FOR THE TREATMENT OF ADULT PATIENTS WITH MODERATELY TO SEVERELY ACTIVE CROHN’S DISEASE OR MODERATELY TO SEVERELY ACTIVE ULCERATIVE COLITIS (UC)
EXPLORE POSSIBILITIES WITH TREMFYA

In both Crohn’s disease and ulcerative colitis, or UC, inflammation can keep coming back like relentless weeds. IL-23, an inflammatory cytokine, is one of the known drivers of inflammation in Crohn’s disease and UC. Blocking IL-23 after it is produced can limit inflammation.after it is produced can limit inflammation. But what if it were possible to block IL-23 inflammation at its cellular source? CD64-positive immune cells are the main producers, and the root source, of IL-23. TREMFYA (guselkumab) is the only dual-acting IL-23 inhibitor. TREMFYA works by BLOCKING IL-23, a cytokine responsible for inflammation, and BINDING to CD64, a receptor on cells that produce IL-23. The clinical significance of these findings is unknown. TREMFYA is an IL-23 blocker indicated for the treatment of adult patients with moderately to severely active Crohn’s disease or moderately to severely active UC. Similar to other IL-23 inhibitors, TREMFYA binds to the p19 subunit of IL-23 and inhibits its interaction with the IL-23 receptor, thereby inhibiting the release of pro-inflammatory cytokines and chemokines. Unlike other IL-23 inhibitors, only TREMFYA is designed with a dual-acting structure that blocks IL-23 and also binds to CD64, a receptor on cells that produce IL-23. Binding to CD64 positions TREMFYA to block IL-23 at its cellular source, allowing it to work at the root of IL-23–driven inflammation. TREMFYA: the only dual-acting IL-23 inhibitor that neutralizes inflammation at its cellular source. Based on in vitro studies in an inflammatory monocyte model. The clinical significance of these findings is unknown.^1-3