Simendan
Simendan ((rac)-Levosimendan; (rac)-Simsndan; (rac)-OR-1259) is a calcium-sensitizing positive inotropic vasodilator compound that enhances myocardial contractility through calcium-dependent binding to cardiac troponin C and selectively inhibits cardiac phosphodiesterase (Phosphodiesterase) III, while inducing coronary and peripheral vasodilation and anti-ischemic effects. Simendan can be used for research on congestive heart failure, acute heart failure, myocardial infarction, myocardial ischemia, and thrombotic diseases.
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- CAS No.: 131741-08-7
- 화학식: C14H12N6O
- 분자량:280.28
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보관:
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
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vitro
Simendan ((rac)-Levosimendan; (rac)-Simsndan; (rac)-OR-1259) selectively inhibits cardiac phosphodiesterase III in purified enzyme preparations[1].
Simendan binds to cardiac troponin C in a calcium-dependent manner in paced papillary muscle preparations, combining positive inotropic effects with enhanced cardiac relaxation[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:Wistar (Male, 300-350 g, healed myocardial infarction via left anterior descending coronary artery ligation)[3]
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Dosage:2.5 mg/kg
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Administration:p.o.; ad libitum; 312 days
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Result:Reduced mortality rate to 53% at day 312, representing a 28% risk reduction versus control.
Reduced 6-month mortality rate to 19%.
Achieved an infarct size of 43%.
Histological analysis showed an external normal boundary of 11.9 mm, internal normal boundary of 7.6 mm, external infarct boundary of 7.4 mm, internal infarct boundary of 6.2 mm, whole area of 60.7 mm2, normal area of 52.4 mm2, and infarct area of 8.2 mm2.
Chemical Information
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CAS No. 131741-08-7
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분자량 280.28
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화학식 C14H12N6O
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SMILES
N#C/C(C#N)=N/NC1=CC=C(C2=NNC(CC2C)=O)C=C1
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Synonyms
(rac)-Levosimendan; (rac)-Simsndan; (rac)-OR-1259
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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)
Simendan Related Classifications
HY-W745845 Related Classifications
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Keywords
- Simendan
- 131741-08-7
- (rac)-Levosimendan
- (rac)-Simsndan
- (rac)-OR-1259
- Phosphodiesterase (PDE)
- myocardial infarction
- thrombotic diseases
- cardiac troponin C
- myocardial ischaemia
- cardiac phosphodiesterase III
- congestive heart failure
- ATP-sensitive potassium channels
- sarcoplasmic reticulum
- acute heart failure
- human platelet aggregation
- Inhibitor
- inhibitor
- inhibit