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Ref Type Journal Article
PMID (35344029)
Authors Lassman AB, Sepúlveda-Sánchez JM, Cloughesy TF, Gil-Gil MJ, Puduvalli VK, Raizer JJ, De Vos FYF, Wen PY, Butowski NA, Clement PMJ, Groves MD, Belda-Iniesta C, Giglio P, Soifer HS, Rowsey S, Xu C, Avogadri F, Wei G, Moran S, Roth P
Title Infigratinib in Patients with Recurrent Gliomas and FGFR Alterations: A Multicenter Phase II Study.
Journal Vol Issue Date Pages Journal Short Title
Clinical cancer research : an official journal of the American Association for Cancer Research 28 11 2022 Jun 01 2270-2277 Clin Cancer Res
URL
Abstract Text 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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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
Drug Name Trade Name Synonyms Drug Classes Drug Description
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
FGFR3 K650E high grade glioma predicted - sensitive Infigratinib Case Reports/Case Series Actionable In a Phase II trial, Truseltiq (infigratinib) treatment resulted in limited efficacy with a 6-month progression-free survival (PFS) rate of 16.0%, a median PFS of 1.7 months, an objective response rate of 4.8% (1/21), and median overall survival of 6.7 months in patients with recurrent gliomas harboring alterations in FGFR1 or FGFR3, however, resulted in stable disease with PFS of 12.9 months in a patient harboring FGFR3 K650E (PMID: 35344029; NCT01975701). 35344029
FGFR1 K656E high grade glioma predicted - sensitive Infigratinib Case Reports/Case Series Actionable In a Phase II trial, Truseltiq (infigratinib) treatment resulted in limited efficacy with a 6-month progression-free survival (PFS) rate of 16.0%, a median PFS of 1.7 months, an objective response rate of 4.8% (1/21), and median overall survival of 6.7 months in patients with recurrent glioma harboring alterations in FGFR1 or FGFR3; however, resulted in a partial response with PFS of 21.9 months and stable disease with PFS of 13.2 months in two patients harboring FGFR1 K656E (PMID: 35344029; NCT01975701). 35344029