Kongensin A is a natural product isolated from Croton kongensis . Kongensin A is an effective, covalent HSP90 inhibitor that blocks RIP3 -dependent necroptosishas. Kongensin A is a potent necroptosis inhibitor and an apoptosis inducer. Kongensin A has potential anti-necroptosis and anti-inflammation applications In Vitro Kongensin A (0-15 μM; 6 hours; HT29 cells) treatment induces caspase activation and apoptosis in multiple cancer cell lines in a dosage-dependent manner. Kongensin A (0-15 μM; 24 hours; HT29 cells) treatment induces the degradation of RIPK1 and oncogenic kinases such as ERBB2, AKT, EGFR, and B-raf, and induces the up-regulation of HSP90A and HSP90B. Kongensin A covalently binds to cysteine 420 in the middle domain of HSP90 and dissociates HSP90 from its cochaperone CDC37. The HSP90-CDC37 complex is required for RIP3 activation, KA blocks LPS/Smac mimetics/Z-VAD and RIP3 polymerization-induced cell death, in which cell death is dependent on RIP3 but not its upstream kinase RIP1. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Apoptosis AnalysisCell Line: HT29 cells Concentration: 0 μM, 2.5 μM, 5 μM, 15 μM Incubation Time: 6 hours Result: Induced caspase activation and apoptosis in a dosage-dependent manner. Western Blot AnalysisCell Line: HT29 cells Concentration: 0 μM, 2.5 μM, 5 μM, 15 μM Incubation Time: 24 hours Result: Induced the degradation of RIPK1 and oncogenic kinases such as ERBB2, AKT, EGFR, and B-raf, and induced the up-regulation of HSP90A and HSP90B. Form:Solid IC50& Target:HSP90, RIP3, Apoptosis