ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2025
Infigratinib low dose therapy is an effective strategy to treat hypochondroplasia.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- FGFR1 signaling in rheumatoid arthritis: Mechanisms of bone destruction and therapeutic targeting (Review).International journal of molecular medicine · 2026Review
- Diagnosis of hypochondroplasia: international Delphi consensus recommendations.Nature reviews. Endocrinology · 2026Review
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10 authors.
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Abstract
Hypochondroplasia is a rare genetic form of skeletal dysplasia, caused by gain-of-function pathogenic variants in the FGF receptor 3 (FGFR3). It is characterized by disproportionate short stature and has a wide spectrum of clinical features. Currently, there are no precision therapeutic options approved for hypochondroplasia. Infigratinib is an orally bioavailable FGFR1-3 selective tyrosine kinase inhibitor in development for achondroplasia and hypochondroplasia. Infigratinib acts directly at the source of the pathophysiological cause of both conditions by inhibiting the phosphorylation of FGFR3 and attenuating both main downstream signaling pathways that are involved in the conditions. Results from a phase 2 study support the concept that infigratinib has a potential to improve bone growth in achondroplasia. We report results of a step-wise evaluation of the therapeutic relevance of infigratinib for hypochondroplasia: in silico assessment of infigratinib with hypochondroplasia associated FGFR3 variants suggest strong interaction; in vitro, infigratinib showed potent inhibitory effect; in a mouse model of hypochondroplasia (Fgfr3N534K/+), infigratinib resulted in significant improvement in skeletal growth. These data in addition to the clinical results from the phase 2 study conducted in children with achondroplasia provide support for the development of infigratinib in the treatment of hypochondroplasia.
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