Ethinyl EstradiolOral contraceptive CAS# 57-63-6 |
2D Structure
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Quality Control & MSDS
3D structure
Package In Stock
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Cas No. | 57-63-6 | SDF | Download SDF |
PubChem ID | 5991 | Appearance | Powder |
Formula | C20H24O2 | M.Wt | 296.4 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | 17α-Ethynylestradiol; Ethynylestradiol | ||
Solubility | DMSO : ≥ 30 mg/mL (101.21 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | (8R,9S,13S,14S,17R)-17-ethynyl-13-methyl-7,8,9,11,12,14,15,16-octahydro-6H-cyclopenta[a]phenanthrene-3,17-diol | ||
SMILES | CC12CCC3C(C1CCC2(C#C)O)CCC4=C3C=CC(=C4)O | ||
Standard InChIKey | BFPYWIDHMRZLRN-SLHNCBLASA-N | ||
Standard InChI | InChI=1S/C20H24O2/c1-3-20(22)11-9-18-17-6-4-13-12-14(21)5-7-15(13)16(17)8-10-19(18,20)2/h1,5,7,12,16-18,21-22H,4,6,8-11H2,2H3/t16-,17-,18+,19+,20+/m1/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Ethynyl estradiol is an orally bio-active estrogen used in almost all modern formulations of combined oral contraceptive pills.
Target: Estrogen Receptor
Ethinyl estradiol (EE), also sometimes written as ethinylestradiol, ethynyl estradiol, or ethinyl estradiol, is a derivative of 17β-estradiol (E2), the major endogenous estrogen in humans. EE is an orally bioactive estrogen used in many formulations of combined oral contraceptive pills. It is one of the most commonly used medications for this purpose. Transdermal ethinyl estradiol carries a greater risk of clot formation and venous thromboembolism than 17 beta estradiol, which some have theorized to be related to different amounts of hepatic metabolism after absorption. The same contraindications and precautions apply for EE as with other estrogen medications.
Estinyl was a preparation of EE alone that was used for the management of menopausal symptoms and female hypogonadism. EE is released into the environment as a xenoestrogen from the urine and feces of people who take it as a medication. The major concern with unopposed estrogen is of endometrial cancer. As such, the medication is generally prescribed with progesterone in the setting of birth control. The first orally active semisynthetic steroidal estrogen, EE (17α-ethynylestradiol), the 17α-ethynyl analog of E2, was synthesized in 1938 by Hans Herloff Inhoffen and Walter Hohlweg at Schering AG in Berlin. References: |
Ethinyl Estradiol Dilution Calculator
Ethinyl Estradiol Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.3738 mL | 16.8691 mL | 33.7382 mL | 67.4764 mL | 84.3455 mL |
5 mM | 0.6748 mL | 3.3738 mL | 6.7476 mL | 13.4953 mL | 16.8691 mL |
10 mM | 0.3374 mL | 1.6869 mL | 3.3738 mL | 6.7476 mL | 8.4345 mL |
50 mM | 0.0675 mL | 0.3374 mL | 0.6748 mL | 1.3495 mL | 1.6869 mL |
100 mM | 0.0337 mL | 0.1687 mL | 0.3374 mL | 0.6748 mL | 0.8435 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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A synthetic analog of estradiol commonly used as an oral contraceptive, often in combination with a progestin. Efficacy of oral administration is facilitated by the ethynyl substitution at the C-17 position, which inhibits first pass hepatic metabolism. Rapidly absorbed from gastrointestinal tract.
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Hypothalamic transcriptomic alterations in male and female California mice (Peromyscus californicus) developmentally exposed to bisphenol A or ethinyl estradiol.[Pubmed:28196854]
Physiol Rep. 2017 Feb;5(3). pii: 5/3/e13133.
Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC) prevalent in many household items. Rodent models and human epidemiological studies have linked this chemical to neurobehavior impairments. In California mice, developmental exposure to BPA results in sociosexual disorders at adulthood, including communication and biparental care deficits, behaviors that are primarily regulated by the hypothalamus. Thus, we sought to examine the transcriptomic profile in this brain region of juvenile male and female California mice offspring exposed from periconception through lactation to BPA or Ethinyl Estradiol (EE, estrogen present in birth control pills and considered a positive estrogen control for BPA studies). Two weeks prior to breeding, P0 females were fed a control diet, or this diet supplemented with 50 mg BPA/kg feed weight or 0.1 ppb EE, and continued on the diets through lactation. At weaning, brains from male and female offspring were collected, hypothalamic RNA isolated, and RNA-seq analysis performed. Results indicate that BPA and EE groups clustered separately from controls with BPA and EE exposure leading to unique set of signature gene profiles. Kcnd3 was downregulated in the hypothalamus of BPA- and EE-exposed females, whereas Tbl2, Topors, Kif3a, and Phactr2 were upregulated in these groups. Comparison of transcripts differentially expressed in BPA and EE groups revealed significant enrichment of gene ontology terms associated with microtubule-based processes. Current results show that perinatal exposure to BPA or EE can result in several transcriptomic alterations, including those associated with microtubule functions, in the hypothalamus of California mice. It remains to be determined whether these genes mediate BPA-induced behavioral disruptions.
Characterisation of the transcriptome of male and female wild-type guppy brains with RNA-Seq and consequences of exposure to the pharmaceutical pollutant, 17alpha-ethinyl estradiol.[Pubmed:28246045]
Aquat Toxicol. 2017 May;186:28-39.
