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Fibroblast growth factor 23 (FGF23) is a bone-derived hormone primarily produced by osteocytes and osteoblasts that plays a critical role in mineral homeostasis (UniProt: Q9GZV9). It acts on the renal proximal tubules to inhibit phosphate reabsorption by downregulating sodium-phosphate cotransporters and suppresses the production of 1,25-dihydroxyvitamin D (PubMed: 29743338). Pathologically elevated levels of intact FGF23 lead to phosphate wasting and impaired bone mineralization, characterizing conditions such as X-linked hypophosphatemia (XLH) and tumor-induced osteomalacia (StatPearls: NBK539868). Conversely, deficient FGF23 activity results in hyperphosphatemia and tumoral calcinosis. Therapeutic intervention, most notably with the monoclonal antibody Burosumab, targets intact FGF23 to restore phosphate balance in patients with hypophosphatemic disorders (DrugBank: DB12851). Monitoring serum phosphate and FGF23 levels is essential during treatment to avoid complications like hyperphosphatemia and soft tissue calcification.
Monoclonal antibody binding and neutralization of intact FGF23 to inhibit its signaling through the FGFR-Klotho complex.
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