Catalog No.S2466 Synonyms: NSC-12169
Molecular Weight(MW): 288.39
Estriol is an antagonist of the G-protein coupled estrogen receptor in estrogen receptor-negative breast cancer cells.
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Choose Selective Estrogen/progestogen Receptor Inhibitors
|Description||Estriol is an antagonist of the G-protein coupled estrogen receptor in estrogen receptor-negative breast cancer cells.|
MTT assays using G-1 shows that, in SkBr3 cells, the proliferative effect induced by 100 nM G-1 is abolished in the presence of 1 μM estriol which acts as an antagonist of GPR30-dependent pathway.  A cell-free transcription assay demonstrates that the antiestrogenic activity exhibited by estriol is because of interferring with estradiol-induced positive cooperative binding and receptor dimerization, binding of hER complexes to ERE, as well as reducing estradiol-dependent transcription in a dose-dependent manner.  A recent study shows that estrogen (estrone, estradiol, and estriol) inhibits Alzheimer's disease-associated low-order Aβ oligomer formation, and among them, estriol shows the strongest in vitro activity. 
|In vivo||In mPTEN+/- mice, estriol treatments resulted in a 187.54% gain in the relative ratio of uterine wet weight to body weight; estriol also increases the ratio to 176.88% in wild-type mice.  Estriol treatment (20 mg/kg ip), in vivo, sensitizes Kupffer cells to LPS via mechanisms dependent on an increase in CD14 by elevated portal blood endotoxin caused by increased gut permeability in rats; while one-half of the rats given estriol intraperitoneally 24 hours before an injection of a sublethal dose of LPS (5 mg/kg) died within 24 hours. |
-  Lappano R, et al. Mol Cell Endocrinol. 2010, 320(1-2), 162-170.
-  Melamed M, et al. Endocrinol. 1997, 11(12), 1868-1878.
-  Morinaga A, et al. Exp Neurol. 2011, 228(2), 298-302.
|In vitro||DMSO||57 mg/mL (197.64 mM)|
|Ethanol||10 mg/mL (34.67 mM)|
|In vivo||Add solvents to the product individually and in order:
5% DMSO+95% Corn oil
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03032848||Completed||Vaginitis Atropic|Pelvic Organ Prolapse|Endometrial Hyperplasia||Universidade Federal do Paraná||November 26, 2013||Phase 4|
|NCT03044652||Recruiting||Vulvovaginal Atrophy||Dr. August Wolff GmbH & Co. KG Arzneimittel|proDERM Institut für Angewandte Dermatologische Forschung GmbH|Bremer Pharmacovigilance Service GmbH|GCP-Service International Ltd. & Co. KG||November 2016||Phase 4|
|NCT02906111||Not yet recruiting||Genital Prolapse||Salvatore Caruso|Policlinico Universitario, Catania||November 2016||Phase 4|
|NCT02967510||Recruiting||Vaginal Atrophy||ITF Research Pharma, S.L.U.||October 2016||Phase 2|
|NCT02892214||Not yet recruiting||Localized Provoked Vulvodynia||Meir Medical Center||October 2016||--|
|NCT02733731||Recruiting||Atrophic Vaginitis||First Affiliated Hospital, Sun Yat-Sen University||February 2016||Phase 1|
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