Alberto J. Montero, MD, MBA, CPHQ

STX-478 showed efficacy in patients with advanced solid tumors regardless of whether they had kinase domain or helical PI3K mutations.

STX-478 may avoid adverse effects associated with prior PI3K inhibitors that lack selectivity for the mutated protein vs the wild-type protein.

Phase 1 data may show the possibility of rationally designing agents that can preferentially target PI3K mutations in solid tumors.