). "Differential estrogen receptor binding of estrogenic substances: a species comparison". J. Steroid Biochem. Mol. Biol. 74 (4): 223–34. doi:10.1016/s0960-0760(00)00126-6. PMID 11162928.
- ^ Bovee TF, Helsdingen RJ, Rietjens IM, Keijer J, Hoogenboom RL (July 2004). "Rapid yeast estrogen bioassays stably expressing human estrogen receptors alpha and beta, and green fluorescent protein: a comparison of different compounds with both receptor types". J. Steroid Biochem. Mol. Biol. 91 (3): 99–109. doi:10.1016/j.jsbmb.2004.03.118. PMID 15276617.
- ^ Mu Y, Peng S, Zhang A, Wang L (February 2011). "Role of pocket flexibility in the modulation of estrogen receptor alpha by key residue arginine 394". Environ. Toxicol. Chem. 30 (2): 330–6. doi:10.1002/etc.389. PMID 21038436.
- ^ Yang R, Li N, Ma M, Wang Z (November 2014). "Combined effects of estrogenic chemicals with the same mode of action using an estrogen receptor binding bioassay". Environ. Toxicol. Pharmacol. 38 (3): 829–37. doi:10.1016/j.etap.2014.10.001. PMID 25461542.
- ^ Luo J, Lei B, Ma M, Zha J, Wang Z (July 2011). "Identification of estrogen receptor agonists in sediments from Wenyu River, Beijing, China". Water Res. 45 (13): 3908–14. doi:10.1016/j.watres.2011.04.045. PMID 21621810.
- ^ Rutishauser BV, Pesonen M, Escher BI, Ackermann GE, Aerni HR, Suter MJ, Eggen RI (April 2004). "Comparative analysis of estrogenic activity in sewage treatment plant effluents involving three in vitro assays and chemical analysis of steroids". Environ. Toxicol. Chem. 23 (4): 857–64. doi:10.1897/03-286. PMID 15095880.