Chondrocyte-affinity peptide

Chondrocyte‑affinity peptide (CAP) (1.3×10¹⁰ pfu; 4.5 h) displayed on phage binds potently to primary rabbit chondrocytes, with a recovery rate of 7.7×10^‑5, and exhibits a far higher affinity for chondrocytes than for rabbit synovial cells or blank phages^[1].
Chondrocyte-affinity peptide (4.5 h) can bind to and be internalized by primary rabbit chondrocytes and primary human chondrocytes without species specificity, with the mean fluorescence intensity of the two cell types being 1260.45 and 327.93, respectively, and it exhibits extremely low affinity for primary human synovial cells^[1].
Chondrocyte-affinity peptide (CAP) (10⁸/mL; 2 h) enhances the uptake of exosomes by primary rat chondrocytes, which produces a stronger intracellular fluorescence signal compared with exosomes without this peptide^[2].
Chondrocyte-affinity peptide enables hybrid exosomes to efficiently deliver the Cas9 sgMMP-13 plasmid into primary rat chondrocytes, potently inhibit MMP-13 expression, and prevent type II collagen degradation, even under IL-1β-induced osteoarthritis (OA)-mimicking conditions ^[2].
Chondrocyte-affinity peptide enables hybrid exosomes to deeply penetrate and retain in osteoarthritis (OA) cartilage tissue blocks^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. .