Lepodisiran
Based on 1 Customer Validation
Lepodisiran (LY3819469) is a GalNAc-conjugated small interfering RNA lipid-lowering agent. Lepodisiran 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 can be used in studies related to atherosclerotic cardiovascular disease.
Para uso exclusivo en investigación. No vendemos a pacientes.
- Pureza : 91.95%
- No. CAS: 2808361-18-2
- Peso molecular:20720.00
-
Almacenamiento:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Actividad biológica
Descripciòn
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Ensayo clínico
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
-
No. CAS 2808361-18-2
-
Appearance Solid
-
Peso molecular 20720.00
-
Color White to off-white
-
SMILES
[Lepodisiran]
-
Synonyms
LY3819469
-
Envío
Room temperature in continental US; may vary elsewhere.
-
Almacenamiento
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Protocolo
-
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.
-
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.
Pureza y Documentación
-
Ficha de datos (271 KB)
-
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
-
Instrucciones de manejo (2242 KB)
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)