Zerlasiran sodium
Zerlasiran (SLN360) sodium is a siRNA targeting apolipoprotein A (ApoA). Zerlasiran sodium targets hepatic ApoA synthesis via RNA interference to degrade encoding mRNA. Zerlasiran sodium can be used for the research of atherosclerotic cardiovascular disease and elevated ApoA levels.
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- Formule: C443H556F12N144Na38O277P40S10
- Masse moléculaire:14155.88 (free acid)
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Stockage:
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Activité biologique
Description
In Vitro
Zerlasiran (300-600 mg) sodium reduces serum ApoA levels of up to 96-98%[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Essai clinique
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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Appearance Solid
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Masse moléculaire 14155.88 (free acid)
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Formule C443H556F12N144Na38O277P40S10
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Color White to off-white
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SMILES
[Zerlasiran (sodium)]
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Synonyms
SLN360 sodium
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
-20°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Protocole
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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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RNA interference technology
RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing gene transcription or activating RNA degradation. This mechanism was discovered in plants in 1998 by Andrew Fire and Craig Mello. Today, this phenomenon can be observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals.
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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
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Fiche technique (265 KB)
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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)
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Instruction de manipulation (2242 KB)
Références
[1]. Nissen SE, et al. Single Ascending and Multiple-Dose Trial of Zerlasiran, a Short Interfering RNA Targeting Lipoprotein(a): A Randomized Clinical Trial. JAMA. 2024;331(18):1534-1543. [Content Brief]
[2]. Fazoli RT, et al. RNA interference therapy in cardiology: will new targets improve therapeutic goals?. Drugs Context. 2024;13:2024-3-1. Published 2024 Aug 20. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)