布鲁顿酪氨酸激酶
化学
酪氨酸激酶
伊布替尼
突变体
共价键
癌症研究
生物化学
生物
信号转导
慢性淋巴细胞白血病
免疫学
基因
白血病
有机化学
作者
Yunpeng Zhao,Yongzhi Shu,Jun Lin,Zhendong Chen,Qiong Xie,Yanning Bao,Lixue Lu,Nannan Sun,Yonghui Wang
标识
DOI:10.1016/j.ejmech.2021.113820
摘要
Bruton's tyrosine kinase (BTK) is a key drug target for B-cell related malignancies. Irreversible covalent BTK inhibitors have been approved for the treatment of B-cell malignancies, yet BTK C481S mutation at the covalent binding site has caused drug-resistance of BTK covalent binding inhibitors. The proteolysis targeting chimera (PROTAC) technology increases the sensitivity to drug-resistant targets compared to classic inhibitors, which provides a new strategy for mutant BTK related B-cell malignancies. ARQ531, a reversible non-covalent BTK inhibitor that inhibits wild type (WT) and mutated BTK with high selectivity, could be an ideal warhead for PROTACs targeting the mutant BTK. Herein, we designed a novel series of PROTACs using the selective non-covalent BTK inhibitor ARQ531 as warhead, with the goal of improving the degradation of both wild-type and C481S mutant BTKs, and increasing the selectivity of BTK over other kinases. This effort will provide some basis for further preclinical study of BTK PROTACs as a novel strategy for treatment of B-cell lymphomas.
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