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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- CAS No.: 83982-78-9
- 화학식: C12H12N2O3S
- 분자량:264.30
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
In Vitro
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.
In Vivo
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.
Chemical Information
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CAS No. 83982-78-9
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분자량 264.30
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화학식 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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Synonyms
MDL 19438
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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)