ent-Estradiol
Ent-Estradiol is the enantiomer of Estradiol (HY-B0141). Ent-Estradiol is a highly selective estrogen receptor ligand, but does not possess estrogenic activity. Ent-Estradiol displays IC50 values of 24.9 nM, 9.59 nM and 8.17 nM for human, rat and mouse ERβ, and 151 nM, 246 nM and 268 nM for human, rat and mouse ERα, respectively. Ent-Estradiol can be used for the study of menopausal physiological changes.
For research use only. We do not sell to patients.
- CAS No.: 3736-22-9
- Formula: C18H24O2
- Molecular Weight:272.38
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
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hERα 151 nM (IC50) |
mouse ERα 268 nM (IC50) |
rat ERα 246 nM (IC50) |
hERβ 24.9 nM (IC50) |
rat ERβ 9.59 nM (IC50) |
mouse ERβ 8.17 nM (IC50) |
In Vitro
Ent-Estradiol (eight dilutions; 5-18 h) selectively binds to ER-β over ER-α across human, rat, and mouse receptors, with the highest selectivity observed for mouse ER-β, and exhibits IC50 values of 24.9 nM (human ER-β), 9.59 nM (rat ER-β), 8.17 nM (mouse ER-β), 151 nM (human ER-α), 246 nM (rat ER-α), and 268 nM (mouse ER-α)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 3736-22-9
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Molecular Weight 272.38
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Formula C18H24O2
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SMILES
C[C@]12[C@@](CC[C@H]2O)([H])[C@]3([H])[C@](CC1)([H])C4=CC=C(O)C=C4CC3
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Synonyms
ent-β-Estradiol; ent-17β-Estradiol; ent-17β-Oestradiol
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)