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Life sciences · Journal article
Journal of Medicinal Chemistry · October 19, 2026
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Abstract Fibroblast growth factor receptor 3 (FGFR3) gain-of-function alterations drive a spectrum of conditions, including cancers and skeletal dysplasias, making FGFR3 an attractive therapeutic target. While second-generation pan-FGFR inhibitors established clinical proof-of-concept, their utility has been constrained by toxicities associated with inhibition of FGFR1, FGFR2, and FGFR4. Despite the high degree of structural homology within the FGFR family, structure-guided medicinal chemistry efforts have recently enabled the development of the first FGFR3-selective inhibitors to enter clinical evaluation. These agents are now being investigated for indications including bladder cancer and achondroplasia. Improved isoform selectivity has the potential to enhance tolerability, enable more durable target inhibition, and expand the therapeutic application of FGFR3-directed therapies. In this Perspective, we discuss the biological rationale for selective FGFR3 inhibition, the structure-based design strategies that have enabled FGFR3 selectivity, and emerging clinical opportunities to address unmet needs in FGFR3-driven disease.