DSG-PEG2000-PP1
DSG-PEG2000-PP1 (DSG-PEG2000-Mal-Cys-LSLERFLRCWSDAPA) is a functionalized PEGylated phospholipid conjugate composed of three modular components: distearoylglycerol (DSG) as a lipid anchoring group, a 2000 Da polyethylene glycol (PEG) spacer arm, and a PP1 (HY-P12012) peptide as a terminal targeting/functional ligand. DSG-PEG2000-PP1 can be used in research on targeted drug delivery for atherosclerosis.
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보관:
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
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vitro
DSG-PEG2000-PP1 is composed of three covalently linked components: 1. DSG (distearoylglycerol) : Lipid anchoring group-a diacylglycerol with two saturated C18 chains; provides strong membrane rigidity and sustained nanoparticle stability, suitable for applications requiring prolonged circulation time. 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. PP1 peptide: Targeting/functional ligand-the PP1 peptide specifically binds to scavenger receptor type A type I (SR-AI), targeting inflammatory atherosclerotic plaques.
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
[DSG-PEG2000-PP1]
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Synonyms
DSG-PEG2000-Mal-Cys-LSLERFLRCWSDAPA
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
DSG-PEG2000-PP1 Related Classifications
HY-189161A Related Classifications
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