CRYSVITA directly targets the biological activity of fibroblast growth factor 23 (FGF23)

CRYSVITA (burosumab-twza) is a FGF23 blocking antibody1

Excess FGF23 in XLH leads to renal phosphate wasting

XLH is caused by increased FGF23 activity, which suppresses renal tubular phosphate reabsorption and renal production of 1,25 dihydroxy-vitamin D, which plays a role in phosphate absorption in the small intestines.1,2

CRYSVITA binds to and inhibits the biological activity of FGF23 to restore renal phosphate absorption and increase Vitamin D production

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

Inhibition of FGF23 may restore phosphate homeostasis by increasing renal expression of sodium phosphate cotransporters and increasing expression 1-a hydroxylase, a vitamin D metabolizing enzyme

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 1-α hydroxylase, a vitamin D-metabolizing enzyme involved in vitamin D production.3,4

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CRYSVITA addresses the underlying cause of XLH

References

  1. CRYSVITA (burosumab-twza) US Prescribing Information; April 2018.

  2. 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.

  3. 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.

  4. Erben RG, Andrukhova O. FGF23-Klotho signaling axis in the kidney. Bone. 2017;100:62-68.