Vincapusine
Vincapusine is an inhibitor of CaV3.1 calcium channel, with a IC50 of 11.83 μM against the human target. Vincapusine suppresses the functional activity of the CaV3.1 calcium channel. Vincapusine exerts antihypertensive activity by inhibiting the CaV3.1 calcium channel. Vincapusine is used in hypertension-related research.
For research use only. We do not sell to patients.
- CAS No.: 80248-97-1
- Formula: C21H24N2O4
- Molecular Weight:368.43
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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
All Calcium Channel Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
CaV3.1 11.83 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | IC50 |
11.83 μM
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Inhibition of CaV3.1 calcium channels in transiently transfected HEK-293 cells.
Inhibition of CaV3.1 calcium channels in transiently transfected HEK-293 cells.
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36017978 |
In Vitro
Vincapusine inhibits CaV3.1 calcium channels in transiently transfected HEK-293 cells with an IC50 of 11.83 μM, indicating potential antihypertensive activity via modulation of pacemaker cell calcium currents[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. 80248-97-1
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Molecular Weight 368.43
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Formula C21H24N2O4
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SMILES
CC[C@]12[C@@]3([H])C4=C5CCN3C[C@H](O)[C@@]1([H])O[C@](C(OC)=O)(C2)N4C6=CC=CC=C56
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Structure Classification
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Initial Source
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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)
Vincapusine Related Classifications
HY-N21842 Related Classifications
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