title: [Inhitibion of FGF23 activities as a possible new treatment for patients with FGF23-related hypophosphatemic diseases].
abstract: Excessive actions of fibroblast growth factor 23(FGF23)result in several kinds of hypophosphatemic rickets and osteomalacia. A combination of oral active vitamin D3 and phosphate is the current standard therapy for FGF23-related hypophosphatemia. However, these medications can lead to long-term complications, such as secondary hyperparathyroidism and renal impairment. Therefore, safer and more efficient therapy to correct excessive actions of FGF23 is needed. X-linked hypophosphatemic rickets(XLHR)is the most prevalent form of FGF23-related hypophosphatemia. The efficacy of anti-FGF23 antibody was confirmed in a Hyp mouse, a murine model of XLHR. A recent phase 1 double-blind, placebo-controlled study and the subsequent open-label phase 1/2 study in adults with XLHR showed the safety and the efficacy of human anti-FGF23 antibody, KRN23. KRN23 has a potential for effectively treating patients with XLHR and other types of FGF23-related hypophosphatemia as well.
authors.affiliation: Division of Nephrology & Endocrinology, Department of Medicine, The University of Tokyo Hospital, Japan.
authors.forename: Yuka
authors.initials: Y
authors.lastname: Kinoshita
mesh_terms: D000328:Adult; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D002908:Chronic Disease; D002986:Clinical Trials as Topic; D004195:Disease Models, Animal; D053098:Familial Hypophosphatemic Rickets / Q000188:drug therapy* / Q000209:etiology*; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000037:antagonists & inhibitors / Q000502:physiology*; D006801:Humans; D051379:Mice
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; C000717427:FGF23 protein, human; C000717428:Fgf23 protein, mouse; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; C000601956:burosumab