Proof-of-concept clinical trial of etokimab shows a key role for IL-33 in atopic dermatitis pathogenesis
Abstract
First-in-class clinical trial of IL-33 blockade shows inhibition of neutrophil migration into human skin and modulates atopic dermatitis symptoms. Interrupting inflammation in atopic dermatitis The alarmin cytokine IL-33 is implicated in a variety of conditions, including atopy, and is an emerging therapeutic target. Chen et al. report a clinical trial of a single dose of an anti–IL-33 antibody (etokimab) in adults with moderate to severe atopic dermatitis. The trial design included a placebo condition and assessment of skin immune responses to challenges with house dust mite. Clinically, anti–IL-33 was well tolerated and reduced peripheral eosinophils and symptoms of atopic dermatitis. Blocking IL-33 interfered with neutrophil recruitment. These results reveal human immunobiology and demonstrate that anti–IL-33 is a promising therapeutic for atopic dermatitis. Targeted inhibition of cytokine pathways provides opportunities to understand fundamental biology in vivo in humans. The IL-33 pathway has been implicated in the pathogenesis of atopy through genetic and functional associations. We investigated the role of IL-33 inhibition in a first-in-class phase 2a study of etokimab (ANB020), an IgG1 anti–IL-33 monoclonal antibody, in patients with atopic dermatitis (AD). Twelve adult patients with moderate to severe AD received a single systemic administration of etokimab. Rapid and sustained clinical benefit was observed, with 83% achieving Eczema Area and Severity Index 50…
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