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FGF23-blocking antibodies

Antibodies that neutralise FGF23, the hormone that makes the kidney waste phosphate. Phosphate rises and rickets heals.

Updated

What they are

Monoclonal antibodies against fibroblast growth factor 23 (FGF23). Too much FGF23 causes X-linked hypophosphataemia (XLH) and tumour-induced osteomalacia: phosphate is lost in the urine, active vitamin D is low, and bones become soft (rickets in children, osteomalacia in adults). Burosumab is the member in use.

Mechanism of action

FGF23, made by bone cells, acts on the kidney to reduce phosphate reabsorption in the proximal tubule and to suppress the enzyme that makes active vitamin D (calcitriol). Neutralising FGF23 restores tubular phosphate reabsorption and calcitriol production, so serum phosphate rises and bone mineralisation improves.

Target: Fibroblast growth factor 23 (FGF23), a phosphate-regulating hormone from bone

Drugs in this class

Test yourself

Think of the answer, then tap the question to see it.

What are the two kidney actions of FGF23 that an anti-FGF23 antibody reverses?

Reduced proximal tubular phosphate reabsorption and suppressed calcitriol synthesis.

Why are oral phosphate and calcitriol stopped before burosumab?

Combined with the antibody they could raise phosphate too much (hyperphosphataemia and mineral deposits).

Which inherited disease is the main indication for FGF23 antibodies?

X-linked hypophosphataemia (XLH).

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Burosumab-twza Injection: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2026).

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