IKVAVC
IKVAVC is a derivative peptide of IKVAV with an artificially added cysteine (Cys) at its C-terminus. IKVAVC retains all the biological activities of the original IKVAV, mainly acting as a neural adhesion/differentiation signaling peptide, and is equipped with an engineered linker arm that enables covalent conjugation to molecular materials. IKVAV inhibits the migration and activation of fibroblasts, downregulates the TGF-β1 signaling pathway and endoplasmic reticulum stress, and promotes nerve repair. IKVAV regulates the phenotype of macrophages, shifting them from the pro-inflammatory M1 type to the pro-reparative M2 type.
For research use only. We do not sell to patients.
- CAS No.: 1187540-64-2
- Formula: C28H53N7O7S
- Molecular Weight:631.83
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
IKVAVC is covalently conjugated to biomaterials such as hydrogels and dendrimers via chemical reactions. This functionalized material can provide bioactive signals in a long-term, stable manner, construct a bionic microenvironment conducive to nerve regeneration and angiogenesis, and shows application potential in the treatment of diseases such as spinal cord injury[1][2][3].
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. 1187540-64-2
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Molecular Weight 631.83
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Formula C28H53N7O7S
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Sequence
Ile-Lys-Val-Ala-Val-Cys
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Sequence Shortening
IKVAVC
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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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Cell migration
Cell migration is a method that plays an important role in wound healing, cell differentiation, embryonic development, etc.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
[1]. Yin Y, et al. Pentapeptide IKVAV-engineered hydrogels for neural stem cell attachment. Biomater Sci. 2021;9(8):2887-2892. [Content Brief]
[2]. Jiang T, et al. IKVAV peptide-containing hydrogel decreases fibrous scar after spinal cord injury by inhibiting fibroblast migration and activation. Behav Brain Res. 2023;455:114683. [Content Brief]
[3]. Jha A, et al. Laminin-derived peptide, IKVAV, modulates macrophage phenotype through integrin mediation. Matrix Biol Plus. 2024;22:100143. Published 2024 Feb 15. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)