Turning KRAS into a Molecular Trigger: Covalent-Induced Drug Conjugates for Conditional Tubulin Poisoning

Covalent-induced drug conjugates introduce a provocative precision-oncology strategy: mutant KRAS serves not merely as the therapeutic target but as the molecular trigger for drug release. By coupling KRASG12C recognition to intracellular release of potent tubulin inhibitors, this strategy seeks to convert oncogene engagement into localized cytotoxicity while limiting systemic payload exposure.