DMG-PEG2000-WLSEAGPVVTVRALRGTGSW
DMG-PEG2000-WLSEAGPVVTVRALRGTGSW is a functionalized PEGylated phospholipid conjugate composed of three modular components: 1,2-dispalmitoyl-sn-glycerol-3-phosphoethanolamine (DMG) as a lipid anchoring group, a 2000 Da polyethylene glycol (PEG) spacer arm, and the WLSEAGPVVTVRALRGTGSW (HY-P3436) peptide as a terminal targeting/functional ligand. DMG-PEG2000-WLSEAGPVVTVRALRGTGSW can be used in research on targeted drug delivery for cardiovascular diseases (such as myocardial infarction and heart failure).
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
DMG-PEG2000-WLSEAGPVVTVRALRGTGSW is composed of three covalently linked components: 1. DMG (dimyristoylglycerol): Lipid anchoring group-a diacylglycerol with two C14 chains, providing moderate membrane anchorage; its short-chain, high-fluidity characteristics enable faster dissociation of PEG-lipids from nanoparticle surfaces, facilitating endosomal escape and cellular uptake. 2. PEG 2000 (polyethylene glycol, molecular weight 2000): A hydrophilic polymer spacer arm that forms a steric hindrance crown around the 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. WLSEAGPVVTVRALRGTGSW peptide: A cardiomyocyte-targeting peptide that specifically recognizes tenosynovin X on the surface of 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
CCCCCCCCCCCCCC(OCC(OC(CCCCCCCCCCCCC)=O)COCCOCCOCCC([WLSEAGPVVTVRALRGTGSW])=O)=O.[n]
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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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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)
DMG-PEG2000-WLSEAGPVVTVRALRGTGSW Related Classifications
HY-181749A Related Classifications
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