Anti-FGF23 monoclonal antibody Made to order

Klotho protein is a powerful regulator of various metabolic pathways including endothelial integration, cell adaptation processes, ion transport, signal transduction, regulation of calcium, potassium, parathyroid hormone, phosphates and glucose metabolism, and reduction of oxidative stress. Klotho protein ensures its biological effects through binding with fibroblast growth factor (FGF)-23 and altered Klotho/FGF23 axis was found a core element in the pathogenesis of the cardiovascular and metabolic disease. It has been found that predisposition for CV disease can be related to Klotho gene polymorphism, while the clinical significance of this finding is required to be elucidated in large clinical studies. The aim of the review was to summarize findings regarding the role of the FGF23/Klotho axis in the CV and metabolic conditions, as well as to identify perspectives to use Klotho protein as a promising pharmacological target for personifying therapy.

A Summary This study investigated the alterations of mineral metabolism in patients with Graves' disease (GD) who achieved euthyroidism. They had higher fibroblast growth factor 23 (FGF23) and phosphorus as compared with healthy subjects. Serum FGF23 was negatively correlated with serum phosphorus. These indicated abnormal mineral metabolism even after 1.6 years of euthyroid status. Introduction FGF23 is involved in the mineral homeostasis, especially the regulation of serum phosphorus. Graves' disease (GD) is associated with accelerated bone turnover, hyperphosphatemia, and elevated serum FGF23. Evidence suggested that serum FGF23 decreased after a 3-month treatment of GD. However, it remains unclear whether serum FGF23, serum phosphorus, and other markers of mineral metabolism will be normalized after euthyroid status achieved. Methods A total of 62 patients with euthyroid GD and 62 healthy control subjects were enrolled, and the median duration of euthyroid status was 1.6 years. Endocrine profiles including thyroid function test, autoantibodies, serum FGF23, and bone turnover markers were obtained and compared between the two groups. Results Euthyroid GD patients had significantly higher serum FGF23 and phosphorus, and lower 25-hydroxyvitamin D (25(OH)D) and intact parathyroid hormone (iPTH) levels as compared with the control group. Serum FGF23 was significantly and negatively correlated with phosphorus level after adjusted for age, gender, calcium, iPTH, and 25(OH)D in the euthyroid GD group. Conclusion Serum phosphorus and FGF23 levels remain higher in GD patients even after euthyroid status has been achieved for a median of 1.6 years. Serum FGF23 was negatively correlated with serum phosphorus in euthyroid GD patients. Underlying mechanisms warrant further investigations.