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.
For research use only. We do not sell to patients.
- Formula: C21H27ClN2O
- Molecular Weight:358.90
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All P2X Receptor Isoforms
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Biological Activity
Description
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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Formula 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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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)