|FGF-23 regulates phosphate homeostasis and transport in the kidney . The full-length 327 amino acid protein is functional, and is deactivated by proteolytic cleavage which generates N-terminal and C-terminal chains. Mutation of the cleavage site causes autosomal dominant hypophosphatemic rickets (ADHR), and other gene alterations are associated with hyperphosphatemic familial tumoral calcinosis (HFTC). Antibody-driven inactivation of FGF-23 is being investigated as a pharmacological intervention in these indications. Burosumab (KRN23) is one such FGF-23 neutralising antibody in clinical development.