Anti-inflammatory agent 116

Anti-inflammatory agent 116 (Compound 9a) (5-20 μM; 2 h pretreatment followed by 24 h LPS stimulation) potently inhibits NO production in LPS (HY-D1056)-stimulated RAW264.7 macrophages, with an IC₅₀ of 0.75 μM, and shows no significant cytotoxicity at a concentration of 20 μM^[1].
Anti-inflammatory agent 116 (5-20 μM; 24 h treatment with LPS) concentration-dependently inhibits pseudopodium formation and reduces cell aggregation in LPS-stimulated RAW264.7 macrophages^[1].
Anti-inflammatory agent 116 (5-20 μM; pretreated for 2 h followed by 6 h of LPS stimulation for TNF-α detection; pretreated for 2 h followed by 24 h of LPS stimulation for IL-1β detection) suppresses LPS-induced IL-1β and TNF-α secretion in RAW264.7 macrophages in a concentration-dependent manner^[1].
Anti-inflammatory agent 116 (5-20 μM; pretreated for 2 h followed by LPS stimulation for 30 min; pretreated for 2 h followed by LPS stimulation for 24 h) inhibits LPS-induced MtROS production in RAW264.7 macrophages in a concentration-dependent manner at 30 min and 24 h post-stimulation^[1].
Anti-inflammatory agent 116 (5-20 μM for NO inhibition assay; 150 μM for CETSA; pre-treatment for 2 h with or without RU486 followed by LPS stimulation for 24 h for NO inhibition assay; incubation at 37 °C for 30 min followed by heating at 40-61 °C for CETSA) exerts anti-inflammatory effects in RAW264.7 macrophages, and these effects are independent of the glucocorticoid receptor signaling pathway. This is because it does not bind to GR, and its NO inhibitory activity is not affected by the GR antagonist RU486 (HY-13683)^[1].
Anti-inflammatory agent 116 (5-20 μM, pretreated for 2 hours followed by LPS stimulation for 24 hours) concentration-dependently inhibits LPS-induced iNOS and COX-2 protein expression in RAW264.7 macrophages^[1].
Anti-inflammatory agent 116 (5-20 μM; 2 h pretreatment followed by 2 h LPS stimulation) concentration-dependently inhibits LPS-induced phosphorylation of IKK, IκB and p65 in RAW264.7 macrophages, and suppresses the activation of the NF-κB pathway without affecting IκB degradation^[1].
Anti-inflammatory agent 116 (5-20 μM; 2 h pretreatment followed by 2 h LPS stimulation) concentration-dependently inhibits LPS-induced phosphorylation of p38, ERK and JNK in RAW264.7 macrophages, thereby suppressing the activation of the MAPK pathway^[1].
Anti-inflammatory agent 116 (20 μM; 2 h pretreatment followed by 2 h LPS stimulation) blocks LPS-induced nuclear translocation of p65 in RAW264.7 macrophages^[1].
Anti-inflammatory agent 116 (20 μM for pull-down assay; 150 μM for CETSA; incubated with LPS-stimulated cell lysates at room temperature for 60 min in pull-down assay; incubated at 37 °C for 30 min followed by heating at 40-61 °C in CETSA) directly binds to the p50 subunit of the p65-p50 heterodimer in RAW264.7 macrophages, thereby impairing the DNA-binding ability of this heterodimer^[1].

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