产品
编 号：F751400
分子式：C30H28N6O3S
分子量：552.65
分子式：C30H28N6O3S
分子量：552.65
产品类型
规格
价格
是否有货
1mg
询价
询价
结构图
CAS No: 2344825-52-9
产品详情
生物活性：
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).
体内研究：
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.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.
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).
体内研究：
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.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.
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