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.
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: 131741-08-7
- 分子式: C14H12N6O
- 分子量:280.28
-
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
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.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Wistar (Male, 300-350 g, healed myocardial infarction via left anterior descending coronary artery ligation)[3]
-
Dosage:2.5 mg/kg
-
Administration:p.o.; ad libitum; 312 days
-
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.
化学情報
-
CAS 番号 131741-08-7
-
分子量 280.28
-
分子式 C14H12N6O
-
SMILES
N#C/C(C#N)=N/NC1=CC=C(C2=NNC(CC2C)=O)C=C1
-
別名
(rac)-Levosimendan; (rac)-Simsndan; (rac)-OR-1259
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
-
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)
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