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.
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- CAS No.: 1065110-43-1
- 화학식: C17H22N4
- 분자량:282.38
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보관:
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
- Protocol
- 순도&문서
- References
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Help & FAQs
All 5-HT Receptor Isoforms
More
Biological Activity
제품 설명
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 No. 1065110-43-1
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분자량 282.38
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화학식 C17H22N4
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SMILES
CNC1=C2C([C@H](CNCC2)C)=NC(CC3=CC=CC=C3)=N1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PF-4479745 Related Classifications
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