Clinical EfficacyELVN-001 produced strong and durable molecular responses in heavily pretreated CML patients, supporting its potential to deliver meaningful clinical benefit for refractory cases.
Combination StrategyEvidence that ELVN-001 and asciminib effectively suppress resistant clones suggests a complementary combination approach that could expand therapeutic options.
Mechanism DifferentiationELVN-001 targets a distinct ATP-binding pocket, providing a differentiated mechanism that could treat patients who failed therapies binding the alternate pocket.