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(S)-Equol is a potent estrogen receptor β (ERβ) agonist (EC50 = 65 nM). Exhibits 13-fold selectivity for ERβ over ERα. Atheroprotective. Protects against t-BHP induced apoptosis and attenuates ER stress in HUVECs. Activates Nrf2 signaling in vitro and in vivo. Inhibits tumor growth. Also dihydrotestosterone antagonist in vivo.
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Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Yuan et al (2016) Tyrosine phosphorylation regulates ERβ ubiquitination, protein turnover, and inhibition of breast cancer. Oncotarget. 7 42585 PMID: 27323858
Zhang et al (2016) Equol attenuates atherosclerosis in apolipoprotein e-deficient mice by inhibiting endoplasmic reticulum stress via activation of Nrf2 in endothelial cells. PLoS One. 11 e0167020 PMID: 27907038
Muthyala et al (2004) Equol, a natural estrogenic metabolite from soy isoflavones: convenient preparation and resolution of R- and S-equols and their differing binding and biological activity through estrogen receptors alpha and beta. Bioorg.Med.Chem. 12 1559 PMID: 15018930
Setchell et al (2005) S-equol, a potent ligand for estrogen receptor beta, is the exclusive enantiomeric form of the soy isoflavone metabolite produced by human intestinal bacterial flora. Am.J.Clin.Nutr. 81 1079 PMID: 15883431
Keywords: (S)-Equol, (S)-Equol supplier, agonist, estrogen, receptor, beta, ERb, ERbeta, ERβ, Nrf2, Estrogen, and, Related, Receptors, Androgen, Receptor, 6158, Tocris Bioscience
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