Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia. - Wikidata - awgldk - TriplyDB

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

http://www.wikidata.org/entity/Q37679946

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Endocrine FGFs: Evolution, Physiology, Pathophysiology, and Pharmacotherapy A unified model for bone-renal mineral and energy metabolism Tumour-induced osteomalacia: a literature review and a case report Optimal management of bone mineral disorders in chronic kidney disease and end stage renal disease Evolution of Cardiovascular Disease During the Transition to End-Stage Renal Disease.Response of Npt2a knockout mice to dietary calcium and phosphorus.Serum calcitriol levels in a patient with X-linked hypophosphatemia complicated by autosomal dominant polycystic kidney disease.Hypophosphatemic rickets: revealing novel control points for phosphate homeostasis.Pharmacokinetics and pharmacodynamics of a human monoclonal anti-FGF23 antibody (KRN23) in the first multiple ascending-dose trial treating adults with X-linked hypophosphatemia.FGF23 neutralization improves bone quality and osseointegration of titanium implants in chronic kidney disease mice.Prolonged Correction of Serum Phosphorus in Adults With X-Linked Hypophosphatemia Using Monthly Doses of KRN23.FGF23 is elevated in multiple myeloma and increases heparanase expression by tumor cells.Hereditary hypophosphatemia in Norway: a retrospective population-based study of genotypes, phenotypes, and treatment complications.Pruning the ricket thicket CYP24 inhibition as a therapeutic target in FGF23-mediated renal phosphate wasting disorders Systemic Control of Bone Homeostasis by FGF23 Signaling.1,25-Dihydroxyvitamin D Alone Improves Skeletal Growth, Microarchitecture, and Strength in a Murine Model of XLH, Despite Enhanced FGF23 Expression.Sclerostin antibody (Scl-Ab) improves osteomalacia phenotype in dentin matrix protein 1(Dmp1) knockout mice with little impact on serum levels of phosphorus and FGF23.Effect of four monthly doses of a human monoclonal anti-FGF23 antibody (KRN23) on quality of life in X-linked hypophosphatemia Therapeutic management of hypophosphatemic rickets from infancy to adulthood.The metabolic bone disease associated with the Hyp mutation is independent of osteoblastic HIF1α expression.Diagnostic Modalities for FGF23-Producing Tumors in Patients with Tumor-Induced Osteomalacia Hypophosphatemic rickets: lessons from disrupted FGF23 control of phosphorus homeostasis.Mineral and bone disorders in kidney transplant recipients: reversible, irreversible, and de novo abnormalities.FGF23-FGF Receptor/Klotho Pathway as a New Drug Target for Disorders of Bone and Mineral Metabolism.The PTH-Vitamin D-FGF23 axis.Therapeutic potential of the endocrine fibroblast growth factors FGF19, FGF21 and FGF23.Cutaneous skeletal hypophosphatemia syndrome (CSHS) is a multilineage somatic mosaic RASopathy Cutaneous skeletal hypophosphatemia syndrome: clinical spectrum, natural history, and treatment.X-linked hypophosphatemia and growth.The Role of the Osteocyte in Bone and Nonbone Disease.Heritable and acquired disorders of phosphate metabolism: Etiologies involving FGF23 and current therapeutics.Tumour-induced osteomalacia.Hypophosphatemic Rickets in Siblings: A Rare Case Report.Population pharmacokinetic and pharmacodynamic analyses from a 4-month intradose escalation and its subsequent 12-month dose titration studies for a human monoclonal anti-FGF23 antibody (KRN23) in adults with X-linked hypophosphatemia.Conditional Deletion of Murine Fgf23: Interruption of the Normal Skeletal Responses to Phosphate Challenge and Rescue of Genetic Hypophosphatemia.FGF23 in chronic kidney disease: are we lost in translation?Chiari malformation, syringomyelia and bulbar palsy in X linked hypophosphataemia.The Foot That Broke Both Hips: A Case Report and Literature Review of Tumor-Induced Osteomalacia.Maternally derived anti-fibroblast growth factor 23 antibody as new tool to reduce phosphorus requirement of chicks.

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Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

http://www.wikidata.org/entity/Q37679946

description

article científic

@ca

article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 24 February 2014

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

@en

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

@nl

type

label

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

@en

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

@nl

prefLabel

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

@en

Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

@nl

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Journal of Clinical Investigation

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Randomized trial of the anti-FGF23 antibody KRN23 in X-linked hypophosphatemia.

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Jeffrey Humphrey

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Margaret M Wooddell

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Mark A Klausner

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Mary D Ruppe

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Munro Peacock

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Takahiro Ito

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Tetsuyoshi Kawakami

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Thomas J Weber

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Thomas O Carpenter

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Xiaoping Zhang

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P2860

Fibroblast growth factor 23: roles in health and disease

How fibroblast growth factor 23 works

FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1.

A clinician's guide to X-linked hypophosphatemia

Nomogram for derivation of renal threshold phosphate concentration.

Ectopic cardiac calcification associated with hyperparathyroidism in a boy with hypophosphatemic rickets.

Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia.

Anti-FGF23 neutralizing antibodies show the physiological role and structural features of FGF23.

Transgenic mice expressing fibroblast growth factor 23 under the control of the alpha1(I) collagen promoter exhibit growth retardation, osteomalacia, and disturbed phosphate homeostasis.

Anti-FGF-23 neutralizing antibodies ameliorate muscle weakness and decreased spontaneous movement of Hyp mice.

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1587-1597

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scholarly article

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10.1172/JCI72829

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4

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124

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2014-02-24T00:00:00Z

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24569459

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3973088

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