17-Epiestriol
(Synonyms: 17-环雌三醇) 目录号 : GC48819
A metabolite of estrone
Cas No.:1228-72-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
17-Epiestriol is a metabolite of estrone .1 It is formed from estrone via a 16α-hydroxy estrone intermediate by reduction of the C-17 ketone. 17-Epiestriol binds to estrogen receptor α (ERα) and ERβ with relative binding affinities of 29 and 80 compared with 17β-estradiol .2
1.Brinton, L.A., Trabert, B., Anderson, G.L., et al.Serum estrogens and estrogen metabolites and endometrial cancer risk among postmenopausal womenCancer Epidemiol. Biomarkers Prev.25(7)1081-1089(2016) 2.Kuiper, G.G.J.M., Lemmen, J.G., Carlsson, B., et al.Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor βEndocrinology139(10)4252-4263(1998)
| Cas No. | 1228-72-4 | SDF | |
| 别名 | 17-环雌三醇 | ||
| Canonical SMILES | C[C@@]12[C@](C[C@H]([C@H]2O)O)([H])[C@@]3([H])[C@@](CC1)([H])C4=CC=C(O)C=C4CC3 | ||
| 分子式 | C18H24O3 | 分子量 | 288.4 |
| 溶解度 | Methanol: slightly soluble | 储存条件 | -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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4674 mL | 17.337 mL | 34.6741 mL |
| 5 mM | 0.6935 mL | 3.4674 mL | 6.9348 mL |
| 10 mM | 0.3467 mL | 1.7337 mL | 3.4674 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。
Regiospecificity and stereospecificity of human UDP-glucuronosyltransferases in the glucuronidation of estriol, 16-epiestriol, 17-Epiestriol, and 13-epiestradiol
Drug Metab Dispos 2013 Mar;41(3):582-91.PMID:23288867DOI:10.1124/dmd.112.049072.
The glucuronidation of estriol, 16-epiestriol, and 17-Epiestriol by the human UDP-glucuronosyltransferases (UGTs) of subfamilies 1A, 2A, and 2B was examined. UGT1A10 is highly active in the conjugation of the 3-OH in all these estriols, whereas UGT2B7 is the most active UGT toward one of the ring D hydroxyls, the 16-OH in estriol and 16-epiestriol, but the 17-OH in 17-Epiestriol. Kinetic analyses indicated that the 17-OH configuration plays a major role in the affinity of UGT2B7 for estrogens. The glucuronidation of the different estriols by the human liver and intestine microsomes reflects the activity of UGT1A10 and UGT2B7 in combination with the tissues' difference in UGT1A10 expression. The UGT1A10 mutant 1A10-F93G exhibited much higher V(max) values than UGT1A10 in estriol and 17-Epiestriol glucuronidation, but a significantly lower value in 16-epiestriol glucuronidation. To this study on estriol glucuronidation we have added experiments with 13-epiestradiol, a synthetic estradiol in which the spatial arrangement of the methyl on C18 and the hydroxyl on C17 is significantly different than in other estrogens. In comparison with estradiol glucuronidation, the C13 configuration change decreases the turnover of UGTs that conjugate the 3-OH, but increases it in UGTs that primarily conjugate the 17-OH. Unexpectedly, UGT2B17 exhibited similar conjugation rates of both the 17-OH and 3-OH of 13-espiestradiol. The combined results reveal the strong preference of UGT1A10 for the 3-OH of physiologic estrogens and the equivalently strong preference of UGT2B7 and UGT2B17 for the hydroxyls on ring D of such steroid hormones.
17-Epiestriol, an estrogen metabolite, is more potent than estradiol in inhibiting vascular cell adhesion molecule 1 (VCAM-1) mRNA expression
J Biol Chem 2003 Apr 4;278(14):11746-52.PMID:12547825DOI:10.1074/jbc.M207800200.
