Nafagrel
Nafagrel (DP-1904 free acid) is a Thromboxane A2 synthase inhibitor. Nafagrel inhibits the production of Thromboxane A2 and increases the production of Prostaglandin I2 (HY-A0126A). Nafagrel prevents thrombotic material accumulation in acute arterial thrombosis models. Nafagrel can be used in research on peripheral vascular disease, restenosis after PTCA, and lupus nephritis.
For research use only. We do not sell to patients.
- CAS No.: 97901-21-8
- Formula: C15H16N2O2
- Molecular Weight:256.31
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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
In Vitro
Nafagrel inhibits thromboxane synthase as an imidazole derivative[1].
DP-1904 (0.1 μM-1 mM; 2 h) completely suppresses TXB2 production and dramatically increases 6-keto-PGF1α production from human umbilical vein EC and platelets stimulated by HA-IgG in a coculture system, acting as a TXA2 synthetase inhibitor[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Human umbilical vein endothelial cells and human platelets
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Concentration:10^-3, 10^-4, 10^-5, 10^-6, 10^-7 M
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Incubation Time:2 h
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Result:Suppressed TXB2 production at 10^-3 to 10^-6 M to levels similar to controls.
Increased 6-keto-PGF1α production at 10^-4 to 10^-7 M.
Decreased the TXB2/6-keto-PGF1α ratio at all concentrations.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 97901-21-8
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Molecular Weight 256.31
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Formula C15H16N2O2
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SMILES
O=C(O)C1=CC=C2C(=C1)CCC(C2)CN3C=NC=C3
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Synonyms
DP-1904 free acid
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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)
Nafagrel Related Classifications
HY-106111 Related Classifications
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Keywords
- Nafagrel
- 97901-21-8
- DP-1904
- DP1904
- DP 1904
- Prostaglandin Receptor
- prostaglandin endoperoxides
- thromboxane A2
- prostaglandin I2
- thromboxane A2 synthase inhibitor
- cytochrome P450 enzyme thromboxane synthase
- endothelial cell and platelet coculture systems
- prostaglandin H2
- acute arterial thrombosis models
- heat-aggregated IgG
- lupus nephritis
- Inhibitor
- inhibitor
- inhibit