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.
For research use only. We do not sell to patients.
- CAS No.: 83982-78-9
- Formula: C12H12N2O3S
- Molecular Weight:264.30
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
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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Molecular Weight 264.30
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Formula 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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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Enoximone sulfoxide Related Classifications
HY-187722 Related Classifications
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