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An Automated Radiosynthesis of [68Ga]Ga-FAPI-46 for Routine Clinical Use
Published on: May 24, 2024
Anti-fibroblast growth factor 23 antibody therapy
1Department of Medicine, Division of Nephrology and Endocrinology, University of Tokyo Hospital, Tokyo, Japan.
Purpose Of Review:
The review is intended to provide an update on the expanding knowledge regarding diseases caused by the excess actions of fibroblast growth factor 23 (FGF23) and also on the new therapeutic measures for these diseases, with an emphasis on the anti-FGF23 antibody.
Recent Findings:
FGF23 decreases serum phosphate and 1,25-dihydroxyvitamin D levels. After the cloning of FGF23, several hypophosphatemic diseases, including tumor-induced osteomalacia and X-linked hypophosphatemic rickets (XLHR), were shown to be caused by excess actions of FGF23. In addition, recent studies indicated that mutations in the family with sequence similarity 20, member C (FAM20C), HRAS and NRAS genes, also caused FGF23-related hypophosphatemic diseases. The inhibition of FGF23 production or activity is, theoretically, an ideal treatment for these hypophosphatemic diseases. The C-terminal fragment of FGF23, inhibitors of FGF receptor and extracellular signal-regulated kinase, and anti-FGF23 antibody were shown to inhibit FGF23 actions both in vitro and in vivo. A phase I clinical trial of anti-FGF23 antibody has shown that this antibody increases serum phosphate in patients with XLHR.
Summary:
These recent findings confirm that FGF23 has a pivotal role in phosphate metabolism. The inhibition of FGF23 production or activity is promising as a new therapy for FGF23-related hypophosphatemic diseases. Further studies are clearly necessary to establish the clinical utility and long-term safety of these measures.
Insights
Excess fibroblast growth factor 23 (FGF23) causes hypophosphatemic diseases. Inhibiting FGF23, particularly with an anti-FGF23 antibody, shows promise for new therapies, with early trials increasing phosphate levels in patients.
Area of Science:
- Endocrinology
- Metabolic Diseases
- Molecular Biology
Background:
- Fibroblast growth factor 23 (FGF23) regulates phosphate and vitamin D metabolism.
- Excess FGF23 activity leads to hypophosphatemic disorders.
- Genetic mutations in FAM20C, HRAS, and NRAS are implicated in FGF23-related diseases.
Purpose of the Study:
- To review current knowledge on diseases caused by excess FGF23.
- To discuss emerging therapeutic strategies targeting FGF23.
- To highlight the potential of anti-FGF23 antibodies.
Main Methods:
- Literature review of studies on FGF23 and related hypophosphatemic diseases.
- Analysis of in vitro and in vivo data on FGF23 inhibition.
- Review of clinical trial outcomes for anti-FGF23 antibody therapy.
Main Results:
- FGF23 is confirmed to decrease serum phosphate and 1,25-dihydroxyvitamin D.
- Tumor-induced osteomalacia and X-linked hypophosphatemic rickets (XLHR) are linked to excess FGF23.
- A phase I clinical trial demonstrated that anti-FGF23 antibody therapy increased serum phosphate in XLHR patients.
Conclusions:
- FGF23 plays a critical role in phosphate homeostasis.
- Inhibiting FGF23 production or activity offers a promising therapeutic avenue for FGF23-related hypophosphatemic diseases.
- Further research is essential to validate the clinical utility and long-term safety of these novel treatments.
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