IBD, including ulcerative colitis (UC) and crohn’s disease (CD) can be caused by genetic and environmental factors and can induces uncontrolled activation of intestinal immune cells. Pro-inflammatory cytokines, such as IL-6 and TNF, produced by activated immune cells are suggested to drive the perpetuation of inflammation and tissue damage.
IBD is a global disorder with a high incidence in developed countries (prevalence rate > 0.3%) and accelerating incidence in industrialized countries.
Even though anti-TNF antibodies have been widely used to treat IBD and hold the largest market share in the IBD therapeutics market, the response rate of antibody treatment is rapidly falling due to alternative signaling mechanisms contributing to resistance to the antibody therapy.
This offers added value to multi-cytokine blockers such as tofacitinib (Jak1 and Jak3 inhibitors) for the effective suppression of gut inflammation.
According to our findings, the phenotypes of IBD induced by dextran sodium sulfate (DSS) treatment were significantly recovered in PDK4 knockout mice, indicating that PDK4 is tightly connected with IBD progression.
These findings indicate that PDK4 inhibitors can provide a new therapeutic method for IBD. Thus, we synthesized both competitive and allosteric PDK4 inhibitors.
Commercialized multi-cytokine blockers such as tofacitinib have limited the rapeutic effects because they can only suppress a limited number of helper T cells. However, since PDK4 inhibitors can modulate the mitochondrial function of immune cells, they can modulate more diverse helper T cells than tofacitinib
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