In mammalian cells, proliferation is controlled by the cell
cycle, where cyclin-dependent kinases regulate critical
checkpoints. CDK4 is considered a highly validated anticancer
drug target due to its essential role in regulating cell cycle
progression at the G1 restriction point. Our objective is
to design novel CDK4 inhibitors using Structure-Based Drug
Design and Quantitative Structure-Activity Relationship
techniques. We used bioinformatics tools and biological
databases. QSAR study of CDK4 inhibitors has given us an
idea of the physicochemical features of studied compounds
and their correlation with the IC50 activity. The docking study
has helped to highlight the molecule key elements to refine
in order to get a more potent compound of CDK4.The
Molecule under the code 21366124 which has the low IC50=
3 nmole shows the most binding affinity with a score value of
ΔG=-9,8 kcal/mol. As prospects, it would be very interesting
to synthesize this drug candidate and to test its inhibitory
activity on cell culture of breast cancer.
MOJ Drug Design Development & Therapy
