DC-PGKI is an orally active ATP-competitive PGK1 inhibitor(IC50 = 0.16 Mm, Kd = 99.08 nM). DC-PGKI stabilizes PGK1 in vitro and in vivo, and suppresses both glycolytic activity and the kinase function of PGK1. DC-PGKI-mediated inhibition of PGK1 leads to the accumulation of NRF2 (nuclear factor-erythroid factor 2-related factor 2, NFE2L2), which then translocates to the nucleus, binds to the proximal regions of IL-1beta and IL-6 genes, and suppresses the LPS-induced expression of these genes. DC-PGKI can be used for the study of colitis[1].
