NF-κB-IN-4 (compound 17) is a potent inhibitor of NF-κB pathway which can cross blood brain barrier (BBB). NF-κB-IN-4 shows potential anti-neuroinflammatory activity with low toxicity which can be used for the research of neuroinflammation related diseases. NF-κB-IN-4 can block the IκBα activation and phosphorylation, reduce NLRP3 expression, therefore inhibiting NF-κB activation [1].

NF-κB-IN-4 (compound 17) (0-10 μM, 24 h) shows high anti-inflammatory activity [1]. NF-κB-IN-4 (0-5 μM, 24 h) significantly decreases the LPS-induced p-IκBα expression levels, significantly inhibits the phosphorylation of IκBα and the expression of three proteins (NLRP3, ASC and caspase-1) in BV2 cells [1]. NF-κB-IN-4 (0-5 μM, 24 h) induces LPS-induced apoptosis in BV2 cells in a dose-dependent manner [1]. Cell Cytotoxicity Assay Cell Line: BV2 microglia cells [1] Concentration: 0, 2.5, 5, 10 μM Incubation Time: 24 h Result: Showed high anti-inflammatory activity, with the survival rate of BV2 microglia cells of 97.4%, inhibition rates against TNF-α and IL-6 release of 60.8% and 80.2%, respectively. Western Blot Analysis Cell Line: BV2 cells [1] Concentration: 0, 1.25, 2.5, 5 μM Incubation Time: 24 h Result: Significantly decreased the LPS-induced p-IκBα expression levels, significantly inhibited the phosphorylation of IκBα and the expression of three proteins (NLRP3, ASC and caspase-1) in BV2 cells. Apoptosis Analysis Cell Line: BV2 cells [1] Concentration: 0, 2.5, 5 μM Incubation Time: 24 h Result: Induced LPS-induced apoptosis in BV2 cells in a dose-dependent manner, with the apoptosis rates of 30.7% (2.5 μM) and 13.0% (5 μM), respectively.