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The role of the structurally related interleukin-(IL) 12 and IL-23, as key drivers of Th1 and Th17 differentiation, in the pathogenesis of inflammatory chronic conditions has led to the development of various monoclonal antibodies targeted either at the common p40 subunit shared both cytokines (ustekinumab) or at the IL-23-specific p19 subunit (guselkumab, tildrakizumab, and risankizumab). These IL-12/23-targeted agents are currently approved for the treatment of plaque psoriasis, psoriatic arthritis, and inflammatory bowel disease in patients with inadequate response or intolerance to conventional or antitumor necrosis factor (TNF)-α therapies. Pivotal trials from the clinical development programs and post-marketing observational studies have shown an overall favorable safety profile in terms of infectious complications, with rates comparable to control groups. Although IL-12 and IL-23 blockade entails a theoretical risk of tuberculosis (TB) and superficial candidiasis, respectively, available clinical evidence suggests that the incidence of such events is actually lower compared to anti-TNF-α or anti-IL-17 agents. Pretreatment screening for latent TB infection and viral hepatitis, however, remains mandatory.

DOI: 10.1007/978-3-031-11363-5_11