Lnd 796
LND 796 is an aminosteroidal derivative with positive inotropic effects similar to those of digitalis. It exhibits electrophysiological, toxic, and inotropic effects in normal and partially potassium-depolarized ventricular muscles. LND 796 requires higher concentrations than digoxin to induce the same toxic symptoms. It exhibits a concentration-dependent positive inotropic effect on guinea pig papillary muscles in normal potassium solution. In partially potassium-depolarized papillary muscles, LND 796 enhances both components of contraction and increases the amplitude of slow action potentials. The mechanism of positive inotropic action of LND 796 involves enhanced calcium entry in calcium channels and inhibition of sodium-potassium ATPase. Due to its expanded positive inotropic range, LND 796 may have potential application in the treatment of congestive heart failure.
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- CAS No.: 118549-42-1
- 화학식: C27H45NO7
- 분자량:495.65
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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
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Biological Activity
제품 설명
Chemical Information
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CAS No. 118549-42-1
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분자량 495.65
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화학식 C27H45NO7
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SMILES
N[C@@]([C@@]12C)(CC[C@@H]1C(OC)=O)[C@@](CC[C@]3([H])C[C@H]4O[C@H](O[C@H]5C)[C@@H]([C@@H]([C@H]5O)O)O)([H])[C@@](CC2)([H])[C@]3(CC4)C
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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)
Lnd 796 Related Classifications
HY-136677 Related Classifications
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