化学
细胞周期蛋白依赖激酶2
选择性
细胞周期蛋白依赖激酶6
药代动力学
流出
分子动力学
机制(生物学)
组合化学
药理学
结构-活动关系
生物物理学
生物化学
新陈代谢
嘧啶
细胞生长
分子模型
计算生物学
多重耐药
药物代谢
癌细胞
体外
动力学(音乐)
肿瘤细胞
癌症研究
生长抑制
肽
立体化学
细胞周期蛋白依赖激酶
激酶
作者
Vishal Verma,Jessica M. Grandner,Brendan T. Parr,Mingshuo Zeng,Melissa Ashley,Yong Wang,Paul Beroza,Pasquale Carione,Kevin M. Johnson,A K Oh,Jeremy Murray,James R. Kiefer,John G. Moffat,Madeleine Prangley,Karl Merrick,Steffan Vartanian,M J Hafner,Christine Orr,Ehud Segal,Elizabeth S. Levy
标识
DOI:10.1021/acs.jmedchem.5c03803
摘要
Targeting HR-positive breast cancer via the inhibition of CDK4 and CDK6 has become the standard of care. However, progression inevitably occurs, and emerging data suggest the implication of CDK2 in this resistance mechanism. As part of our efforts to target this resistance, we embarked on a medicinal chemistry campaign to selectively inhibit CDK2 over the broadly essential CDK1. In order to obtain selectivity against CDK1, we utilized a molecular dynamics approach focused on interaction with a conserved lysine in the active site. Additionally, we uncovered a unique mechanism of clearance driven by both metabolism and efflux in rats and demonstrated that we could counter efflux-driven clearance with high permeability. Our efforts resulted in compound 19, which was potent against CDK2, exhibited good selectivity vs CDK4 and CDK1, and had pharmacokinetic properties that enabled evaluation in a CDK2 xenograft model of cancer, where it achieved nearly 80% tumor growth inhibition.
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