- Mechanism of Action
Mechanism of Action
TREMFYA® MECHANISM OF ACTION IN PATIENTS WITH MODERATE TO SEVERE PLAQUE PSORIASISTREMFYA® SELECTIVELY TARGETS AND BINDS WITH HIGH SPECIFICITY AND AFFINITY TO IL-231-3
TREMFYA® is the only fully human anti–IL-23.
- IL-23 is a naturally occurring cytokine that is involved in normal inflammatory and immune responses1
- Interaction between IL-23 and its receptor drives the differentiation, proliferation, and survival of Th17 cells, which produce inflammatory cytokines4-6
By blocking IL-23, TREMFYA® inhibits the release of important pro-inflammatory cytokines4-6
- Serum levels of IL-17A, IL-17F, and IL-22 were reduced relative to pretreatment levels based on an exploratory analysis
- The clinical significance of these findings is not known
The mean half-life of guselkumab in patients with plaque psoriasis: ≈15 to 18 days.1
References: 1. TREMFYA® (guselkumab) [prescribing information]. Horsham, PA: Janssen Biotech, Inc. 2. Zhuang Y, Calderon C, Marciniak SJ Jr, et al. First-in-human study to assess guselkumab (anti-IL-23 mAb) pharmacokinetics/safety in healthy subjects and patients with moderate-to-severe psoriasis. Eur J Clin Pharmacol. 2016;72(11):1303-1310. 3. Data on file. Janssen Biotech, Inc. 4. Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361(5):496-509. 5. Fitch E, Harper E, Skorcheva I, Kurtz SE, Blauvelt A. Pathophysiology of psoriasis: recent advances on IL-23 and Th17 cytokines. Curr Rheumatol Rep. 2007;9(6):461-467. 6. Fujita H. The role of IL-22 and Th22 cells in human skin diseases. J Dermatol Sci. 2013;72(1):3-8.