Waterways are increasingly being contaminated by chemical compounds that can disrupt the endocrinology of organisms. One such compound is 17alpha-Ethinyl Estradiol (EE2), a synthetic estrogen used in the contraceptive pill. Despite considerable research interest in the effects of EE2 on reproduction and gene expression, surprisingly, only a few studies have capitalised on technologies, such as next-generation sequencing (NGS), to uncover the molecular pathways related to EE2 exposure. Accordingly, using high-throughput sequencing technologies, the aim of our study was to explore the effects of EE2 on brain transcriptome in wild-type male and female guppy (Poecilia reticulata). We conducted two sets of experiments, where fish were exposed to EE2 (measured concentrations: 8ng/L and 38ng/L) in a flow-through system for 21days. The effects on the brain transcriptome on both males and females were assessed using Illumina sequencing (MiSeq and HiSeq) platform followed by bioinformatics analysis (edgeR, DESeq2). Here, we report that exposure to EE2 caused both up- and downregulation of specific transcript abundances, and affected transcript abundance in a sex-specific manner. Specifically, we found 773 transcripts, of which 60 were male-specific, 61 female-specific and 285 treatment-specific. EE2 affected expression of 165 transcripts in males, with 88 downregulated and 77 upregulated, while in females, 120 transcripts were affected with 62 downregulated and 58 upregulated. Finally, RT-qPCR validation demonstrated that expression of transcripts related to transposable elements, neuroserpin and heat shock protein were significantly affected by EE2-exposure. Our study is the first to report brain transcriptome libraries for guppies exposed to EE2. Not only does our study provide a valuable resource, it offers insights into the mechanisms underlying the feminizing effects on the brains of organisms exposed to environmentally realistic concentrations of EE2.
No clinically meaningful pharmacokinetic interaction between the hepatitis C virus inhibitors elbasvir and grazoprevir and the oral contraceptives ethinyl estradiol and levonorgestrel.[Pubmed:28233047]
Eur J Clin Pharmacol. 2017 May;73(5):593-600.
PURPOSE: Oral contraceptive pills (OCPs) are an important element of hepatitis C virus (HCV) treatment in women of childbearing potential. These studies evaluated the safety and pharmacokinetic interactions between elbasvir (EBR) and grazoprevir (GZR) and Ethinyl Estradiol/levonorgestrel (EE/LNG). METHODS: Both studies were open-label, single-site, two-period, fixed-sequence, one-way interaction studies. In period 1, subjects received one tablet of EE/LNG (0.03 mg/0.15 mg). In period 2, subjects received EBR (50 mg once daily) for 13 days or GZR (200 mg once daily) for 10 days, with one tablet of EE/LNG on day 7 (GZR group) or 10 (EBR group). Each study enrolled 20 healthy, nonsmoking adult females. RESULTS: There was no clinically meaningful effect of multiple doses of EBR or GZR on the pharmacokinetics of EE or LNG. Geometric mean ratios (GMRs) for AUC0-infinity and Cmax in the presence and absence of EBR were 1.01 and 1.10 for EE and 1.14 and 1.02 for LNG, with 90% confidence intervals (CIs) that were contained in the interval [0.80, 1.25]. Similarly, the AUC0-infinity and Cmax GMRs in the presence and absence of GZR were 1.10 and 1.05 for EE and 1.23 and 0.93 for LNG, respectively. The 90% CIs for EE AUC0-infinity and for EE and LNG Cmax were contained in the interval [0.80, 1.25]; however, the 90% CI for the LNG AUC0-infinity [1.15, 1.32] slightly exceeded the upper bound. CONCLUSIONS: These results suggest that EBR/GZR can be co-administered to female patients with HCV of childbearing potential who are on OCPs to prevent pregnancy.
Mammalian target of rapamycin (mTOR)/nitric oxide system possibly modulate antidepressant-like effect of 17alpha-ethinyl estradiol in ovariectomized mice.[Pubmed:28259097]
Biomed Pharmacother. 2017 May;89:591-604.
Due to a close association between depressive disorders and altered estrogen levels, this study was conducted to examine the hypothesis that antidepressant-like effect of Ethinyl Estradiol (EE2) in ovariectomized mice is modulated by mammalian target of rapamycin (mTOR)/nitric oxide pathways. Female mice were undergone bilateral ovariectomy and different doses of EE2 were intraperitoenally injected alone and combined with specific mTOR inhibitor, rapamycin, non-specific NOS inhibitor, L-NAME, nNOS inhibitor, 7-NI, NO precursor, l-arginine, and selective PDE5I, sildenafil. After locomotion assessment, immobility times were recorded in FST and TST. Moreover, hippocampal mTOR expression was assessed using western blot assay. The hippocampal concentrations of nitrite, a major metabolite of NO, were measured. Although EE2 demonstrated a significant antidepressant-like activity in OVX mice, acute rapamycin exerted an unmarked decrease of the anti-immobility effect of EE2 in FST and TST (P>0.05). In contrast, combination of minimal effective dose of EE2 with sub- effective doses of either L-NAME (10mg/kg) or 7-NI (25mg/kg) resulted in a robust antidepressant-like effect in OVX mice. Administration of either L-NAME or 7-NI enhanced the decreased antidepressant activity of EE2 induced by combination with rapamycin. Moreover, decrement of hippocampal mTOR expression in OVX mice was significantly enhanced by acute EE2. The increased hippocampal nitrite concentrations caused by ovariectomy were also reversed by EE2 administration. The study demonstrated that acute treatment with lowest dose of EE2 exerts significant antidepressant-like behavior in OVX mice, possibly, through mTOR activation. This effect seems to be also mediated by the suppression of nitric oxide pathway.