SB 247083
SB 247083 is a selective, competitive and orally active endothelin-A receptor antagonist with a Ki of 0.41 nM. SB 247083 shows a Ki of 467 nM to endothelin-B receptor. SB 247083 shows a Kb of 3.5 nM for ET-1-induced contraction of rat aorta. SB 247083 can be used for the research of cardiovascular disease.
For research use only. We do not sell to patients.
- CAS No.: 188186-61-0
- Formula: C34H33ClN2O7
- Molecular Weight:617.09
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
ETA 0.41 nM (Ki) |
ETB 467 nM (Ki) |
Chemical Information
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CAS No. 188186-61-0
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Molecular Weight 617.09
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Formula C34H33ClN2O7
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SMILES
COC(C=C1C(OCC1)=C2)=C2C/C(C(O)=O)=C\C3=C(C4=C(C=C(C=C4)Cl)OCC5=C(C=CC=C5)C(O)=O)N(N=C3)CCCC
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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 Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)