New Data Show TREMFYA ® (guselkumab) Binds to Both Inflammatory Cells and Interleukin (IL)-23, Supporting a Hypothesis for a Differentiated Mechanism from Risankizumab

SPRING HOUSE, PENNSYLVANIA, May 18, 2022 – The Janssen Pharmaceutical Companies of Johnson & Johnson today announced the first results of the in vitro MODIF-Y studies, supporting a hypothesis that may differentiate the mechanism of first-in-class TREMFYA® (guselkumab) from risankizumab due to the ability of TREMFYA to bind to CD64 positive (CD64+) cells in addition to interleukin (IL)-23 — both of which are key components of the immune system. 1,2 These findings, which are being presented at the Society for Investigative Dermatology (SID) annual meeting May 18-21, 2022 in Portland, Oregon, demonstrate TREMFYA binds simultaneously to CD64 via its native fragment crystallizable (Fc) region and to IL-23 via its antigen-binding region, suggesting the potential to neutralize IL-23 right at the site where it is secreted.1 Further studies will be conducted in vitro and in vivo to generate additional evidence supporting this hypothesis. IL-23, a cytokine secreted by activated monocyte/macrophage and dendritic cells, is known to be a driver of inflammatory diseases, including plaque psoriasis (PsO), psoriatic arthritis (PsA), and inflammatory bowel disease (IBD).3,a CD64 is a receptor that binds the Fc region of immunoglobulin G4 and is highly expressed on the surface of certain immune cells that are major producers of IL-23.4-7 “The initial results of these studies show the potential differentiating mechanism of TREMFYA,” said presenting study author James G. Krueger, M....
Source: Johnson and Johnson - Category: Pharmaceuticals Tags: Innovation Source Type: news