XP-524 是一种有效的BET和EP300抑制剂。XP-524 在体内显示出强大的杀肿瘤活性。 XP-524 可防止 KRAS 诱导的体内肿瘤转化，并延长两种侵袭性 PDAC 转基因小鼠模型的存活时间。XP-524 还增强了自身肽的表达和将肿瘤细胞向细胞毒性 T 淋巴细胞的募集。XP-524 具有研究胰腺导管腺癌（PDAC）的潜力。

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) [1].

XP-524 (5 mg/kg; i.p.; daily for 150 days) extends survival and inhibits KRAS signaling in uurinePDAC [1]. XP-524 (5 mg/kg; i.p.; daily for 250 days) Cooperates with PD-1 inhibition to further extends survivalin KPC Mice [1]. Animal Model: 15 weeks KPC mice [1] 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 [1] 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.

2344825-52-9

C30H28N6O3S

552.65

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years