Mirati Therapeutics hopes to later this year win U.S. approval of only the second drug able to target tumors spurred by mutations in an elusive gene called KRAS.
Updated clinical trial results disclosed Thursday show the San Diego biotech’s drug to be roughly as effective as the first, Amgen’s Lumakras, in treating a common form of advanced lung cancer. Lumakras won a milestone clearance from the Food and Drug Administration last spring and the agency is expected to make a decision on Mirati’s therapy, called adagrasib, by December.
The new data were revealed in a study abstract published ahead of the American Society of Clinical Oncology’s annual meeting next month and are the first to emerge since an update from Mirati last September. Treatment with adagrasib shrank tumors in 43% of the 112 patients included in the analysis and held cancer in check for a median of 6.5 months, as measured by what’s known as progression-free survival.
Study participants, almost all of whom were previously treated with chemotherapy and immunotherapy, lived a median of just over one year, the data show.
Mirati’s results mirror those recently reported by Amgen after two years of follow-up from the early study that led to Lumakras’ approval. In that trial, Lumakras led to a response rate of 41%, median progression-free survival of 6.3 months and median overall survival of 12.5 months.
Yet, Mirati’s data also signal adagrasib treatment comes with a high rate of side effects rated as more severe, with 43% of patients in the study experiencing reactions classified as Grade 3 or Grade 4. Two patients died; one from pulmonary hemorrhage and the other from cardiac failure. In the latter patient, who had a history of heart problems, Mirati said there were no signs of heart rhythm disturbances that can sometimes warn of a drug-related effect.
Adagrasib has been closely followed as the nearest rival to Lumakras, which Amgen has marked as a future blockbuster product. While the KRAS gene is frequently mutated in lung, colon and pancreatic cancers, targeting it with drugs remained out of researchers’ reach for more than three decades. Only recently did scientists learn how best to design treatments that could latch onto the protein produced by mutant KRAS and help shut it down.