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Much of the recent focus on drug development in IBD has centered on the IL-23 pathway.
In new data presented during the 18th Congress of the European Crohn’s and Colitis Organization (ECCO), taking place in Copenhagen, investigators found guselkumab is able to dose-dependently bind to CD64+a myeloid cells, which is the primary source of interleukin 23 (IL-23) driven inflammation in in vitro models of patients with inflammatory bowel disease (IBD).
In an interview with HCPLive®, Maria T. Abreu, MD, Professor of Microbiology and Immunology Director Crohn's & Colitis Center Martin Kalser Chair in Gastroenterology Vice Chair of Research, Department of Medicine Chair, International Organization for the Study of Inflammatory Diseases University of Miami Miller School of Medicine, explained the positive results and how researchers plan on building on this initial pursuit of targeting the IL-23 pathway with guselkumab.
In the past year there has been a lot of attention in drug development for IBD on IL-23, particularly after the US Food and Drug Administration approved risankizumab-rzaa (SKYRIZI) for the treatment of adults with moderately to severely active Crohn’s disease, the first ever IL-23 inhibitor approved for IBD.
“That was a step forward for mankind because it’s been recognized for quite a while that this cytokine interleukin 23 is really important in turning on these T cells that can be turned into pathogenic cells when they are around interleukin 23,” Abreu said from the meeting in Denmark.
The next step for the treatment is to test it in human tissue and potentially combine it as a therapy with other biologics.