CXCR2-IN-3

CXCR2-IN-3 (compound 5) shows potent ROS scavenging activity in RAW 264.7 macrophages^[1].
In combination of 5-Fluorouracil (HY-90006), CXCR2-IN-3 is strikingly showing significant cytotoxicity in CAL27 cells with the LD50 of 48.00 μM^[1].
CXCR2-IN-3 (25-100 μM) inhibits the migration as well as reduce the clonogenic potency of the CAL27 cells^[1].
CXCR2-IN-3 decreases IL-8 expression in both CAL27 and LPS stimulated CAL27 cells. CXCR2-IN-3 reduces the Ca2+ level in the CAL27^[1].
CXCR2-IN-3 (10-50 μM) induces autophagy in a dose-dependent manner, as evidenced through higher LC3 puncta formation in the CAL27 cells. CXCR2-IN-3 reduces the autophagosome-lysosome fusion initiated by Rapamycin (HY-10219)^[1].
CXCR2-IN-3 shows dependent autophagic flux inhibition fuels anti-inflammatory response in the oral cancer cells via downregulating the canonical CXCR2-NLRP3 signalling cascade^[1].
CXCR2-IN-3 (5 μM, 50 μM; 21 days, 24 h) primes oral cancer cells and enhances chemo-sensitization in CAL27^[1].
CXCR2-IN-3 (5-50 μM; 24-72 h) induces autophagy-dependent cell death in PGCCs (CDDP-resistant oral cancer cells) and reduces autophagic flux and triggers autophagy-mediated apoptotic cell death in CAL27^[1].

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