Abstract
CDK1 and CDK4 are highly similar isoforms but with apparently diverse cellular functions, which makes it fundamental to discover selective CDK4 inhibitors that could accurately control the process of cell cycle of the specific organization so as to restore normal physiological state. In current research, interaction modes of CDK1 and CDK4 inhibitors were investigated through combined in silico strategies to elucidate the selectivity mechanism against CDK4 over CDK1, revealing that H-bond networks formed with key amino acids such as LYS33 and LEU83 of CDK1 and VAL93 of CDK4 are crucial for CDK4 selective inhibition, which would provide a theoretical basis for the design of selective CDK4 inhibitors.
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