DMG-PEG2000-PP1
DMG-PEG2000-PP1 (DMG-PEG2000-Mal-Cys-LSLERFLRCWSDAPA) is a functionalized PEGylated phospholipid conjugate composed of three modular components: dimyristoylglycerol (DMG) 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. DMG-PEG2000-PP1 can be used in research on targeted drug delivery for atherosclerosis.
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。
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
体外実験
DMG-PEG2000-PP1 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): 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.
化学情報
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SMILES
CCCCCCCCCCCCCC(OCC(OC(CCCCCCCCCCCCC)=O)COCCOCCOCCNC([Mal-Cys-LSLERFLRCWSDAPA])=O)=O.[n]
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別名
DMG-PEG2000-Mal-Cys-LSLERFLRCWSDAPA
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)