FDA Clears Daraxonrasib, First Broad RAS Inhibitor, for Second-Line Metastatic Pancreatic Cancer

Targeted therapies have leapt before—imatinib in 2001 turned chronic myeloid leukemia from a death sentence into a chronic disease, and trastuzumab in 1998 re-defined HER2-positive breast cancer—but neither tackled a mutation once labeled “undruggable.” KRAS, driving >90 % of pancreatic tumors and ~25 % of all cancers, resisted medicinal chemistry for four decades. Daraxonrasib’s molecular-glue strategy echoes the 1940s discovery that penicillin worked by binding a helper protein, suggesting a broader renaissance in using induced proximity rather than lock-and-key fit. If subsequent studies confirm benefit and manage inevitable resistance, the drug could inaugurate a wave of pan-RAS inhibitors and combination regimens, much as imatinib seeded dozens of tyrosine-kinase agents. Yet the median survival gain still leaves patients living barely a year, and the $39,800 monthly sticker price reprises the ongoing tension between biomedical breakthroughs and affordability. On a century scale, the approval marks a possible pivot from empiric cytotoxics to rational, intracellular “switch-off” oncology, but history warns that early euphoria (e.g., interferon in the 1980s) can fade; only sustained, accessible benefits will determine whether 2026 is remembered as a true turning point or merely another incremental step.