PP1 peptide
PP1 peptide is an antagonist that specifically binds to scavenger receptor AI (SR-AI), with an IC50 of 29 μM against bovine SR-AI. By recognizing SR-AI which is highly expressed on macrophages, PP1 peptide enables precise targeting and internalization of inflammatory regions within atherosclerotic plaques. PP1 peptide can be used in research related to atherosclerosis.
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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。
- CAS 番号: 870274-84-3
- 分子式: C79H122N22O22S
- 分子量:1764.01
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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
PP1 peptide (0-300 μM) potently inhibits the binding of SR-AI-targeting phages to immobilized recombinant SR-AI, with an IC50 of 29 μM, and its N-terminal region is critical for activity[1].
The PP1 peptide binds to mouse RAW264.7 macrophages in an SR-AI-dependent manner, as demonstrated by fucoidan-mediated inhibition assays, with an IC50 of 4.2 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
体内実験
PP1 (0.38 μM; intravenous injection; single administration) selectively targets advanced atherosclerotic plaques in ApoE-/- mice, increases the maximum carrier accumulation by 93.7%, colocalizes with 52.4% of macrophages in plaques, and does not alter plaque size[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ApoE-/- (male, ~65 weeks old, back-crossed for 9 generations on a C57Bl/6 background)[1]
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Dosage:0.38 μM
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Administration:i.v.; single dose
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Result:Showed an 84.12% increase in aortic plaque accumulation compared with untargeted 125I-streptavidin, with no difference in plaque size between groups.
Showed a 93.65% increase in aortic plaque accumulation compared with untargeted Quantumdot Nanocrystals.
Colocalized with 52.4% of intraplaque F4/80-positive macrophages, compared with 6.3% for untargeted Quantumdots.
化学情報
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CAS 番号 870274-84-3
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分子量 1764.01
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分子式 C79H122N22O22S
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SMILES
O=C(N[C@@H](CO)C(N[C@@H](CC(C)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC1=CC=CC=C1)C(N[C@@H](CC(C)C)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CS)C(N[C@@H](CC2=CNC3=CC=CC=C23)C(N[C@@H](CO)C(N[C@@H](CC(O)=O)C(N[C@@H](C)C(N4[C@@H](CCC4)C(N[C@@H](C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CC(C)C)N
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配列
Leu-Ser-Leu-Glu-Arg-Phe-Leu-Arg-Cys-Trp-Ser-Asp-Ala-Pro-Ala
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シーケンスの短縮
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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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)