CRYSVITA® (burosumab-twza) is an FGF23 blocking antibody1
XLH is caused by a variant in the PHEX gene, which leads to increased FGF23 activity through an unknown mechanism. 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
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 active vitamin D production.3,4
CRYSVITA is a human monoclonal antibody specifically designed to inhibit the activity of FGF23
CRYSVITA targets the underlying cause of XLH
CRYSVITA (burosumab-twza) US Prescribing Information; September 2019.
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.