| Bioactivity | CC-401 dihydrochloride is a potent inhibitor of all three forms of JNK with Ki of 25 to 50 nM[1]. |
| Target | Ki: 25 to 50 nM (JNK). |
| Invitro | CC-401 dihydrochloride 对 JNK 的选择性至少是其他相关激酶的 40 倍，包括 p38、细胞外信号调节激酶 (ERK)、κB 激酶抑制剂 (IKK2)、蛋白激酶 C、Lck、70 的 zeta 相关蛋白kDa (ZAP70)。在基于细胞的测定中，CC-401 dihydrochloride (1 - 5 μM) 特异性抑制 JNK。CC-401 dihydrochloride，一种小分子，是所有三种 JNK 亚型的特异性抑制剂。CC-401 dihydrochloride 竞争性结合 JNK 中的 ATP 结合位点，从而抑制转录因子 c-Jun 的 N 末端激活域的磷酸化。使用 HK-2 人肾小管上皮细胞系的渗透压在体外测试了该抑制剂的特异性。CC-401 dihydrochloride 以剂量依赖性方式抑制 Sorbitol 诱导的 c-Jun 磷酸化。然而，CC-401 dihydrochloride 不会阻止 Sorbitol 诱导的 JNK、p38 或 ERK磷酸化[1]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> CC-401 dihydrochloride 相关抗体: |
| In Vivo | 与对照组相比，Bevazicumab 和 Oxaliplatin 处理适度诱导 p-JNK 染色，并且在 CC-401 处理的样品中 p-cJun 含量显著降低，与有效的 JNK 抑制一致。 与 CC-401 联合治疗时 DNA 损伤适度升高[2]。第 7 天至第 24 天的 CC-401 处理减缓了蛋白尿的进展，与第 14 天和第 21 天的无治疗组和载体组相比显著降低。但是，与第 5 天的蛋白尿相比，在第 21 天时 CC-401 处理的大鼠蛋白尿程度仍然有所增加。载体组和未治疗组在第 24 天出现肾功能损害，表现为血清肌酐升高，可通过 CC-401 处理来防止[3]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only. |
| CAS | 2319601-04-0 |
| Formula | C22H26Cl2N6O |
| Molar Mass | 461.39 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [1]. Vasilevskaya IA, et al. Inhibition of JNK Sensitizes Hypoxic Colon Cancer Cells to DNA-Damaging Agents. Clin Cancer Res. 2015 Sep 15;21(18):4143-52. [2]. Ma FY, et al. Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab Invest. 2009 Apr;89(4):470-84. [3]. Ma FY, et al. A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J Am Soc Nephrol. 2007 Feb;18(2):472-84. |