(-)-(S)-Equol

531-95-3

C15H14O3

DMSO : 100 mg/mL (412.76 mM; Need ultrasonic and warming)

Others; Metabolic Enzyme/Protease

(-)-(S)-Equol is a high affinity ligand for estrogen receptor beta with a K_i of 0.73 nM. IC50 & Target: Ki: 0.73 nM (Estrogen receptor beta)^[1] In Vitro: (-)-(S)-Equol shows the greatest affinity for ERbeta (Ki=0.73+/-0.2 nM), whereas its affinity for ERalpha (Ki=6.41+/-1 nM) is relatively poor^[1]. (-)-(S)-Equol inhibits the growth of LnCaP, DU145 and PC3 human prostate cancer cell lines. (-)-(S)-Equol causes cell cycle arrest in the G2/M phase in PC3 cells by down regulating cyclin B1 and CDK1 and upregulating CDK inhibitors (p21 and p27), as well as inducing apoptosis by upregulating Fas ligand (FasL) and the expression of pro-apoptotic Bim. (-)-(S)-Equol increases the expression of FOXO3a, decreases the expression of p-FOXO3a and enhances the nuclear stability of FOXO3a. (-)-(S)-Equol also decreases the expression of MDM2, which serves as an E3 ubiquitin ligase forp-FOXO3a, thus preventing p-FOXO3a degradation by the proteasome^[2]. (-)-(S)-Equol enantioselectively increases the survival of INS-1 cells presumably through activating PKA signaling. (-)-(S)-Equol might have applications as an anti-type 2 diabetic agent. In INS-1 pancreatic beta-cells, (-)-(S)-Equol induces phosphorylation of cAMP-response element-binding protein at Ser 133, and induced cAMP-response element-mediated transcription^[3]. In Vivo: (-)-(S)-Equol inhibits the tumor growth by 43.2% and 28.4% compared to the control on day 33, suggesting that the compound is not overtly toxic^[2].