17-beta estradiol (17-beta E(2)) attenuates the expression of vascular cell adhesion molecule 1 (VCAM-1) in vivo at physiological levels (pg/ml), whereas supraphysiological concentrations of 17-beta E(2) (ng/ml) are required in vitro. We assessed whether a metabolite of estrogen, which could only be generated in vivo, might be a more potent inhibitor of VCAM-1 expression and thereby explain this discrepancy. We report here that 17-Epiestriol, an estrogen metabolite and a selective estrogen receptor (ER) beta agonist, is approximately 400x more potent than 17-beta E(2) in suppressing tumor necrosis factor (TNF) alpha-induced VCAM-1 mRNA as well as protein expression in human umbilical vein endothelial cells. Genistein, an ERbeta agonist, at low concentrations (1 and 10 nm) also suppressed TNFalpha-induced VCAM-1 mRNA expression. These actions of 17-Epiestriol and genistein were significantly attenuated in the presence of the estrogen receptor antagonist ICI-182780. Other estrogenic compounds such as ethinyl estradiol and estrone did not have any effect on TNFalpha-induced VCAM-1 expression at the concentrations tested. We further show that, 1) 17-Epiestriol induces the expression of endothelial nitric-oxide synthase mRNA and protein, 2) 17-Epiestriol prevents TNFalpha-induced migration of NFkappaB into the nucleus, 3) N(G)-nitro-l-arginine methyl ester, an inhibitor of NO synthesis, abolishes 17-epiestriol-mediated inhibition of TNFalpha-induced VCAM-1 expression and migration of NFkappaB from the cytoplasm to the nucleus. Our results indicate that 17-Epiestriol is more potent than 17-beta E(2) in suppressing TNFalpha-induced VCAM-1 expression and that this action is modulated at least in part through NO.
Urinary estrogen metabolites and gastric cancer risk among postmenopausal women
Cancer Rep (Hoboken) 2022 Jul;5(7):e1574.PMID:34766475DOI:10.1002/cnr2.1574.
Background: The overall incidence of gastric cancer in women is half that in men for most global populations. Sex hormone pathways may be involved in carcinogenesis and estrogens have been postulated to protect women against gastric cancer. Aim: To evaluate associations of gastric cancer with estrogen metabolites in postmenopausal women. Methods and results: We performed an analysis of 233 gastric cancer cases and 281 age-matched controls from three prospective cohorts and two case-control studies of early-stage gastric cancer, mainly conducted in high-risk Asian populations. Fifteen estrogen-parent (estrone and estradiol) and -metabolite analytes (2-hydroxyestrone, 2-hydroxyestradiol, 2-hydroxyestrone-3-methyl ether, 4-hydroxyestrone; 4-methoxyestrone, 4-methoxyestradiol, 2-methoxyestrone, 2-methoxyestradiol, estriol, 16α-hydroxyestrone, 16-ketoestradiol, 16-epiestriol, and 17-Epiestriol) were measured in spot urines using liquid chromatography-tandem mass spectrometry. Odds ratios for association with each marker were estimated by logistic regression. Heterogeneity was assessed by Cochran's Q test. Study-specific odds ratios were pooled by fixed-effects meta-analysis. Urinary levels of estrogen-related molecules were not associated with gastric cancer (adjusted odds ratios ranged from 0.87 to 1.27; p-values >.05), with low between-study heterogeneity (p-values >.1) for all but two metabolites (2-hydroxyestrone-3-methyl ether and 2-methoxyestradiol). Conclusion: To date, this is the first comprehensive assessment of endogenous estrogens with gastric cancer risk in women. Estrogens do not appear to have an etiologic role in gastric cancer risk among postmenopausal women. Given the complex network of sex steroid hormones and their extreme variation over the lifespan, further evaluation of this hypothesis is warranted.
