Anti–IL-13 (cendakimab) administration improves esophageal gene expression in eosinophilic esophagitis

Abstract

The molecular pathogenesis of the type 2 inflammatory disease eosinophilic esophagitis (EoE) is largely driven by IL-13-mediated effects. A humanized monoclonal anti-IL-13 antibody (cendakimab) lowered esophageal eosinophils and improved outcomes in clinical trials. We aimed to determine how systemic cendakimab administration impacted local esophageal gene expression in a substudy of a double-blind, placebo-controlled phase 2 trial (NCT02098473).