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C87 directly binds to TNFα, potently inhibits TNFα-induced cytotoxicity (IC50=8.73 μM) and effectively blocks TNFα-triggered signaling activities. C87 exhibits good solubility and consistent dose-dependent functions in vitro. C87 completely blocks TNFα-induced activation of caspase-3 and caspase-8. The activity of c-Jun N-terminal kinase (JNK) is significantly reduced by C87 in L929 cells. C87 also prevents the degradation of IκBα in cells treated with TNFα. C87 potently blocks multiple signaling transduction pathways and downstream target gene activation triggered by TNFα[1].

C87 attenuates TNFα-induced inflammation, thereby markedly reducing injuries to the liver and improving animal survival. C87 injection delays the incidence of death and increases the survival rate by two folds compared with the vehicle control. The level of alanine transaminase and aspartate transaminase is consistently reduced in mice with C87 treatment[1].

[1]. Ma L, et al. A novel small-molecule tumor necrosis factor α inhibitor attenuates inflammation in a hepatitis mouse model. J Biol Chem. 2014 May 2;289(18):12457-66.

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