布鲁顿酪氨酸激酶
伊布替尼
Janus激酶3
化学
药理学
酪氨酸激酶
类风湿性关节炎
贾纳斯激酶
激酶
医学
免疫学
信号转导
生物化学
体外
白血病
白细胞介素12
细胞毒性T细胞
慢性淋巴细胞白血病
作者
Tingting Liang,Lifang Cen,Junjie Wang,Ming Cheng,Weibo Guo,Wenjie Wang,Chunqiu Yu,Haifeng Zhang,Yuan Wang,Zhongyan Hao,Jiaming Jin,Yaoyao Wu,Jiang Teng,Qihua Zhu,Yungen Xu
标识
DOI:10.1016/j.bmc.2023.117354
摘要
Rheumatoid arthritis (RA) is a chronically systemic autoimmune disorder, which is related with various cellular signal pathways. Both BTK (Bruton's Tyrosine Kinase) and JAK3 (Janus Kinase 3) play important roles in the pathogenesis of rheumatoid arthritis. Herein, we reported the discovery of dual BTK/JAK3 inhibitors through bioisosterism and computer-aided drug design based on the structure of BTK inhibitor ibrutinib. We reported the discovery of dual BTK/JAK3 inhibitors which are based on the structure of BTK inhibitor ibrutinib via the method of bioisosterism and computer-aided drug design) Most of the target compounds exhibited moderate to strong inhibitory activities against BTK and JAK3. Among them, compound XL-12 stood out as the most promising candidate targeting BTK and JAK3 with potent inhibitory activities (IC
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