17β-HSD1-IN-2
17β-HSD1-IN-2 (PBRM) is a non-estrogenic and steroidal covalent irreversible inhibitor of 17β-Hydroxysteroid dehydrogenase type 1 (17β-HSD1) (Ki=368 nM). 17β-HSD1-IN-2 can be used for the research of estrogen-dependent disorders.
For research use only. We do not sell to patients.
- CAS No.: 1318265-18-7
- Formula: C28H34BrNO2
- Molecular Weight:496.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All 17β-HSD Isoforms
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Biological Activity
Description
IC50 & Target
17β-HSD1[1]
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| T47D | IC50 |
68 nM
Compound: 23b
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Inhibition of 17-beta HSD1 in human T47D cells assessed as transformation of [14C]E1 to [14C]E2 after 24 hrs by thin layer chromatography
Inhibition of 17-beta HSD1 in human T47D cells assessed as transformation of [14C]E1 to [14C]E2 after 24 hrs by thin layer chromatography
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[PMID: 24328103] |
| T47D | IC50 |
68 nM
Compound: 5
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Inhibition of 17beta-HSD1 in human T47D cells assessed as decrease in transformation of [14C]estrone to [14C]-estradiol after 24 hrs by thin layer chromatography
Inhibition of 17beta-HSD1 in human T47D cells assessed as decrease in transformation of [14C]estrone to [14C]-estradiol after 24 hrs by thin layer chromatography
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[PMID: 21927646] |
| T47D | IC50 |
97 nM
Compound: 23b
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Inhibition of 17-beta HSD1 in human T47D cells
Inhibition of 17-beta HSD1 in human T47D cells
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[PMID: 24328103] |
Chemical Information
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CAS No. 1318265-18-7
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Molecular Weight 496.48
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Formula C28H34BrNO2
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SMILES
O=C(N)C1=CC=CC(C[C@H]2C[C@@]3([H])[C@]4([H])CCC5=C(C=CC(CCBr)=C5)[C@@]4([H])CC[C@]3(C)[C@H]2O)=C1
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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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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)
17β-HSD1-IN-2 Related Classifications
HY-129433 Related Classifications
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