GSK3527497
GSK3527497 is an orally active TRPV4 inhibitor. GSK3527497 is applicable for the research of heart failure.
For research use only. We do not sell to patients.
- CAS No.: 2215855-22-2
- Formula: C17H16ClFN4O4S
- Molecular Weight:426.85
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
TRPV4 |
In Vitro
GSK3527497 potently inhibits hTRPV4 with an IC50 of 12 nM in a FLIPR assay[1].
GSK3527497 inhibits hERG with an IC50 of 20 μM[1].
GSK3527497 inhibits CYP3A4 with an IC50 of 12 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
Chemical Information
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CAS No. 2215855-22-2
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Molecular Weight 426.85
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Formula C17H16ClFN4O4S
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SMILES
NC[C@](O)(CN(C1)S(=O)(C2=CC=C(C=N2)Cl)=O)[C@H]1OC3=CC(F)=C(C=C3)C#N
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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)