化学
癌症
机制(生物学)
癌症研究
内科学
医学
认识论
哲学
作者
Zhongcheng Yang,Yuxia Liu,Zibin Liao,Lianru Chen,Zhiling Liang,Luyong Zhang,Zheng Li
标识
DOI:10.1021/acs.jmedchem.5c00062
摘要
MAPK-interacting kinases (MNKs) are the only known kinases that phosphorylate eIF4E at Ser209, playing a critical role in tumor progression. However, the current MNK inhibitors have been limited due to the deficiency of effectiveness. Herein, we reported the design of the first-in-class MNK1-targeting PROTACs based on the MNK1 inhibitor DS12881479 . Among them, P11–2 exhibited robust antitumor activity against MV4–11 cells (IC 50 = 45 nM) by efficiently degrading MNK1 (DC 50 = 11.92 nM, D max > 96%) mediated by the ubiquitin-proteasome system. Notably, P11–2 does not degrade MNK2, which played an important role in maintaining normal function. Moreover, P11–2 significantly suppressed the phosphorylation of eIF4E (IC 50 = 22.07 nM), induced apoptosis, and arrested the cell cycle at the G1 phase. In addition, P11–2 exhibited favorable PK profiles and robust antitumor effects in the xenograft model. These findings highlight the potential of P11–2 as a novel therapeutic strategy for targeting the degradation of MNK1.
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