Article
PI3Kα Inhibitor and Degrader Inavolisib Can Co-opt FGFR2 to Enhance Responses in Patients with PIK3CA-Mutated Solid Tumors and in Preclinical Models.
Clinical cancer research : an official journal of the American Association for Cancer Research - 6 Jan 2026
Juric Dejan, Song Kyung, Johnson Radia M, Accordino Melissa K, Bedard Philippe L, Cervantes Andrés, Gambardella Valentina, Hamilton Erika, Italiano Antoine, Kalinsky Kevin, Krop Ian E, Oliveira Mafalda, Saura Cristina, Schmid Peter, Turner Nicholas C, Varga Andreea, Gendreau Steven, Hwang Michael S, Kuang Zheng, Lau Jeffrey T, Lin Eva, Pham Trang, Maddalo Danilo, Rees Matthew G, Ronan Melissa M, Roth Jennifer A, Martin Scott, Sodir Nicole M, Sokol Ethan S, Whitfield Zachary J, Wong Alice, Yauch Robert L, Aimi Junko, Cheeti Sravanthi, Fredrickson Jill, Hilz Stephanie, Hafner Marc, Hutchinson Katherine E, Jin Yanling, Peters Ubong, Zingg Daniel, Royer-Joo Stephanie, Shankar Noopur, Schutzman Jennifer L, Jhaveri Komal L, Dey Anwesha
Abstract excerpt
PURPOSE: PIK3CA mutations frequently drive solid tumors, particularly hormone receptor-positive breast cancer. Inavolisib, an ATP-competitive p110α inhibitor, also promotes the degradation of mutated p110α. PI3K inhibitors have generally shown modest single-agent activity and have safety concerns. PATIENTS AND METHODS: A first-in-human phase 1 study (NCT03006172) evaluated oral inavolisib in patients with...
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