B022 is a potent and selective NF-κB-inducing kinase (NIK) inhibitor ( K i of 4.2 nM; IC 50 =15.1 nM). B022 protects liver from toxin-induced inflammation, oxidative stress, and injury In Vitro B022 (0-5 μM; 12 hours; Hepa1 cells) treatment suppresses NIK-induced p52 formation in a dose-dependent manner. B022 (0-5 μM; 12 hours; Hepa1 cells) treatment for 8 h completely blocks NIK-induced expression of TNF-a, IL-6, iNOS, CCL2, and CXCL5. B022 prevents NIK- or H2O2-induced β cell death and also ameliorates streptozotocin (STZ)-induced β cell death and hyperglycemia. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: Hepa1 cells Concentration: 0 μM, 0.5 μM, 5 μM Incubation Time: 12 hours Result: Suppressed NIK-induced p52 formation in a dose-dependent manner. RT-PCRCell Line: Hepa1 cells Concentration: 0 μM, 0.5 μM, 5 μM Incubation Time: 12 hours Result: Dose-dependently blocked NIK-induced expression of chemokines, cytokines, and iNOS in these cells. Completely blocked NIK-induced expression of TNF-a, IL-6, iNOS, CCL2, and CXCL5. In Vivo B022 (30 mg/kg; intravenous injection; twice a day; for 10 days; STOP-NIK male mice) treatment inhibits NIK-triggered liver inflammation and injury in STOP-NIK mice infected with cre adenoviruses . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: STOP-NIK male mice (8 weeks) infected with Ad-cre Dosage: 30 mg/kg Administration: Intravenous injection; twice a day; for 10 days Result: Completely prevents the lethal effect of abnormally high levels of hepatic NIK in mice. Inhibited the majority of the deteriorating effects of aberrant activation of hepatic NIK. Form:Solid IC50& Target:Ki: 4.2 nM (NF-κB-inducing kinase (NIK))