MAPK-IN-8

MAPK-IN-8 (compound 20) (20 µM; 24 h) exhibits no significant toxicity toward RAW 264.7 cells^[1].
MAPK-IN-8 (20 µM; pretreatment for 4 h + co-incubation with LPS (HY-D1056) (100 ng/mL for 12 h) significantly inhibits nitric oxide (NO) production in RAW 264.7 cells with an inhibition rate of 67.64%. MAPK-IN-8 significantly downregulates the protein and mRNA expression levels of LPS-induced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW 264.7 cells. MAPK-IN-8 reduces the secretion of the pro-inflammatory cytokines TNF-α and IL-6 ^[1].
MAPK-IN-8 (20 µM; pretreatment for 4 h + co-incubation with LPS (100 ng/mL) + IFN-γ (20 ng/mL) for 12 h) modulates macrophage polarization in RAW 264.7 cells. MAPK-IN-8 almost completely blocks polarization toward pro-inflammatory M1 macrophages while actively promoting polarization toward anti-inflammatory M2 macrophages^[1].
MAPK-IN-8 (5-20 µM; pretreatment for 4 h + co-incubation with LPS (100 ng/mL for 12 h) inhibits the overactivation of the MAPK signaling pathway in RAW 264.7 cells. MAPK-IN-8 significantly reduces the phosphorylation levels of key components of the MAPK cascade (p38, JNK and ERK) in a dose-dependent manner^[1].
MAPK-IN-8 (20 µM; pretreatment for 4 h + co-incubation with exposure to macrophage-conditioned medium for 16 h) significantly protects Caco2 intestinal epithelial cells against the degradation and disruption of tight junction proteins (ZO-1, Occludin, Claudin-4) induced by inflammatory mediators^[1].
MAPK-IN-8 (> 128 µg/mL) does not exhibit direct antibacterial activity against various Gram-negative pathogenic bacteria (Escherichia coli, Salmonella typhimurium, Klebsiella pneumoniae and Acinetobacter baumannii) (MIC > 128 µg/mL)^[1].

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