16-Epiestriol
(Synonyms: 异雌三醇,16-epi-Estriol; 16β,17β-Estriol) 目录号 : GC49068
A metabolite of estrone
Cas No.:547-81-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
16-Epiestriol is a metabolite of the endogenous estrogen estrone .1 It is formed from estrone via a 16β-hydroxy estrone intermediate by reduction of the C-17 ketone. 16-Epiestriol (200 µg/ml) inhibits the growth of carbapenem-resistant A. baumannii.2 It inhibits carrageenan-induced paw edema in rats when administered at a dose of 20 mg/kg.3 Unlike hydrocortisone, 16-epiestriol (240 µg/animal) does not increase plasma or liver glucose levels in adrenalectomized rats.
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.Skariyachan, S., Muddebihalkar, A.G., Badrinath, V., et al.Natural epiestriol-16 act as potential lead molecule against prospective molecular targets of multidrug resistant Acinetobacter baumannii-Insight from in silico modelling and in vitro investigationsInfect. Genet. Evol.82104314(2020) 3.Latman, N.S., Kishore, V., and Bruot, B.C.16-Epiestriol: An anti-inflammatory steroid without glycogenic activityJ. Pharm. Sci.83(6)874-877(1994)
| Cas No. | 547-81-9 | SDF | |
| 别名 | 异雌三醇,16-epi-Estriol; 16β,17β-Estriol | ||
| 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 | Ethanol: 1 mg/ml | 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。
16-Epiestriol, a novel anti-inflammatory nonglycogenic steroid, does not inhibit IFN-gamma production by murine splenocytes
J Interferon Cytokine Res 1998 Nov;18(11):921-5.PMID:9858313DOI:10.1089/jir.1998.18.921.
All the steroidal anti-inflammatory drugs currently available are glucocorticoids. The desired anti-inflammatory activities of glucocorticoids frequently are accompanied by adverse side effects, notably glycogenic activities and profound immunosuppression, that can limit clinical use. We recently identified 16-Epiestriol, a naturally occurring steroid, as exhibiting significant anti-inflammatory activity without glycogenic activity. In the present study, we compared the effects of 16-Epiestriol and hydrocortisone on the capacity of murine splenocytes to produce interferon-y (IFN-y). We injected young adult male BDF1 mice once with 20 mg/kg hydrocortisone or 20, 5, or 1 mg/kg 16-Epiestriol and 4 h later harvested the splenocytes. Flow cytometric analysis confirmed that 16-Epiestriol did not alter the number of CD3+ T cells in the spleen. In contrast to the suppressive effects of hydrocortisone, none of the 16-Epiestriol concentrations inhibited concanavalin A-stimulated IFN-gamma production by spleen cells, as determined by ELISA. Incubating spleen cells from untreated mice in concentrations of 16-Epiestriol ranging from 1 mg/ml to 100 pg/ml did not alter profiles of IFN-gamma production, in contrast to the suppressive dose-response effects of hydrocortisone. Collectively, these results support the contention that 16-Epiestriol may be a clinically useful safe anti-inflammatory steroid without profound immunosuppressive activities.
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.
16-Epiestriol: an anti-inflammatory steroid without glycogenic activity
J Pharm Sci 1994 Jun;83(6):874-7.PMID:9120824DOI:10.1002/jps.2600830623.
All of the steroidal anti-inflammatory drugs currently available are glucocorticoids. They exhibit both glycogenic and anti-inflammatory activities. These two activities are usually considered inseparable. This glycogenic activity is responsible for most of the adverse side effects that severely limit clinical use of currently available steroidal anti-inflammatory drugs. The purpose of this study was to determine if a steroid, 16-Epiestriol, could exhibit significant anti-inflammatory activity without glycogenic activity. The anti-inflammatory activity of 16-Epiestriol was determined using a modified Winter's carrageenin rat paw edema model. The glycogenic activity of 16-Epiestriol was determined by a modification of Venning's methods on liver and plasma glucose concentrations. In each study, 16-epiestriol-treated animals were compared to untreated control and hydrocortisone-treated animals. In the anti-inflammatory study, 16-Epiestriol was more than twice as effective as hydrocortisone, on an equimolar basis, in preventing edema. 16-Epiestriol exhibited no effect on the liver or plasma glucose concentration in the glycogenic study. 16-Epiestriol exhibited potent anti-inflammatory activity without glycogenic activity. 16-Epiestriol does not conform to classical steroidal structure-activity relationship theory.
Intestinal metabolism of estrogens
J Clin Endocrinol Metab 1976 Sep;43(3):497-505.PMID:956337DOI:10.1210/jcem-43-3-497.
Estrogen metabolism in the human intestine was studied in two ways. Firstly, by measuring the excretion of 12 estrogens in pooled human late pregnancy feces before and during the administration of ampicillin (2 g/day). Secondly, by administering 5.4 and 20 mg of 16alpha-hydroxyestrone orally to two postmenopausal women and analyzing the estrogens in simultaneously drawn portal and peripheral venous blood samples at time intervals from 0 to 150 min after steroid administration. The majority of the estrogens in normal pregnancy feces were unconjugated. The amounts of estradiol, estreon and 16-Epiestriol excreted, relative to the principal estrogen estriol, were greater than in pregnancy bile or urine and 16alpha-hydroxyestrone, an important biliary estrogen, was only present in trace amounts. Considerable quantities of 15alpha-hydroxyestradiol-17beta were also found. Ampicillin administration, which decreases intestinal bacterial steroid metabolism, caused a huge increase in the fecal excretion of conjugated estrogens. In particular it caused very striking increases in the excretion of both unconjugated and conjugated, estriol, 15alpha-hydroxyestrone, 15alpha-hydroxyestradiol and 2-methoxyestrone. These findings emphasize the active role played by the intestinal microflora in estrogen metabolism under normal conditions. Administration of 16alpha-hydroxyestrone resulted in increases in portal venous unconjugated and conjugated 16alpha-hydroxyestrone, 16-oxoestradiol-17beta, 15alpha-hydroxyestrone, 16-Epiestriol and conjugated estriol levels. The most significant finding in both subjects was the large increase in portal venous unconjugated 15alpha-hydroxyestrone. This would suggest that the human intestine (or intestinal contents) has the ability to carry out the transformation, 16alpha-hydroxyestrone leads to 15alpha-hydroxyestrone. Increases in the same estrogens were found in peripheral plasma, with the increase in conjugated estriol occurring in peripheral blood before it was seen in portal blood. The largest elevations in peripheral plasma values were seen in unconjugated estriol and conjugated 16alpha-hydroxyestrone in the subject who received the 20 mg dose and in unconjugated 16alpha-hydroxyestrone and 16-oxoestradiol-17beta in the subject who had the 5.4 mg dose. The intestinal and enterohepatic metabolism of estrogens is discussed in relation to these findings.
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.