(R)-Equol
(Synonyms: R-雌马酚,(+)-Equol) 目录号 : GC40643
An estrogen receptor α agonist
Cas No.:221054-79-1
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Cell viability is determined using the well-established MTT assay. Cells are seeded (1.25×105 cells/mL) in 96-well plates in experimental medium (100 μL/well) and incubated for 48 h at 37°C in a 95 % air/5 % CO2 humidified atmosphere. Medium is then replaced with fresh medium containing (R)-Equol (R-equol) (2.5, 10 or 50 μM) or DMSO only as a control. Following 48-h incubation, cell viability is assessed[2]. |
Animal experiment: | To investigate the chemopreventive effects of dietary (R)-Equol against chemically induced mammary cancer, female Sprague-Dawley rats bred in-house are fed a soy-free AIN-93G diet from birth to 35 days of age, then separated into different groups. Group 1 (Control group, n=40) continues on this diet, whereas the other group of animals are fed the AIN-93G diet supplemented with 250 mg/kg of (R)-Equol (Group 3, n=41) beginning on day 35 until killing on day 190[3]. |
References: [1]. Setchell KD, et al. 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. 2005 May;81(5):1072-9. | |
(R)-Equol is an agonist of both ERα and ERβ with Kis of 27.4 and 15.4 nM, respectively.
(R)-Equol is an agonist of both ERα and ERβ with Kis of 27.4 and 15.4 nM, respectively[1]. (R)-Equol induces a dose-dependent inhibitory effect on the invasive capacity of MDA-MB-231 cells that is significant at the highest concentration tested (50 μM). Following 48-h exposure to (R)-Equol, invasion is reduced by 62% (p=0.009, versus untreated cells) with 50 μM (R)-Equol. Matrix metalloproteinase-2 (MMP-2) expression is significantly down-regulated following treatment with 50 μM (R)-Equol (p=0.035)[2].
Animals fed (R)-Equol have a significantly reduced number of palpable tumors over time when compare with Controls (P=0.002). Furthermore, the number of palpable tumors formed per rat in the (R)-Equol-fed group is significantly lower than that of rats treated with S-(-)equol (P=0.008). (R)-Equol-fed animals have 43% fewer tumors than the control group and this difference is highly statistically significant (P=0.004). The number of tumors/tumor-bearing animal is significantly lower in the animals fed (R)-Equol compare with Controls (3.3±0.4 versus 5.5±0.5, P=0.004). At necropsy, the mean (±SEM) tumor weight per animal for (R)-Equol fed rats (5.3±1.1 mg) is significantly reduced (P=0.04) when compare with Controls (9.9±1.4 mg). Feeding the (R)-Equol diet results in significantly increased tumor latency (P=0.003)[3].
References:
[1]. Setchell KD, et al. 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. 2005 May;81(5):1072-9.
[2]. Magee PJ, et al. Daidzein, R-(+)equol and S-(-)equol inhibit the invasion of MDA-MB-231 breast cancer cells potentially via the down-regulation of matrix metalloproteinase-2. Eur J Nutr. 2014 Feb;53(1):345-50.
[3]. Brown NM, et al. The chemopreventive action of equol enantiomers in a chemically induced animal model of breast cancer. Carcinogenesis. 2010 May;31(5):886-93.
| Cas No. | 221054-79-1 | SDF | |
| 别名 | R-雌马酚,(+)-Equol | ||
| Canonical SMILES | OC1=CC=C2C(OC[C@@H](C3=CC=C(O)C=C3)C2)=C1 | ||
| 分子式 | C15H14O3 | 分子量 | 242.3 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml,Ethanol:PBS (pH 7.2) (1:10): 0.1 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 4.1271 mL | 20.6356 mL | 41.2712 mL |
| 5 mM | 0.8254 mL | 4.1271 mL | 8.2542 mL |
| 10 mM | 0.4127 mL | 2.0636 mL | 4.1271 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
(S)-Equol Is More Effective than (R)-Equol in Inhibiting Osteoclast Formation and Enhancing Osteoclast Apoptosis, and Reduces Estrogen Deficiency-Induced Bone Loss in Mice
J Nutr 2022 Aug 9;152(8):1831-1842.PMID:35675296DOI:10.1093/jn/nxac130.
