Identification | Back Directory | [Name]
L-Leucine, L-phenylalanyl-L-asparaginyl-L-prolyl-L-serylglycyl-L-prolyl-L-tyrosyl-L-glutaminyl-L-lysyl-L-lysyl-L-prolyl-L-valyl-L-histidyl-L-α-glutamyl-L-lysyl-L-lysyl-L-α-glutamyl-L-valyl- | [CAS]
960358-79-6 | [Synonyms]
CKLF1-C19 L-Leucine, L-phenylalanyl-L-asparaginyl-L-prolyl-L-serylglycyl-L-prolyl-L-tyrosyl-L-glutaminyl-L-lysyl-L-lysyl-L-prolyl-L-valyl-L-histidyl-L-α-glutamyl-L-lysyl-L-lysyl-L-α-glutamyl-L-valyl- | [Molecular Formula]
C103H161N27O28 | [MOL File]
960358-79-6.mol | [Molecular Weight]
2225.58 |
Hazard Information | Back Directory | [Uses]
CKLF1-C19 is the C-terminal peptide of human chemokine-like factor 1 (CKLF1). CKLF1-C19 interacts with CCR4, and inhibits chemotaxis induced by both CKLF1 and CCL17. CKLF1-C19 can suppress allergic lung inflammation via inhibiting chemotaxis mediated by CCR3 and CCR4[1]. | [in vivo]
CKLF1-C19 (0.01-100 μg, 200 μL; i.p.; single dose at day 24-26, 30 min before OVA induced) results in a significant reduction of airway hyperresponsiveness (AHR) compared to ovalbumin (OVA) group with saline[1].
CKLF1-C19 (0.5 mg or 1 mg, 200 μL; s.c.; single dose) reduces CCL11-mediated recruitment of eosinophils into the peritoneal cavity in a mouse model of asthma[1].
| [IC 50]
CCL17-CCR4; CCR3 | [References]
[1] Tian L, et al. The CKLF1-C19 peptide attenuates allergic lung inflammation by inhibiting CCR3- and CCR4-mediated chemotaxis in a mouse model of asthma. Allergy. 2011 Feb;66(2):287-97. DOI:10.1111/j.1398-9995.2010.02478.x |
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