Keto lovastatin
Keto lovastatin (Monacolin X) is an impurity of Lovastatin (HY-N0504) and also a competitive inhibitor of HMG-CoA reductase. Keto lovastatin exerts its cholesterol-lowering effect by blocking the rate-limiting step of endogenous cholesterol synthesis. Keto lovastatin can be used in research on hypercholesterolemia and atherosclerosis, and can also serve as an impurity reference standard in the research on the production and quality control of Lovastatin.
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- CAS No.: 96497-73-3
- Formule: C24H34O6
- Masse moléculaire:418.52
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
In Vitro
Keto lovastatin (Monacolin X) (up to 1000 ng/mL; 2 h) inhibits cholesterol synthesis in human umbilical vein endothelial cells (HUVEC), human enterocytes, normal human skin fibroblasts, and familial homozygous hypercholesterolemia LDL receptor-deficient human skin fibroblasts, with no significant inhibitory effect on protein synthesis or fatty acid synthesis[2].
Keto lovastatin (up to 1000 ng/mL; 2 h) inhibits cholesterol synthesis in human hepatoma cells HEPG2, and its lactone and ring-opened acid forms exhibit comparable inhibitory activity, with no significant inhibitory effect on protein synthesis or fatty acid synthesis[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 96497-73-3
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Masse moléculaire 418.52
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Formule C24H34O6
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SMILES
O=C1OC(CC(C1)O)CCC2C(C)C=CC3=CC(CC(C32)OC(C(C)C(C)=O)=O)C
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Synonyms
Monacolin X
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keto lovastatin Related Classifications
HY-169818 Related Classifications
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