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Full Prescribing Information
FOR THE TREATMENT OF ADULTS WITH ACTIVE PSORIATIC ARTHRITIS (PsA)
The first biologic that
selectively inhibits IL-231-3
FOR THE TREATMENT OF ADULTS WITH ACTIVE PSORIATIC ARTHRITIS (PsA)
The first biologic that selectively inhibits IL-231-3
Watch TREMFYA® mechanism of action
IL=interleukin.
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
- By blocking IL-23, TREMFYA® inhibits the release of important pro-inflammatory cytokines and chemokines
- In evaluated patients with plaque psoriasis, TREMFYA® reduced serum levels of IL-17A, IL-17F, and IL-22 relative to pretreatment levels based on exploratory analyses of the pharmacodynamic markers
- In evaluated subjects with PsA, serum levels of acute phase proteins C-reactive protein, serum amyloid A and IL-6, and Th17 effector cytokines IL-17A, IL-17F, and IL-22 were elevated at baseline. Serum levels of these proteins measured at Week 4 and Week 24 were decreased compared to baseline following guselkumab treatment
- The clinical significance of these findings is not known
The mean half-life of guselkumab in patients with plaque psoriasis: ~15 days to 18 days1
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.
Learn how TREMFYA® is structurally different
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