ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2017
Therapeutic Effects of FGF23 c-tail Fc in a Murine Preclinical Model of X-Linked Hypophosphatemia Via the Selective Modulation of Phosphate Reabsorption.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- The PHEX deletion variant (p.Thr605MetfsTer14) causes X-linked hypophosphatemic rickets by reducing protein expression and promoting mineralization.Orphanet journal of rare diseases · 2026Article
- Expression of FGF23 and α-KLOTHO in Normal Human Kidney Development and Congenital Anomalies of the Kidney and Urinary Tract (CAKUT).Biomolecules · 2025Article
- Pathology and Therapeutic Significance of Fibroblast Growth Factors.Targets (Basel) · 2025Article
- Bone-derived C-terminal FGF23 cleaved peptides increase iron availability in acute inflammation.Blood · 2023Article
- Structural basis for FGF hormone signalling.Nature · 2023Article
- Strategies to lower fibroblast growth factor 23 bioactivity.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- FGF23 and Hypophosphatemic Rickets/Osteomalacia.Current osteoporosis reports · 2021Review
- A novel therapeutic strategy for skeletal disorders: Proof of concept of gene therapy for X-linked hypophosphatemia.Science advances · 2021Article
- The Role of Fibroblast Growth Factor 23 in Inflammation and Anemia.International journal of molecular sciences · 2019Review
- Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia.Nature reviews. Nephrology · 2019Article
- FGF23, Biomarker or Target?Toxins · 2019Review
- Role of phosphate sensing in bone and mineral metabolism.Nature reviews. Endocrinology · 2018Review
- Fibroblast Growth Factor 23 Associates with Death in Critically Ill Patients.Clinical journal of the American Society of Nephrology : CJASN · 2018Article
- Targeting Fibroblast Growth Factor 23 Signaling with Antibodies and Inhibitors, Is There a Rationale?Frontiers in endocrinology · 2018Review
- FGF23 Actions on Target Tissues-With and Without Klotho.Frontiers in endocrinology · 2018Review
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Authors and funding
21 authors at 3 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factor 23 (FGF23) is the causative factor of X-linked hypophosphatemia (XLH), a genetic disorder effecting 1:20,000 that is characterized by excessive phosphate excretion, elevated FGF23 levels and a rickets/osteomalacia phenotype. FGF23 inhibits phosphate reabsorption and suppresses 1α,25-dihydroxyvitamin D (1,25D) biosynthesis, analytes that differentially contribute to bone integrity and deleterious soft-tissue mineralization. As inhibition of ligand broadly modulates downstream targets, balancing efficacy and unwanted toxicity is difficult when targeting the FGF23 pathway. We demonstrate that a FGF23 c-tail-Fc fusion molecule selectively modulates the phosphate pathway in vivo by competitive antagonism of FGF23 binding to the FGFR/α klotho receptor complex. Repeated injection of FGF23 c-tail Fc in Hyp mice, a preclinical model of XLH, increases cell surface abundance of kidney NaPi transporters, normalizes phosphate excretion, and significantly improves bone architecture in the absence of soft-tissue mineralization. Repeated injection does not modulate either 1,25D or calcium in a physiologically relevant manner in either a wild-type or disease setting. These data suggest that bone integrity can be improved in models of XLH via the exclusive modulation of phosphate. We posit that the selective modulation of the phosphate pathway will increase the window between efficacy and safety risks, allowing increased efficacy to be achieved in the treatment of this chronic disease. © 2017 American Society for Bone and Mineral Research.
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