UB-MBX-46
UB-MBX-46 is a potent and selective P2X7 receptor antagonist with IC50s of 0.514 nM (hP2X7R), 40.6 nM (rP2X7R), and 4.52 nM (mP2X7R), respectively. UB-MBX-46 interacts with the classical allosteric pocket of the human P2X7 receptor. UB-MBX-46 can be used for cancer, atherosclerosis, and neurode generation research.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C21H27ClN2O
- Molecular Weight:358.90
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
hP2X7R 0.514 nM (IC50) |
rP2X7R 40.6 nM (IC50) |
mP2X7R 4.52 nM (IC50) |
Chemical Information
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Molecular Weight 358.90
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Formel C21H27ClN2O
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SMILES
O=C(NNC1=C(C=CC=C1)Cl)C23C(CC4(C)C5(C)C3)CC4(C)C5(C)C2
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)