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Updated: Aug 26, 2025
06:56
Author Spotlight: Developing Tools to Tune the Activity of Tyrosine Phosphatases
Published on: September 6, 2024
450
Phosphatonins: From Discovery to Therapeutics
Kittrawee Kritmetapak1, Rajiv Kumar2
1Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Summary
Fibroblast growth factor 23 (FGF23) plays a key role in phosphate homeostasis. The anti-FGF23 antibody burosumab effectively treats FGF23-related hypophosphatemic disorders like XLH and TIO in children and adults.
Area of Science:
- Endocrinology
- Nephrology
- Bone Metabolism
Background:
- Phosphate is vital for cellular functions and bone health.
- The gut-bone-parathyroid-kidney axis regulates phosphate homeostasis via hormones like FGF23.
- Dysregulation of FGF23 causes hypophosphatemic disorders.
Purpose of the Study:
- To review phosphate homeostasis and FGF23 pathophysiology.
- To discuss clinical implications of FGF23-related hypophosphatemic disorders.
- To focus on burosumab treatment for these conditions.
Main Methods:
- Focused literature search of PubMed.
Main Results:
- Excess FGF23 leads to hyperphosphaturia and hypophosphatemia by inhibiting phosphate cotransporters and vitamin D synthesis.
- FGF23-related disorders include XLH, ADHR, ARHR, fibrous dysplasia/McCune-Albright syndrome, and TIO.
- Burosumab, an anti-FGF23 antibody, shows a favorable safety profile and efficacy in healing rickets and osteomalacia in XLH and TIO patients.
Conclusions:
- Recent clinical trials are transforming the treatment of XLH and TIO.
- Burosumab demonstrates effectiveness and safety for pediatric and adult patients with XLH or TIO.
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