F15845
F 15845 is a highly effective persistent sodium current blocker. F 15845 also is a cardioprotective agent, has anti-ischemic activity and exerts short- and long-term cardioprotection after myocardial infarction. F 15845 can be used for the research of myocardium functional impairment.
For research use only. We do not sell to patients.
- CAS No.: 470454-73-0
- Formula: C20H25NO2S2
- Molecular Weight:375.55
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
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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
F 15845 (10 nM-10 μM) concentration-dependently reduces veratrine-induced diastolic contracture with an IC50 value of 0.14 μM in isolated atria[1].
F 15845 (0.1-10 μM) preserves viability in isolated cardiomyocytes exposed to lysophosphatidylcholine (LPC)[1].
F 15845 (0.3 μM) significantly counteracts [Na+] increase during no-flow ischemia[1].
F 15845 (0.3 μM, 0-35 min) delays the reduction in [Na+], but marks and maintains upon reperfusion[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Rat[1]
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Dosage:2.5 mg/kg, 5 mg/kg
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Administration:intravenously
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Result:Significantly reduced infarct size, decreased of troponin I levels and limited the long-term expansion of infarct size.
Chemical Information
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CAS No. 470454-73-0
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Molecular Weight 375.55
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Formula C20H25NO2S2
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SMILES
COC(C=CC=C1)=C1SC[C@@H](C)CN[C@@H]2COC3=CC=CC=C3SC2
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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)
F15845 Related Classifications
HY-19463A Related Classifications
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