VPC 23153
VPC 23153 is a S1P4 receptor agonist and vasoconstrictor. VPC 23153 activates the S1P4 receptor, thereby triggering vasoconstriction. VPC 23153 induces pulmonary artery contraction. VPC 23153 can be used in studies related to pulmonary arterial hypertension.
For research use only. We do not sell to patients.
- CAS No.: 787582-98-3
- Formula: C17H28N3O4P
- Molecular Weight:369.40
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
S1PR4 |
In Vitro
VPC 23153 (0.01-3 μM) induces dose-dependent vasoconstriction in isolated perfused normotensive rat lungs[1].
VPC 23153 (0.1-10 μM) induces concentration-dependent contraction of isolated pulmonary arteries (but not renal or mesenteric arteries) from chronically hypoxic rats[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 787582-98-3
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Molecular Weight 369.40
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Formula C17H28N3O4P
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SMILES
[C@@H](COP(=O)(O)O)(N)C=1NC=2C(N1)=CC=C(CCCCCCCC)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)
VPC 23153 Related Classifications
HY-W040167 Related Classifications
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