PF-4479745
PF-4479745 is a potent and selective 5-HT2C receptor agonist (EC50: 10 nM, ki: 15 nM). PF-4479745 can be used in the research of cardiovascular disease like hypertension.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 1065110-43-1
- Formel: C17H22N4
- Molecular Weight:282.38
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Speicherung:
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
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Alle 5-HT Receptor Isoform-spezifische Produkte anzeigen
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Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
5-HT2C Receptor |
5-HT2C Receptor 10 nM (EC50) |
5-HT2C Receptor 15 nM (Ki) |
5-HT2A Receptor 360 nM (IC50) |
5-HT2B Receptor 67 nM (IC50) |
5-HT1A Receptor 500 nM (IC50) |
5-HT6 Receptor 280 nM (IC50) |
In Vitro
PF-4479745 (copmpound 17) exhibits metabolic stability in both human liver microsomes (HLM) and human hepatocytes[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
PF-4479745 demonstrates a robust dose-dependent effect in canine PUP (peak urethral pressure) model of SUI (stress urinary incontinence)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS. Nr. 1065110-43-1
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Molecular Weight 282.38
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Formel C17H22N4
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SMILES
CNC1=C2C([C@H](CNCC2)C)=NC(CC3=CC=CC=C3)=N1
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
PF-4479745 Related Classifications
HY-118339 Related Classifications
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