American Association for Cancer Research
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Supplementary Figure from Infigratinib in Patients with Recurrent Gliomas and FGFR Alterations: A Multicenter Phase II Study

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posted on 2023-03-31, 23:12 authored by Andrew B. Lassman, Juan Manuel Sepúlveda-Sánchez, Timothy F. Cloughesy, Miguel J. Gil-Gil, Vinay K. Puduvalli, Jeffrey J. Raizer, Filip Y.F. De Vos, Patrick Y. Wen, Nicholas A. Butowski, Paul M.J. Clement, Morris D. Groves, Cristóbal Belda-Iniesta, Pierre Giglio, Harris S. Soifer, Steven Rowsey, Cindy Xu, Francesca Avogadri, Ge Wei, Susan Moran, Patrick Roth
Supplementary Figure from Infigratinib in Patients with Recurrent Gliomas and FGFR Alterations: A Multicenter Phase II Study


QED Therapeutics Inc.

The William Rhodes and Louise Tilzer-Rhodes Center for Glioblastoma at New York-Presbyterian Hospital

The Michael Weiner Glioblastoma Research Into Treatment Fund

Voices Against Brain Cancer (VABC)

National Cancer Institute (NCI)

United States Department of Health and Human Services

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FGFR genomic alterations (amplification, mutations, and/or fusions) occur in ∼8% of gliomas, particularly FGFR1 and FGFR3. We conducted a multicenter open-label, single-arm, phase II study of a selective FGFR1–3 inhibitor, infigratinib (BGJ398), in patients with FGFR-altered recurrent gliomas. Adults with recurrent/progressive gliomas harboring FGFR alterations received oral infigratinib 125 mg on days 1 to 21 of 28-day cycles. The primary endpoint was investigator-assessed 6-month progression-free survival (PFS) rate by Response Assessment in Neuro-Oncology criteria. Comprehensive genomic profiling was performed on available pretreatment archival tissue to explore additional molecular correlations with efficacy. Among 26 patients, the 6-month PFS rate was 16.0% [95% confidence interval (CI), 5.0–32.5], median PFS was 1.7 months (95% CI, 1.1–2.8), and objective response rate was 3.8%. However, 4 patients had durable disease control lasting longer than 1 year. Among these, 3 had tumors harboring activating point mutations at analogous positions of FGFR1 (K656E; n = 2) or FGFR3 (K650E; n = 1) in pretreatment tissue; an FGFR3-TACC3 fusion was detected in the other. Hyperphosphatemia was the most frequently reported treatment-related adverse event (all-grade, 76.9%; grade 3, 3.8%) and is a known on-target toxicity of FGFR inhibitors. FGFR inhibitor monotherapy with infigratinib had limited efficacy in a population of patients with recurrent gliomas and different FGFR genetic alterations, but durable disease control lasting more than 1 year was observed in patients with tumors harboring FGFR1 or FGFR3 point mutations or FGFR3-TACC3 fusions. A follow-up study with refined biomarker inclusion criteria and centralized FGFR testing is warranted.

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