前列腺癌
化学
癌症研究
BRD4
效力
癌症
前列腺
下调和上调
紫杉醇
癌细胞
细胞生长
药理学
乙酰化
生物活性
细胞培养
细胞凋亡
癌细胞系
细胞周期
药物发现
结构-活动关系
细胞
细胞周期检查点
作者
Yizhe Zhang,Huijuan Zhu,Xiao-Xiao Zhou,Shijie Li,Di Han,Fengxiang Liu,Hui-min Zhou,Xin-Yu Jiang,Yuan-Yuan Guan,Hui-Ru Ren,Ying Wang,Wenjing Dai,Yi-Bo Ban,Nan Su,Yong‐Cheng Ma,Yong-Tao Xu,Saiqi Wang,Ying‐Chao Duan
标识
DOI:10.1021/acs.jmedchem.5c03168
摘要
CBP/p300 and BRD4 synergistically drive prostate cancer progression. Here, we report the rational design, synthesis, and biological evaluation of novel PROTACs capable of simultaneously degrading CBP/p300 and BRD4. The representative compounds 10h and 29c induced robust degradation of both targets with DC50 values ranging from 8.8 pM to 10.5 nM in PC-3 prostate cancer cells, accompanied by marked downregulation of c-Myc and acetylated H3K27. Both compounds displayed potent antiproliferative activity across multiple cancer cell lines, with higher potency than NEO2734, paclitaxel (PTX), and ARV-771. In a PC-3 xenograft mouse model, compound 29c achieved dose-dependent tumor growth inhibition (TGI) of up to 81.5% at a low dose of 0.2 mg/kg, administered every other day, significantly surpassing the efficacy of NEO2734 and PTX at higher doses. Together, 29c, a highly efficient CBP/p300 and BRD4 dual-target degrader, demonstrates significant therapeutic potential in prostate cancer and warrants further development.
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