XP-524 is a potent BET and EP300 inhibitor. XP-524 shows great tumoricidal activity in vivo. XP-524 prevents KRAS-induced, neoplastic transformation in vivo and extends survival in two transgenic mouse models of aggressive PDAC. XP-524 also enhances the presentation of self-peptide and tumor recruitment of cytotoxic T lymphocytes. XP-524 has the potential for the research of pancreatic ductal adenocarcinoma (PDAC). In Vivo XP-524 (5 mg/kg; i.p.; daily for 150 days) extends survival and inhibits KRAS signaling in uurinePDAC . XP-524 (5 mg/kg; i.p.; daily for 250 days) Cooperates with PD-1 inhibition to further extends survivalin KPC Mice . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: 15 weeks KPC mice Dosage: 5 mg/kg Administration: I.p., daily for 150 days Result: Significantly delayed mortality in KPC mice, extending median survival from 43- to 108-d postenrollment and reduced ERK activation, with parallel reductions in cell prolif-eration and uniform increases in apoptosis. Animal Model: 15 weeks KPC mice Dosage: 5 mg/kg Administration: I.p.; daily (200-μg dose of anti–PD-1 every other day) for 250 days Result: Increased in cell-mediated cytotoxicity andreduction in T cell exhaustion, the combination of XP-524 andanti–PD-1 enhanced expression of the surrogate marker of cyto-toxicity perforin-1 in tumor-infiltrating CD8+T cell. Form:Solid