Allosteric co-binding restores tyrosine kinase inhibitor affinity in T790M-mutant EGFR through conformational reprogramming.
Docking predicted stronger binding to wild-type EGFR and reduced affinity for the T790M mutant, whereas co-binding produced compound-dependent improvements, and an integrated framework provides structural, dynamic, and energetic criteria for prioritize cooperative allosteric-orthosteric co-binding chemotypes for experi...