KT-1
KT-1 is a vasodilator. KT 1 can decrease aortic pressure, renal blood flow, left ventricular enddiastolic pressure and resistances of total peripheral, vertebral, coronary and renal vasculatures and increase aortic blood flow, vertebral blood flow, coronary blood flow, peak positive left ventricular dP/dt and heart rate in anesthetized open-chest dogs. KT-1 can be used for the research of cardiovascular disease.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
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: 47487-05-8
- 分子式: C16H22N4O6
- 分子量:366.37
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
Adenosine 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
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A1R |
化学情報
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CAS 番号 47487-05-8
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分子量 366.37
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分子式 C16H22N4O6
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SMILES
COC1=C(C(OC)=CC2=C(N=CN=C12)NCCCCCO[N+]([O-])=O)OC
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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)