Recombinant Human FGF23 protein

Fibroblast Growth Factor 23 (FGF23) is a hormone primarily secreted by osteocytes and osteoblasts, playing a critical role in phosphate and vitamin D homeostasis. It regulates renal phosphate excretion by binding to the α-Klotho-FGF receptor complex in the proximal tubules, suppressing phosphate reabsorption and 1.25-dihydroxyvitamin D synthesis. Dysregulation of FGF23 is linked to several disorders. Elevated FGF23 levels are associated with hypophosphatemic conditions, such as X-linked hypophosphatemia (XLH) and chronic kidney disease (CKD), where excessive phosphate wasting leads to bone mineralization defects. Conversely, FGF23 deficiency or resistance causes hyperphosphatemia, as seen in familial tumoral calcinosis.

Recombinant FGF23 protein, produced via mammalian expression systems (e.g., CHO or HEK293 cells), is engineered to mimic the native protein’s biological activity. It serves as a vital tool for studying FGF23 signaling pathways, drug screening, and developing therapeutic interventions. For instance, anti-FGF23 antibodies (e.g., burosumab) are used to treat XLH by neutralizing excess FGF23 activity. Conversely, recombinant FGF23 could theoretically address conditions caused by its deficiency, though clinical applications remain exploratory.

In diagnostics, recombinant FGF23 aids in standardizing assays to measure circulating FGF23 levels, critical for differentiating renal phosphate disorders. Challenges persist in therapeutic use due to FGF23’s short half-life and pleiotropic effects, prompting research into engineered variants with improved stability and tissue specificity. Additionally, understanding its interactions with co-receptors and downstream effectors may unveil targeted therapies for mineral metabolism disorders. Overall, recombinant FGF23 bridges basic research and clinical innovation, offering insights into phosphate-related pathologies and potential treatment avenues.