Caffeine, coffee, and tea intake and urinary estrogens and estrogen metabolites in premenopausal women
Cancer Epidemiol Biomarkers Prev 2015 Aug;24(8):1174-83.PMID:26063478DOI:10.1158/1055-9965.EPI-15-0246.
Background: Prior studies have found weak inverse associations between breast cancer and caffeine and coffee intake, possibly mediated through their effects on sex hormones. Methods: High-performance liquid chromatography/tandem mass spectrometry was used to quantify levels of 15 individual estrogens and estrogen metabolites (EM) among 587 premenopausal women in the Nurses' Health Study II with mid-luteal phase urine samples and caffeine, coffee, and/or tea intakes from self-reported food frequency questionnaires. Multivariate linear mixed models were used to estimate geometric means of individual EM, pathways, and ratios by intake categories, and P values for tests of linear trend. Results: Compared with women in the lowest quartile of caffeine consumption, those in the top quartile had higher urinary concentrations of 16α-hydroxyestrone (28% difference; Ptrend = 0.01) and 16-epiestriol (13% difference; Ptrend = 0.04), and a decreased parent estrogens/2-, 4-, 16-pathway ratio (Ptrend = 0.03). Coffee intake was associated with higher 2-catechols, including 2-hydroxyestradiol (57% difference, ≥4 cups/day vs. ≤6 cups/week; Ptrend = 0.001) and 2-hydroxyestrone (52% difference; Ptrend = 0.001), and several ratio measures. Decaffeinated coffee was not associated with 2-pathway metabolism, but women in the highest (vs. lowest) category of intake (≥2 cups/day vs. ≤1-3 cups/month) had significantly lower levels of two 16-pathway metabolites, estriol (25% difference; Ptrend = 0.01) and 17-Epiestriol (48% difference; Ptrend = 0.0004). Tea intake was positively associated with 17-Epiestriol (52% difference; Ptrend = 0.01). Conclusion: Caffeine and coffee intake were both associated with profiles of estrogen metabolism in premenopausal women. Impact: Consumption of caffeine and coffee may alter patterns of premenopausal estrogen metabolism.
Individual and cyclic estrogenic profile in women: Structure and variability of the data
Steroids 2019 Oct;150:108432.PMID:31279660DOI:10.1016/j.steroids.2019.108432.
The concentration of estrogens in the body fluids of women is highly variable, due to the menstrual cycle, circadian oscillations, and other physiological and pathological causes. To date, only the cyclic fluctuations of the principal estrogens (estradiol and estrone) have been studied, with limited outcome of general significance. Aim of the present study was to examine in detail the cyclic variability of a wide estrogens' panel and to interpret it by multivariate statistics. Four estrogens (17α-estradiol, 17β-estradiol, estrone, estriol) and eleven of their metabolites (4-methoxyestrone, 2-methoxyestrone, 16α-hydroxyestrone, 4-hydroxyestrone, 2-hydroxyestrone, 4-methoxyestradiol, 2-methoxyestradiol, 4-hydroxyestradiol, 2-hydroxyestradiol, estriol, 16-epiestriol, and 17-Epiestriol) were determined in urine by a gas chromatography - mass spectrometry method, which was developed by design of experiments and fully validated according to ISO 17025 requirements. Then, urine samples collected every morning for a complete menstrual cycle from 9 female volunteers aged 24-35 years (1 parous) were analysed. The resulting three-dimensional data (subjects × days × estrogens) were interpreted using several statistical tools. Parallel Factor Analysis compared the estrogen profiles in order to explore the cyclic and inter-individual variability of each analyte. Principal Component Analysis (PCA) provided clear separation of the sampling days along the cycle, allowing discrimination among the luteal, ovulation, and follicular phases. The scores obtained from PCA were used to build a Linear Discriminant Analysis classification model which enhanced the recognition of the three cycle's phases, yielding an overall classification non-error rate equal to 90%. These statistical models may find prospective application in fertility studies and the investigation of endocrinology disorders and other hormone-dependent diseases.