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Cancer Drug Narmafotinib Shows Promise Beyond KRAS Mutations
22 Oct
Summary
- Narmafotinib's effectiveness may not depend on KRAS mutations in pancreatic cancer.
- The drug targets FAK protein, crucial for tumor growth and resistance.
- Four clinical trials are advancing for narmafotinib across multiple cancers.
Amplia Therapeutics is advancing narmafotinib, a drug targeting difficult-to-treat cancers, with recent updates focusing on pancreatic, ovarian, and lung cancer trials. A key finding from its pancreatic cancer trial suggests narmafotinib's efficacy may not be contingent on specific KRAS gene mutations, which are prevalent in over 90% of pancreatic cancers.
Narmafotinib functions by inhibiting the FAK protein, which is overexpressed in solid tumors and supports cancer cell growth and resistance to treatment. This FAK inhibition is also thought to degrade the fibrotic tissue surrounding tumors, enhancing chemotherapy's effectiveness.
The ACCENT trial for metastatic pancreatic cancer has shown promising response rates and survival data, with some patients achieving remarkable longevity in the study. Amplia is also initiating the ACCENT-Mini trial in Australia to evaluate daily dosing of narmafotinib with chemotherapy, aiming for data crucial for FDA submission by the first half of 2027.
Further expanding its pipeline, Amplia is pursuing ovarian cancer treatment through the PRROSE study, which combines narmafotinib with standard chemotherapy in patients with high-grade serous ovarian cancer. Additionally, a trial combining narmafotinib with Lilly's KRAS G12C inhibitor is planned for advanced non-small cell lung cancer. These combined efforts aim to attack cancer on multiple fronts by targeting different pathways.
