AR antagonist 6
AR antagonist 6 (compound 6i) is a diphenyl ether androgen receptor (AR) antagonist that binds AR at a concentration of 120 nM. AR antagonist 6 exhibits low toxicity and in vitro activity against the golden Syrian hamster ear model.
For research use only. We do not sell to patients.
- CAS No.: 876760-08-6
- Formula: C16H12F3NO2
- Molecular Weight:307.27
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MDA-MB-231 | IC50 |
47 nM
Compound: 6i
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Antagonist activity at human androgen receptor expressed in human MDA-MB-231 cells assessed as inhibition of DHT-induced response
Antagonist activity at human androgen receptor expressed in human MDA-MB-231 cells assessed as inhibition of DHT-induced response
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[PMID: 19286380] |
| Sf9 | IC50 |
120 nM
Compound: 6i
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Displacement of [3H]DHT from human cloned androgen receptor expressed in insect Sf9 cell system
Displacement of [3H]DHT from human cloned androgen receptor expressed in insect Sf9 cell system
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[PMID: 19286380] |
In Vitro
The inhibitory concentration of AR antagonist 6 on AR in cells is 47 nM[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. 876760-08-6
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Molecular Weight 307.27
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Formula C16H12F3NO2
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SMILES
N#CC1=CC=C(C=C1C(F)(F)F)OC2=C(OCC)C=CC=C2
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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)
AR antagonist 6 Related Classifications
HY-160680 Related Classifications
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