A 131701
A 131701 is a selective α1a- (Ki: 0.22 nM for human α1a) and α1d-adrenoceptor antagonist. A 131701 antagonizes epinephrine-induced increases in intraurethral pressure (IUP). A 131701 causes transient decreases in mean arterial blood pressure (MABP) and transient tachycardia. A 131701 can be used in the research of spontaneous hypertension.
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- CAS No.: 181490-18-6
- Formule: C24H24N4O3S
- Masse moléculaire:448.54
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
IC50 & Target
[1]|
α1A-adrenergic receptor 0.22 nM (Ki) |
Alpha-1D adrenergic receptor |
Chemical Information
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CAS No. 181490-18-6
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Masse moléculaire 448.54
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Formule C24H24N4O3S
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SMILES
O=C1NC(C2=NC=CC=C2S3)=C3C(N1CCN4C[C@]5([H])CCC6=C(OC)C=CC=C6[C@]5([H])C4)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)