Enoximone sulfoxide
Enoximone sulfoxide (MDL 19438) is the primary sulfoxide metabolite of Enoximone (HY-B1639). Enoximone sulfoxide is also a cardiotonic agent with positive inotropic, positive chronotropic, and vasodilatory activities. Enoximone sulfoxide can be used in the research of congestive heart failure.
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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: 83982-78-9
- 分子式: C12H12N2O3S
- 分子量:264.30
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
体外実験
Enoximone sulfoxide (MDL 19438) (5 μM; incubated for 5-120 min) has the effect of being reduced to Enoximone in the 9000 g supernatant of rat liver and kidney[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:unspecified (anaesthetized)[3]
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Dosage:3 mg/kg
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Administration:i.v.; single injection
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Result:Increased cardiac contractile force from baseline, with a duration of inotropic action 13 times longer than that of enoximone.
Demonstrated inotropic activity 0.14 times as potent as enoximone.
Exhibited vasodilator activity.
化学情報
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CAS 番号 83982-78-9
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分子量 264.30
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分子式 C12H12N2O3S
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SMILES
O=C1NC(C(C2=CC=C(S(C)=O)C=C2)=O)=C(C)N1
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別名
MDL 19438
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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)