CREKA peptide
Based on 1 Customer Validation
CREKA peptide is a selective non-covalent binding agent targeting fibrin, type IV collagen, and fibronectin, often used as a targeting ligand to modify delivery carriers. CREKA peptide specifically recognizes fibrin, fibronectin, and type IV collagen that are excessively deposited in the tumor microenvironment or fibrotic tissue, mediating the targeted accumulation of the carrier at the lesion site and promoting drug internalization into target cells (such as cancer cells and activated hepatic stellate cells). CREKA peptide can enhance targeted delivery efficiency, increase drug concentration at the lesion site, and reduce systemic side effects.
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- Reinheit: 99.80%
- CAS. Nr.: 847058-45-1
- Formel: C23H43N9O8S
- Molecular Weight:605.71
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Speicherung:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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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Biologische Aktivität
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Chemical Information
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Biologische Aktivität
CREKA peptide (0.5 mM, 1 mM; 1 hour) covalently bound to PEG particles showed significantly higher binding affinity to fibrin than free CREKA (approximately 70%) and peptide-free particles (45%), with a binding rate of 94% at 0.5 mM[1][3].
CREKA peptide (modified on PEG particles, particle concentration 0.1 mg/mL; 24 hours, 72 hours) showed no significant toxicity to HeLa cervical cancer cells and human BJ skin fibroblasts, with cell viability above 80%[1][3].
CREKA peptide (modified on PEG particles, loaded with DOX, particle concentration 0.1 mg/mL; 1 hour) significantly increased the uptake efficiency of DOX by HeLa cells, with an uptake rate of 111%, higher than PEG particles (50%), PEG-IKVAV particles (34%), and dual-peptide modified particles (34%)[1][3].
CREKA peptide (modified on liposomes, DiD concentration 200 ng/mL; 2-4 hours) promoted cellular uptake by human hepatic stellate cells LX2, with significantly higher fluorescence intensity than unmodified liposomes. Uptake was dependent on clathrin- and caveolin-mediated endocytosis and inhibited by free CREKA and fibronectin antibodies[2].
CREKA peptide (modified on liposomes, loaded with 1 μM sorafenib; 48 hours) significantly inhibited the mRNA expression of α-SMA, Col1a1, Col5a1, and TIMP-2 in LX2 cells, reduced α-SMA and Col1a1 protein levels, and inhibited collagen synthesis[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HeLa cervical cancer cells, human dermal BJ fibroblasts
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Concentration:PEG particles functionalized with CREKA, IKVAV, or CREKA-IKVAV (0.1 mg/mL); Control: Untreated cells
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Incubation Time:24 and 72 hours
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Result:The viability of both HeLa cells and BJ fibroblasts was above 80% in all peptide-functionalized particle groups. No significant cytotoxicity was observed compared to the untreated control group, indicating the good biocompatibility of CREKA-functionalized PEG particles.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male C57BL/6 J mice (male, 7-8 weeks old) CCl4-induced liver fibrosis model[2]
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Dosage:Sorafenib-loaded CREKA-modified liposomes (CREKA-Lip/Sor): 1 mg/kg sorafenib, dissolved in PBS
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Administration:administered intravenously, twice a week for 4 consecutive weeks
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Result:After 4 weeks of treatment, CREKA-Lip/Sor significantly alleviated CCl4-induced liver fibrosis. Sirius red and Masson’s trichrome staining showed a marked reduction in hepatic collagen deposition compared to free sorafenib and sorafenib-loaded unmodified liposomes (Lip/Sor).
The mRNA and protein levels of fibrotic markers including α-SMA, Col1a1, Col3a1, Col5a1, TIMP-1 and TGF-β1 were significantly downregulated. Additionally, CREKA-Lip/Sor attenuated liver inflammation by reducing the mRNA expression of Mcp-1, IL-1β and Tnf-α, and decreasing F4/80-positive inflammatory cell infiltration.
It also inhibited hepatic angiogenesis, as evidenced by reduced CD31-positive vascular density and suppressed phosphorylation of PDGFR-β, Akt and Erk. No obvious toxicity was observed in major organs.
Chemical Information
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CAS. Nr. 847058-45-1
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Appearance Solid
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Molecular Weight 605.71
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Formel C23H43N9O8S
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Color White to off-white
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Sequence
Cys-Arg-Glu-Lys-Ala
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Sequence Shortening
CREKA
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Reinheit & Dokumentation
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Data Sheet (276 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Okur AC, et al. Targeting cancer cells via tumor-homing peptide CREKA functional PEG nanoparticles. Colloids Surf B Biointerfaces. 2016 Nov 1;147:191-200. [Content Brief]
[2]. Li R, et al. CREKA-modified liposomes target activated hepatic stellate cells to alleviate liver fibrosis by inhibiting collagen synthesis and angiogenesis. Acta Biomater. 2023 Sep 15;168:484-496. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
CREKA peptide Related Classifications
HY-P10709 Related Classifications
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