Balversa (erdafitinib)

Combined inhibition of FGFR1 and MET significantly suppressed tumor growth in resistant cells. These findings establish MET amplification and GAB1-SHP2 signaling as central mediators of erdafitinib resistance in FGFR1-amplified MIBC and support dual FGFR1/MET targeting as a promising therapeutic strategy.

Functionally, the FGFR inhibitor erdafitinib suppressed cell proliferation and migration, and FGFR3 silencing also markedly reduced proliferation, migration, invasion, and colony formation in cancer cell lines. The down-regulation of FGFR3 in muscle-invasive bladder cancer, coupled with the inhibitory effect of its inactivation on cell growth, suggests a significant role for FGFR3 in bladder cancer progression.

Awareness of these risks and early intervention can prevent vision loss. Further research is needed to explore underlying mechanisms and preventive strategies.

CAFs exhibited broad sensitivity to multikinase inhibitors, with dasatinib, midostaurin, and FGFR inhibitors (AZD4547, erdafitinib) emerging as top stromal-directed candidates. These findings underscore the plasticity of prostate CAFs and reveal actionable vulnerabilities, supporting the development of targeted stromal therapies to disrupt tumor-stroma interactions in PCa.

Palbociclib (CDK4/6), miltefosine (PI3K/AKT/mTOR), gilteritinib (FLT3/AXL), and erdafitinib (FGFR) led to increased expression of the ICAM1-eGFP reporter and the release of chemokines. Finally, clinically relevant KIs that enhanced ICAM1-eGFP expression in PTLCs were found to be associated with renal adverse events in patients. Our overall findings support the application of imaging-based hiPSC-derived ICAM1-eGFP reporter covering different differentiated cell lineages to identify liabilities of novel kinase inhibitors to modulate TNFα pathways.

Co-administering fibroblast BJ-hTERT cell supernatants with BYL719, JNJ-42756493, and PD-0332991 had an inhibitory effect on their effects on viability and confluence in some cell lines. This was never the case with cisplatin, and very rarely the case with docetaxel or AZD-5363.

Introduction: Gastrointestinal stromal tumors (GISTs) are primarily driven by mutations in KIT (KIT proto-oncogene receptor tyrosine kinase) or PDGFRA (platelet-derived growth factor receptor alpha), but resistance to tyrosine kinase inhibitors (TKIs) such as imatinib remains a major clinical challenge. Although direct evidence remains limited, particularly regarding DNA repair and polymorphisms, FGFR2-targeted therapies (e.g., erdafitinib, pemigatinib) show potential, especially in combination with TKIs or DNA-damaging agents. Future research should prioritize GIST-specific clinical trials, the development of FGFR2-driven models, and standardized molecular diagnostics to validate FGFR2 as a therapeutic target.

These findings establish that erdafitinib exerts off-target anti-angiogenic effects by blocking VEGFR2 phosphorylation and downstream signaling, supporting its repurposing potential for anti-VEGF-resistant retinal vascular diseases. Further studies should address its intraocular pharmacokinetics and long-term safety.

Pan-FGFR-selective inhibitors (erdafitinib, pemigatinib, and futibatinib) have been developed in clinical practice...FGFR2-selective inhibitor lirafugratinib, FGFR3-selective inhibitors LOXO-435 and TYRA-300, FGFR2/3-selective inhibitor ABSK061, and FGFR4-selective inhibitors are in clinical development. Additionally, novel isoform-selective FGFR-targeting degraders, FGFR2b/FGFR3-selective antibodies, and de novo-designed 'c' isoform-selective proteins provide novel treatment strategies. This review provides an overview of the current FGFR-targeted therapeutics and limitations and evaluates next-generation inhibitor development to guide future research.

Accordingly, inhibition of FGFR activation by TK inhibitors (erdafitinib and infigratinib) or FGF trapping (by NSC12) significantly hampered ACC growth and survival in vitro. Altogether these results demonstrate for the first time the impact of FGF/FGFR blockade on ACC cell growth and survival both in vitro and in vivo. This study may set the rationale to start clinical trials investigating the therapeutic potential of FDA approved FGFR-TK inhibitors for the treatment of aggressive ACC.

P1, N=30, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting

Genomic profiling has advanced our understanding of UC diagnosis and treatment, but its routine clinical use remains limited to confirming biomarkers such as FGFR alterations and HER2 amplification for approved targeted therapies such as erdafitinib, a FGFRi, and trastuzumab deruxtecan, a HER2-directed ADC. Testing for other biomarkers such as PD-L1, tumor mutational burden (TMB), and Nectin-4 can be useful, but not required for the use of ICI and enfortumab vedotin. Circulating tumor DNA (ctDNA) is an emerging tool for monitoring disease and guiding therapy, with trials underway to confirm its clinical utility.