VCAM1 binding peptide
VCAM1 binding peptide is a VCAM1 binder with internalization activity. VCAM1 binding peptide can be labeled with 5-FAM. VCAM1 binding peptide serves as a component of biosensing systems for visualizing in vitro VCAM1 endocytic pathways. VCAM1 binding peptide forms the research and development basis for MacroP and NAMP, PET radiotracers targeting VCAM1. VCAM1 binding peptide is applicable to studies related to atherosclerosis.
For research use only. We do not sell to patients.
- CAS No.: 1311293-04-5
- Formula: C57H95N23O16S
- Molecular Weight:1390.57
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All Radionuclide-Drug Conjugates (RDCs) Isoforms
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Biological Activity
Description
IC50 & Target
[1]|
RDC Peptide |
In Vitro
The binding intensity of 5FAM-labeled VCAM1-binding peptide (10 mM; 4 h) to TNFα-treated HUVEC is higher than that to control HUVEC[1].
68Ga-MacroP (a VCAM1-binding peptide conjugate) binds specifically to VCAM-1 on the surface of TNF-α-stimulated HUVECs, and the activated cellular radioactive uptake is 4-fold higher than that of unstimulated control cells[2].
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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CAS No. 1311293-04-5
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Molecular Weight 1390.57
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Formula C57H95N23O16S
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Sequence
Val-His-Pro-Lys-Gln-His-Arg-Gly-Gly-Ser-Lys-Gly-Cys
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Sequence Shortening
VHPKQHRGGSKGC
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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)
VCAM1 binding peptide Related Classifications
HY-P11088 Related Classifications
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