CC-401 is a second generation ATP-competitive anthrapyrazolone c-Jun N terminal kinase (JNK) inhibitor with potential antineoplastic activity. IC50 value: Target: JNK In vitro: JNK inhibition decreased cytochrome c release, caspase 3 activation (P<0.05), and lipid peroxidation (P<0.05). JNK inhibition also transiently blocked phosphorylation of c-Jun at 60 minutes after reperfusion (P<0.05) without affecting other MAPK signaling, including p-38 and Erk activation [1]. in vivo: In acute disease, CC-401 blocked JNK signaling and reduced proteinuria in the first 24 h. The transient neutrophil influx seen at 3 h of disease was not affected, however. Continued CC-401 treatment suppressed glomerular and tubulointerstitial damage usually seen at 14 days [2]. Administration of CC-401 to rats prior to bilateral renal I/R prevented acute renal failure and largely prevented tubular damage, leucocyte infiltration and upregulation of pro-inflammatory molecules. However, delaying CC-401 treatment until 1 h after reperfusion (after the peak of JNK activation) had no protective effect [3].
[1]. Uehara T, et al. c-Jun N-terminal kinase mediates hepatic injury after rat liver transplantation. Transplantation. 2004 Aug 15;78(3):324-32.
[2]. Flanc RS, et al. A pathogenic role for JNK signaling in experimental anti-GBM glomerulonephritis. Kidney Int. 2007 Sep;72(6):698-708.
[3]. Kanellis J, et al. JNK signalling in human and experimental renal ischaemia/reperfusion injury. Nephrol Dial Transplant. 2010 Sep;25(9):2898-908.
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