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Burosumab May Improve Multiple Clinical Outcomes in X-Linked Hypophosphatemia

Burosumab, a fully human monoclonal antibody against fibroblast growth factor 23 (FGF23), may restore phosphorus homeostasis and improve mineralization defect in in patients with X-linked hypophosphatemia (XLH), according to study results published in the Journal of Bone & Mineral Research.

Loss-of-function mutations in the PHEX gene (phosphate-regulating endopeptidase homolog, X-linked) cause XLH, a rare disease associated with increased FGF23 levels, chronic hypophosphatemia, and impaired production of 1,25-dihydroxyvitamin D. Burosumab was approved for the treatment of XLH, with studies reporting improved fracture healing and increased serum phosphorus levels and bone remodeling markers.

An ongoing open-label phase 3 single-group multicenter trial is investigating the efficacy of burosumab in improving osteomalacia in adults with XLH.


Burosumab May Improve Multiple Clinical Outcomes In X-Linked Hypophosphatemia

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