Background: Equol, a metabolite of daidzein, binds to the estrogen receptor with greater affinity than daidzein and exhibits various biological properties. It exists as an enantiomer, either (S)-equol or (R)-Equol. Objectives: We have previously shown that the inhibitory effect of (S)-equol on bone fragility is stronger than that of racemic equol in ovariectomized (OVX) mice; however, the effect of (R)-Equol has not been elucidated. The aim of this study was to compare the activities of equol enantiomers on bone metabolism in vitro and in vivo. Methods: Bone marrow cells (BMCs) and RAW 264.7 cells were treated with equol enantiomers. The number of osteoclasts and caspase-3/7 activity were measured. We examined the effect of equol enantiomers on osteoblast differentiation in MC3T3-E1 cells. In vivo, 8-wk-old female ddY mice were assigned to 4 groups: sham-operated (sham), OVX, OVX + 0.5 mg/d of (S)-equol (S-eq), and OVX + 0.5 mg/d of (R)-Equol (R-eq). Four weeks after the intervention, femoral bone mineral density (BMD) and osteoclastic gene expression were analyzed, along with concentrations of equol enantiomers in the serum and tissues. Results: (S)-equol and (R)-Equol inhibited osteoclast differentiation in BMCs (97% and 60%, P < 0.05) and RAW 264.7 cells (83% and 68%, P < 0.05). (S)-equol promoted apoptosis of mature osteoclasts by inducing caspase-3/7 activity (29%, P < 0.05) and enhanced osteoblast differentiation (29%, P < 0.05). In OVX mice, BMD was ameliorated in (S)-equol-treated mice (11%, P < 0.05), but not in (R)-equol-treated mice. The concentrations of (S)-equol were greater than those of (R)-Equol in the serum, tibia, liver, and kidney (by 148%, 80%, 22%, and 139%, respectively). Conclusions: These results suggest that (S)-equol is more effective than (R)-Equol in inhibiting osteoclast formation and enhancing osteoclast apoptosis in vitro, supporting the beneficial effect of (S)-equol to reduce estrogen deficiency-induced bone loss in OVX mice.
R- and S-equol have equivalent cytoprotective effects in Friedreich's ataxia
BMC Pharmacol Toxicol 2012 Oct 22;13:12.PMID:23088310DOI:10.1186/2050-6511-13-12.
Background: Estradiol (E2) is a very potent cytoprotectant against a wide variety of cellular insults in numerous different cell models, including a Friedreich's ataxia (FRDA) model. Previously, we demonstrated that estrogen-like compounds are able to prevent cell death in an FRDA model independent of any known estrogen receptor (ER) by reducing reactive oxygen species (ROS) and the detrimental downstream effects of ROS buildup including oxidative damage to proteins and lipids and impaired mitochondrial function. Results: We have previously demonstrated by western blot that our cell model lacks ERα and expresses only very low levels of ERβ. Using L-buthionine (S,R)-sulfoximine (BSO) to induce oxidative stress in human FRDA fibroblasts, we determine the potency and efficacy of the soy-derived ERβ agonist S-equol and its ERα-preferring enantiomer, R-equol in vitro on cell viability and ROS accumulation. Here we demonstrate that these equol biphenolic compounds, while significantly less potent and efficacious than E2, provide statistically similar attenuation of ROS and cytoprotection against a BSO-induced oxidative insult. Conclusions: These preliminary data demonstrate that estrogen and soy-derived equols could have a beneficial effect in delaying the onset and decreasing the severity of symptoms in FRDA patients by an antioxidant mechanism. In addition, these data confirm that the protection seen previously with E2 was indeed unrelated to ER binding.
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 2004 Mar 15;12(6):1559-67.PMID:15018930DOI:10.1016/j.bmc.2003.11.035.
