YM-1758735
YM-1758735 is an orally active androgen receptor (AR) antagonist with an IC50 of 0.2 μM. YM-1758735 inhibits AR-mediated transcriptional activation. YM-1758735 can be used for the research of prostate.
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- CAS No.: 262294-30-4
- Formule: C21H19F5N4O
- Masse moléculaire:438.40
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
In Vitro
YM-1758735 (Compound 85) inhibits AR-mediated transcriptional activation with an IC50 of 0.2 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male)[1]
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Dosage:10 mg/kg
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Administration:p.o.; daily; 15 days
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Result:Failed to decrease ventral prostate weight.
Chemical Information
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CAS No. 262294-30-4
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Masse moléculaire 438.40
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Formule C21H19F5N4O
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SMILES
C[C@@H]1N(C2=CC(C(F)(F)F)=C(C#N)C=C2)C[C@@H](C)N(C(NC3=C(F)C=C(F)C=C3)=O)C1
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)