DPPE-PEG2000-CSTSMLKAC
DPPE-PEG2000-CSTSMLKAC is a functionalized PEGylated phospholipid conjugate composed of three modular components: 1,2-dipalmitoyl-sn-glycerol-3-phosphoethanolamine (DPPE) as a lipid anchoring group, a 2000 Da polyethylene glycol (PEG) spacer arm, and the CSTSMLKAC peptide as a terminal targeting/functional ligand. DPPE-PEG2000-CSTSMLKAC can be used in research on targeted drug delivery for ischemic heart disease.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
DPPE-PEG2000-CSTSMLKAC is composed of three covalently linked components: 1. DPPE (1,2-dipalmitoyl-sn-glycerol-3-phosphoethanolamine): Lipid anchoring group-inserts into the lipid bilayer of liposomes/LNPs, providing stable membrane anchoring; its saturated C16 chain imparts bilayer rigidity. 2. PEG 2000 (polyethylene glycol, molecular weight 2000): Hydrophilic polymer spacer arm-forms a steric hindrance crown around nanoparticles, reducing opsonin activity and reticuloendothelial system (RES) clearance, prolonging circulating half-life, and providing steric separation between the lipid surface and the targeting ligand. 3. CSTSMLKAC peptide: Targeting/functional ligand-the CSTSMLKAC peptide mediates phage selective homing to ischemic cardiac tissue and has targeted binding ability to ischemic cardiomyocytes.
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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SMILES
[DPPE-PEG2000-CSTSMLKAC]
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)