Erdafitinib (Balversa) had a predictable toxicity profile and showed early efficacy signals in patients with recurrent or progressive IDH wild-type glioma with FGFR-TACC (F3T3) gene fusions, according to findings from the safety run-in cohort of the phase 2 ETCTN 10559 trial (NCT05859334), which were presented at the 2025 Society for Neuro-Oncology Annual Meeting.1 The agent also generated durable responses in this analysis.
The safety run-in cohort completed therapy in October 2024, and 8 mg daily continuous dosing was identified as the recommended phase 2 dose (RP2D) of erdafitinib. One patient experienced a dose-limiting toxicity (DLT), which was grade 3 central serous retinopathy; this was the only grade 3 treatment-emergent adverse effect (TEAE) reported and was the only TEAE that led to erdafitinib discontinuation. Any TEAEs and grade 1 TEAEs were reported in all patients during the DLT period of cycle 1; no TEAEs were grade 4 or higher. Grade 2 TEAEs included dyspepsia (n = 2), hyperphosphatemia (n = 1), and hyponatremia (n = 1). Grade 1 hyperphosphatemia was common (n = 4). No TEAEs led to erdafitinib dose reductions or treatment interruptions. Notably, 1 patient experienced grade 3 cerebral edema that was deemed unrelated to treatment.
Preliminary efficacy data were available for 5 patients. Best overall responses were complete response (CR; n = 1), partial response (PR; n = 2), stable disease (n = 1), and progressive disease (n = 1).
Erdafitinib in F3T3 Fusion–Positive Glioma: Highlights
- The safety profile of erdafitinib in patients with recurrent or progressive IDH wild-type glioma with F3T3 gene fusions was predictable and within expectations for the agent in other tumor types, leading to the selection of 8 mg daily continuous dosing as the RP2D.
- Erdafitinib showed early efficacy signals and durable responses, with preliminary efficacy data for 5 patients showing best overall responses of CR (n = 1), PR (n = 2), SD (n = 1), and PD (n = 1).
- The investigation of erdafitinib was based on the fact that F3T3 gene fusions are the most prevalent gene fusions in adult glioma and have demonstrated strong oncogenic activity and sensitivity to F3T3 inhibitors in prior studies.
“The safety profile of erdafitinib within gliomas is within [the] expected known safety profile [of the agent] in other tumor types, and we were able to identify durable responses in this population,” lead study author Macarena de la Fuente, MD, stated in the presentation.
de la Fuente is an associate professor of neuro-oncology, chief of the Neuro-Oncology Division, the clinical service leader for the Neuro-Oncology Service Line, chair of the Neuro-Oncology Site Disease Group, the director of the Neuro-Oncology Fellowship Program, and the leader of the Oncology Clinical Service for Neuro-Oncology at the University of Miami Miller School of Medicine and Sylvester Comprehensive Cancer Center in Florida.
What was the rationale for investigating erdafitinib in patients with glioma?
F3T3 gene fusions are the most prevalent gene fusions in adult glioma and are present in approximately 3% to 6% of adult patients with IDH wild-type glioma. F3T3 fusions are truncal alterations that emerge during gliomagenesis and independently predict favorable outcomes in gliomas; these fusions are also retained in recurrent glioblastoma. In vitro and in vivo studies have shown that F3T3 fusions have strong oncogenic activity and sensitivity to F3T3 inhibitors.
Erdafitinib, a potent, oral pan-FGFR TKI, was FDA approved in 2024 for the salvage treatment of patients with locally advanced or metastatic urothelial carcinoma harboring FGFR alterations, as determined by an FDA-approved test, whose disease has progressed during or after treatment with 1 or more prior lines of systemic therapy.2 Responses to erdafitinib in patients with glioma have been reported in basket trials, but prior to the ETCTN 10559 study, no clinical trials focused solely on examining the activity of the agent in gliomas harboring F3T3 fusions.1