产品
编 号：F195531
分子式：C16H14N4O
分子量：278.31
分子式：C16H14N4O
分子量：278.31
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
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1mg
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 1628208-23-0
产品详情
生物活性：
CPI-455 is a specific, pan-KDM5 inhibitor with an IC50 of 10 nM for KDM5A. CPI-455 mediates KDM5 inhibition, elevates global levels of H3K4me3, and decreases the number of drug-tolerant persister cancer cells in multiple cancer cell line models treated with standard chemotherapy or targeted agents.
体内研究：
在小鼠中双重阻断 B7-H4 和 KDM5B (CPI-455，50/70 mg/kg，腹腔注射，每日) 可引发保护性免疫。Animal Model:Six-week-old male C57BL/6 mice (One- to 2-mm fragments of P. gingivalis–positive PDXs were implanted subcutaneously into the flank region of humanized mice.)
Dosage:50 mg/kg or 70 mg/kg (combined with anti–B7-H4).
Administration:IP, daily, 14-28 days.
Result:Histopathology analysis revealed no inflammation in either group at 2 weeks in response to the primary infection. However, at 8 weeks after inoculation, mice receiving monotherapy exhibited mild inflammation, whereas the combined treatment presented with heavy to severe inflammation, which persisted at 12 and 16 weeks after challenge.Treatment with CPI-455 to selectively target H3K4-specific JmjC demethylases increased CXCL11, CXCL9, and CXCL10 following infection, with maximum levels observed 48 hours after infection.
体外研究：
CPI-455 介导 KDM5 抑制，提高 H3K4 三甲基化 (H3K4me3) 的总体水平，并减少使用标准化疗或靶向药物处理的多种癌细胞系模型中的 DTP 数量。 CPI-455，对目标 KDM5 蛋白具有高亲和力。在 24 小时内，在暴露于两种活性化合物 CPI-455 和 CPI-766 中的任何一种后，观察到 H3K4me3 以剂量依赖性方式增加。KDM5 Inhibitor CPI0455 在 3 种管腔乳腺癌细胞系 MCF-7、T-47 和 EFM-19 中的 IC50 计算值分别为 35.4、26.19 和 16.13 μM。
CPI-455 is a specific, pan-KDM5 inhibitor with an IC50 of 10 nM for KDM5A. CPI-455 mediates KDM5 inhibition, elevates global levels of H3K4me3, and decreases the number of drug-tolerant persister cancer cells in multiple cancer cell line models treated with standard chemotherapy or targeted agents.
体内研究：
在小鼠中双重阻断 B7-H4 和 KDM5B (CPI-455，50/70 mg/kg，腹腔注射，每日) 可引发保护性免疫。Animal Model:Six-week-old male C57BL/6 mice (One- to 2-mm fragments of P. gingivalis–positive PDXs were implanted subcutaneously into the flank region of humanized mice.)
Dosage:50 mg/kg or 70 mg/kg (combined with anti–B7-H4).
Administration:IP, daily, 14-28 days.
Result:Histopathology analysis revealed no inflammation in either group at 2 weeks in response to the primary infection. However, at 8 weeks after inoculation, mice receiving monotherapy exhibited mild inflammation, whereas the combined treatment presented with heavy to severe inflammation, which persisted at 12 and 16 weeks after challenge.Treatment with CPI-455 to selectively target H3K4-specific JmjC demethylases increased CXCL11, CXCL9, and CXCL10 following infection, with maximum levels observed 48 hours after infection.
体外研究：
CPI-455 介导 KDM5 抑制，提高 H3K4 三甲基化 (H3K4me3) 的总体水平，并减少使用标准化疗或靶向药物处理的多种癌细胞系模型中的 DTP 数量。 CPI-455，对目标 KDM5 蛋白具有高亲和力。在 24 小时内，在暴露于两种活性化合物 CPI-455 和 CPI-766 中的任何一种后，观察到 H3K4me3 以剂量依赖性方式增加。KDM5 Inhibitor CPI0455 在 3 种管腔乳腺癌细胞系 MCF-7、T-47 和 EFM-19 中的 IC50 计算值分别为 35.4、26.19 和 16.13 μM。
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