
Mechanism of disease (MOD)
Small, usually benign tumors express FGF23, which results in hypophosphatemia. Excess FGF23 activity suppresses renal tubular phosphate reabsorption and production of active vitamin D.4
CRYSVITA® (burosumab-twza) is an FGF23-blocking antibody1
In TIO, benign tumors produce excess FGF23. This suppresses renal tubular phosphate reabsorption and renal production of 1,25 dihydroxy vitamin D, which play a role in phosphate absorption in the small intestine.1,2
CRYSVITA binds to and inhibits the biological activity of FGF23, restoring renal phosphate reabsorption and increasing the serum concentration of 1,25 dihydroxy vitamin D.1
Small, usually benign tumors express FGF23, which results in hypophosphatemia. Excess FGF23 activity suppresses renal tubular phosphate reabsorption and production of active vitamin D.4
Based on preclinical studies, inhibition of FGF23 is thought to restore phosphate homeostasis by promoting renal phosphate reabsorption through increased renal expression of sodium phosphate cotransporters and by increasing the renal expression of 1α-hydroxylase, a vitamin D–metabolizing enzyme involved in vitamin D production.3,4
CRYSVITA (burosumab-twza) US Prescribing Information; June 2020.
Martin A, Quarles LD. Evidence for FGF23 involvement in a bone-kidney axis regulating bone mineralization and systemic phosphate and vitamin D homeostasis. Adv Exp Med Biol. 2012;728:65-83.
Aono Y, Yamazaki Y, Yasutake J, et al. Therapeutic effects of anti-FGF23 antibodies in hypophosphatemic rickets/osteomalacia. J Bone Miner Res. 2009;24(11):1879-1888.
Erben RG, Andrukhova O. FGF23-Klotho signaling axis in the kidney. Bone. 2017;100:62-68.