For decades, KRAS stood as oncology’s archetypal “undruggable” target—a powerful cancer driver with no obvious pocket for conventional medicines to grasp. This episode explores how molecular-glue drugs such as daraxonrasib overturn that assumption by recruiting cyclophilin A to form a synthetic complex around active RAS, physically blocking its growth signals. From the structural ingenuity behind this molecular trap to emerging clinical promise in pancreatic and other KRAS-driven cancers, the daraxonrasib FDA approval reveals a potential turning point in precision oncology—while examining resistance, patient selection, and what KRAS teaches us about drugging the seemingly impossible. Produced by Dr. Jake Chen.
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