With extended remissions, high safety and favorable dosing schedules, interleukin (IL)-23 inhibitors are well-suited for a variety of patients with psoriasis, says an expert who spoke at the South Beach Symposium.
The IL-23 inhibitors’ mechanism of action and infrequent dosing schedule provide advantages over previous-generation biologics, says Mark Lebwohl, M.D. He is the Waldman Professor and Chairman, Kimberly and Eric J. Waldman Department of Dermatology, Icahn School of Medicine at Mount Sinai.
“In the pathophysiology of psoriasis, the key target appears to be IL-17,” he says.
The IL-23 blockers guselkumab, tildrakizumab, risankizumab and mirikizumab block the cytokine that upregulates the Th17 cell, which makes IL-17. The Th17 cell not only stops making IL-17, but then either hibernates or withers away, according to Dr. Lebwohl.
“Then it takes several months to reconstitute those cells. So these drugs work more slowly than the IL-17 inhibitors, but their effect is longer lasting,” he adds.
Brodalumab, ixekizumab and secukinumab can provide 50% Psoriasis Area and Severity Index (PASI) reductions in 1.8 to 3 weeks, but with IL-23 inhibitors, “patients really only start getting going after four weeks,” says Dr. Lebwohl.
Dr. Lebwohl has been an investigator and advisor for guselkumab (Janssen), tildrakizumab (Sun Pharma), risankizumab (AbbVie) and mirikizumab (Eli Lilly), and most of the biologic therapies available for psoriasis. All payments for research go to his employer, the Icahn School of Medicine at Mount Sinai, and he receives no personal direct compensation from the manufacturers of biologic therapies.
Mark Lebwohl MD. “Tips in the Use of Anti-IL-23 Antibodies,” South Beach Symposium. February 8, 2020.