The bromodomain and extra-terminal (BET) inhibitor have emerged as promising new cancer agents via regulation of epigenetic mechanism. Recent studies further demonstrate that BET inhibitors exhibit anti-inflammatory effects in animal models of various inflammatory diseases. In the present study, we examined the effect of BET inhibitor on inflammatory bowel disease (IBD) in experimentally-induced murine Crohn's disease (CD)-like ileitis models. Ileitis was induced in male C57BL/6 mice by subcutaneous administration of indomethacin and the ileum was examined 48 h later. CN210 was given orally 30 min before and 24 h after indomethacin administration. Further, the effect of CN210 on LPS-stimulated cytokine expression in cultured RAW264.7 cells. The administration of CN210 reduced the severity of indomethacin-induced ileitis in a dose-dependent manner. Indomethacin-induced upregulation of inflammatory cytokines such asTNF-α, IL-1β and IL-6was also significantly attenuated by administration of CN210. In RAW264.7 cells, LPS upregulated the expression of inflammatory cytokines, and this response was potently abrogated by CN210. These findings suggest that CN210 ameliorates indomethacin-induced ileitis via inhibition of inflammatory cytokine expression. Thus, CN210 is a novel candidate for the treatment with IBD including CD.