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.
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。
- 純度 : 91.95%
- CAS 番号: 2808361-18-2
- 分子量:20720.00
-
保管条件:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
生物活性
製品説明
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
臨床実験
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
化学情報
-
CAS 番号 2808361-18-2
-
性状 Solid
-
分子量 20720.00
-
Color White to off-white
-
SMILES
[Lepodisiran]
-
別名
LY3819469
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
プロトコル
-
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.
純度とドキュメンテーション
-
データシート (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)
-
取扱説明書 (2242 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)