| 货号 | 18867-10mg |
| 描述 | c-Jun N-terminal kinases (JNKs) are MAP kinase family members that become highly activated after cells are exposed to stress conditions and are poorly activated by exposure to growth factors or mitogens.1 CC-401 is a potent inhibitor of all three JNK isoforms (Ki values range from 25 to 50 nM).2,3 It has at least 40-fold selectivity for JNK compared with other related kinases. CC-401 is bioavailable when delivered by gavage, blocking JNK signaling and renal fibrosis in a rat obstructed kidney model.3 It also has been shown to decrease hepatic necrosis and apoptosis after orthotopic liver transplantation and prevent acute renal failure following ischemia/reperfusion associated with renal transplantation in rats.2,4 |
| 供应商 | Cayman |
| 应用文献 | |
| 1.Cowan, K.J., and Storey, K.B. Mitogen-activated protein kinases: New signaling pathways functioning in cellular responses to environmental stress. Journal of Experimental Biology 206, 1107-1115 (2003). 2.Uehara, T.,Xi Peng, X.,Bennett, B., et al. c-Jun N-terminal kinase mediates hepatic injury after rat liver transplantation. Transplantation 78(3), 324-332 (2004). 3.Ma, F.Y.,Flanc, R.S.,Tesch, G.H., et al. A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. Journal of the American Society of Nephrology 18(2), 472-484 (2007). 4.Kanellis, J.,Ma, F.Y.,Kandane-Rathnayake, R., et al. JNK signalling in human and experimental renal ischaemia/reperfusion injury. Nephrology Dialysis Transplantation 25(9), 2898-2908 (2010). | |
| 运输条件 | Wet ice in continental US; may vary elsewhere |
| 存放说明 | -20 |
| 纯度 | ≥98% |
| 计算分子量 | 388.5 |
| 分子式 | C22H24N6O |
| CAS号 | 395104-30-0 |
| 稳定性 | ≥ 2 years |
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