Equol is a metabolite produced in vivo from the soy phytoestrogen daidzein by the action of gut microflora. It is known to be estrogenic, so human exposure to equol could have significant biological effects. Equol is a chiral molecule that can exist as the enantiomers R-equol and S-equol. To study the biological activity of racemic (+/-)-Equol, as well as that of its pure enantiomers, we developed an efficient and convenient method to prepare (+/-)-Equol from available isoflavanoid precursors. Furthermore, we optimized a method to separate the enantiomers of equol by chiral HPLC, and we studied for the first time, the activities of the enantiomers on the two estrogen receptors, ERalpha and ERbeta. In binding assays, S-equol has a high binding affinity, preferential for ERbeta (K(i)[ERbeta]=16 nM; beta/alpha=13 fold), that is comparable to that of genistein (K(i)[ERbeta]=6.7 nM; beta/alpha=16), whereas R-equol binds more weakly and with a preference for ERalpha (K(i)[ERalpha]=50 nM; beta/alpha=0.29). All equol isomers have higher affinity for both ERs than does the biosynthetic precursor daidzein. The availability and the in vitro characterization of the equol enantiomers should enable their biological effects to be studied in detail.
Equol induces apoptosis in human hepatocellular carcinoma SMMC-7721 cells through the intrinsic pathway and the endoplasmic reticulum stress pathway
Anticancer Drugs 2014 Jul;25(6):633-40.PMID:24487643DOI:10.1097/CAD.0000000000000085.
Equol, a microbial metabolite of the isoflavone daidzein, is currently receiving much attention because of its strong antiproliferative effect on hormone-related human breast cancer cells; however, in our previous study, we observed that racemic equol [(±)-Equol] shows the highest antiproliferative effect on human hepatocellular carcinoma SMMC-7721 cells compared with other cells, including human breast cancer MCF-7 and MDA-MB-231 cell lines. In the present study, we use the SMMC-7721 cancer cell line to investigate the mechanisms of (±)-equol-induced, R-(+)-equol-induced, and S-(-)-equol-induced apoptosis. Our purpose was to provide some guidelines to introduce equol into a clinical situation. R-(+)-Equol and S-(-)-Equol were prepared from (±)-Equol by chiral stationary phase high performance liquid chromatography. The antiproliferative effect of equol on SMMC-7721 cells was investigated by crystal violet staining. Equol-induced apoptosis was detected by acridine orange/ethidium bromide staining and by flow cytometry. Western blotting was performed to study the molecular mechanisms of equol-induced apoptosis. The results showed that (±)-Equol, R-(+)-Equol, and S-(-)-Equol inhibited the proliferation of SMMC-7721 cells in a concentration-dependent manner. Exposure of SMMC-7721 cells to equol caused significant cell cycle arrest in the S-phase. In addition, equol was shown to induce endoplasmic reticulum stress-mediated apoptosis by activating caspase-12 and caspase-8, and by upregulating Chop and Bip. Mitochondrion-mediated apoptosis was caused by upregulation of Bax and downregulation of Bcl-2, followed by activation of caspase-9, caspase-3, and cleaved poly (ADP-ribose) polymerase, respectively. This is the first report that shows that R-(+)-Equol, S-(-)-Equol, and (±)-Equol can induce apoptosis of human hepatocellular carcinoma SMMC-7721 cells through the intrinsic pathway and the endoplasmic reticulum stress pathway.
[Effects of equol on proliferation of colorectal cancer HCT-15 cell]
Wei Sheng Yan Jiu 2019 Sep;48(5):803-806.PMID:31601322doi
Objective: To investigate the effect of racemic equol and equol enantiomers on the proliferation of colorectal cancer HCT-15 cell and the potential mechanism. Methods: 3-( 4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide( MTT) assay was used to detect the effect of different concentrations of racemic equol and equol enantiomers( 0, 0. 5, 1, 5 and 10 μmol/L) on the proliferation of colorectal cancer HCT-15 cell. Western blot was used to detect the expression of estrogen receptor( ER)and nuclear factor 2 related factor 2( Nrf2). Results: Racemic equol and( R) equol inhibited the proliferation of HCT-15 cell in a dose-dependent manner, whereas( S) equol had no effect on the proliferation of HCT-15 cell. Racemic equol increased the expression of ERβ and Nrf2, while( R) equol increased the expression of Nrf2. Conclusion: Racemic equol can inhibit the proliferation of HCT-15 cell through estrogenic and antioxidative activity. R equol can inhibit the proliferation of HCT-15 cell through antioxidative activity, while( S) equol has no effect on the proliferation of HCT-15 cell.