Lepodisiran sodium
Lepodisiran (LY3819469) sodium is a GalNAc-conjugated small interfering RNA lipid-lowering agent. Lepodisiran sodium targets the hepatic LPA gene and degrades apolipoprotein (a) mRNA to silence its expression, thereby effectively reducing the production of apolipoprotein (a) and serum lipoprotein (a) in a dose-dependent manner. Lepodisiran sodium can be used in studies related to atherosclerotic cardiovascular disease.
For research use only. We do not sell to patients.
- CAS No.: 2766131-24-0
- Molecular Weight:21973.00
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 2766131-24-0
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Molecular Weight 21973.00
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SMILES
[Lepodisiran (sodium)]
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Synonyms
LY3819469 sodium
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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)