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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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 181490-18-6
- 分子式: C24H24N4O3S
- 分子量:448.54
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
Adrenergic Receptor アイソフォーム固有の製品をすべて表示
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生物活性
製品説明
IC50 & Target
[1]|
α1A-adrenergic receptor 0.22 nM (Ki) |
Alpha-1D adrenergic receptor |
化学情報
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CAS 番号 181490-18-6
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分子量 448.54
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)