Which therapy directly targets FGF23 in XLH?

• A. Burosumab (anti-FGF23).
• B. Calcitriol.
• C. PTH analog.
• D. Calcitonin.

Answer: (A)

Directly neutralizing FGF23 addresses the root cause of XLH. In XLH, excess FGF23 causes the kidneys to waste phosphate and suppresses 1,25-dihydroxyvitamin D, leading to low serum phosphate and impaired bone mineralization. Burosumab is a monoclonal antibody that binds FGF23, blocking its action, which increases renal phosphate reabsorption and raises 1,25-dihydroxyvitamin D levels, correcting the phosphate-wasting problem rather than just treating symptoms. Calcitriol helps raise vitamin D activity but does not reduce FGF23 or stop phosphate wasting. A PTH analog influences bone turnover and phosphate handling indirectly, not by targeting FGF23. Calcitonin has no direct role in addressing FGF23-driven phosphate wasting.