PPM-18

PPM-18 (0.1-10 µM; 24 h) inhibits lipopolysaccharide (LPS)-induced nitric oxide production (measured by nitrite content) in rat alveolar macrophages in a dose-dependent manner, with the maximal inhibitory effect observed at 10 µM^[1].
PPM-18 (3-10 µM; 24 h) inhibits lipopolysaccharide (LPS)-induced iNOS protein expression in rat alveolar macrophages^[1].
PPM-18 (3-10 µM; preincubated prior to 6 h LPS stimulation) inhibits lipopolysaccharide (LPS)-induced accumulation of iNOS mRNA in rat alveolar macrophages^[1].
PPM-18 (10 µM; 60 min preincubation prior to 30 min LPS stimulation) inhibits lipopolysaccharide (LPS)-induced nuclear translocation of NF-κB p65 in rat alveolar macrophages^[1].
PPM-18 (10-30 µM; 60 min preincubation prior to 30 min LPS stimulation for whole-cell assays) inhibits lipopolysaccharide (LPS)-induced NF-κB-DNA binding activity in intact rat alveolar macrophages, but does not directly interfere with NF-κB-DNA binding in isolated nuclear extracts^[1].
PPM-18 (10 µM; 24 h) inhibits LPS-induced TNF-α release from rat alveolar macrophages^[1].
PPM-18 (5-20 μM; 6-24 h) reduces the viability of bladder cancer T24 and EJ cells in a dose- and time-dependent manner^[2].
PPM-18 (5-15 μM; 24 h) induces autophagy in bladder cancer T24 and EJ cells in a dose-dependent manner, and this effect can be detected by decreased p62 expression and increased LC3B II expression^[2].
PPM-18 (10 μM; 1 h) completely inhibits shear-induced nuclear translocation of NF-κB subunits p50 and p65^[3].

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