ArticleBiochemistry and biophysics reports2026
Inhibition of FGFR signaling attenuates phosphaturia and early kidney injury in sickle cell disease mice.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
We examined whether short term treatment with the pan-FGF Receptor (FGFR) inhibitor BGJ398 (Infigratinib) modulated impaired FGFR downstream signaling, phosphate wasting and markers of kidney damage in sickle cell disease (SCD) mice. Healthy control (Ctrl) and SCD mice were subcutaneously injected with BGJ398 for 24 h. In serum both FGF23 intact and carboxy-terminal-fragment FGF23 were significantly higher in SCD and were not decreased with BGJ398. In SCD mice, serum phosphate level was significantly decreased, and urine phosphate/creatinine ratio were significantly higher and BGJ398 significantly reduced urine phosphate wasting. Immunohistochemistry analysis of kidneys revealed that phosphate transporters NPT2a and PIT-2 proteins were significantly decreased in SCD kidneys and were significantly improved by BGJ398. Signaling molecules that mediate decreased NPT2a, and PIT-2 expression were significantly increased and were significantly reduced by BGJ398. Markers of SCD kidney injury such as glomeruli sclerosis, tubular-damage-marker NGAL, early kidney-damage-marker KIM1, inflammatory M1 iNOS
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