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The most common FGF23\u2010mediated hypophosphatemia is X\u2010linked hypophosphatemia (XLH), caused by mutations in the\n                    <jats:italic>PHEX<\/jats:italic>\n                    gene. FGF23\u2010mediated forms of hypophosphatemia are characterized by phosphaturia and low or low\u2010normal calcitriol concentrations, and unlike nutritional rickets, these cannot be cured with nutritional vitamin D supplementation. Autosomal dominant and autosomal recessive forms of FGF23\u2010mediated hypophosphatemias show a similar pathophysiology, despite a variety of different underlying genetic causes. An excess of FGF23 activity has also been associated with a number of other conditions causing hypophosphatemia, including tumor\u2010induced osteomalacia, fibrous dysplasia of the bone, and cutaneous skeletal hypophosphatemia syndrome. Historically phosphate supplementation and therapy using analogs of highly active vitamin D (eg, calcitriol, alfacalcidol, paricalcitol, eldecalcitol) have been used to manage conditions involving hypophosphatemia; however, recently a neutralizing antibody for FGF23 (burosumab) has emerged as a promising treatment agent for FGF23\u2010mediated disorders. This review discusses the progression of clinical trials for burosumab for the treatment of XLH and its recent availability for clinical use. Burosumab may have potential for treating other conditions associated with FGF23 overactivity, but these are not yet supported by trial data. \u00a9 2019 The Authors.\n                    <jats:italic>JBMR Plus<\/jats:italic>\n                    published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.\n                  <\/jats:p>","DOI":"10.1002\/jbm4.10190","type":"journal-article","created":{"date-parts":[[2019,3,19]],"date-time":"2019-03-19T00:43:23Z","timestamp":1552956203000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["FGF23, Hypophosphatemia, and Emerging Treatments"],"prefix":"10.1093","volume":"3","author":[{"given":"Erik A","family":"Imel","sequence":"first","affiliation":[{"name":"Division of Endocrinology Indiana University School of Medicine, Indianapolis, IN  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