In Patients with Moderate to Severe Plaque Psoriasis
Mechanism of Action
TREMFYATM SELECTIVELY TARGETS AND BINDS WITH HIGH SPECIFICITY AND AFFINITY TO IL-231,3-7

TREMFYA<sup>TM</sup> (guselkumab) mechanism of action

TREMFYATM is a human monoclonal IgG1λ antibody that selectively binds to the p19 subunit of IL-23 and inhibits its interaction with the IL-23 receptor.

  • 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 cytokines5-7

  • By blocking IL-23, TREMFYATM inhibits the release of important pro-inflammatory cytokines

    • 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 days1