Efficacy of biologics in atopic dermatitis

ABSTRACT

Introduction: Atopic dermatitis (AD) is a heterogeneous disease. Recent advancements in understanding AD pathogenesis resulted in the exponential expansion of its therapeutic pipeline, particularly following the success and FDA-approval of dupilumab. Different phenotypes of AD by age and ethnicity have also recently been described and clinical studies of emerging treatments will further clarify the role of each cytokine pathway in AD.

Areas covered: We review the impressive repertoire of biologics for treatment of moderate-to-severe AD, including those targeting Th2, Th22, Th17/IL-23 and IgE. We highlight the scientific rationale behind each approach and provide a discussion of the most recent clinical efficacy and safety data.

Expert opinion: AD is a complex disease and recent research has identified numerous endotypes, reinforcing the rationale for developing targeted therapeutics to antagonize these factors. Dupilumab has revolutionized AD treatment and its mechanistic studies also offer crucial insight into AD pathogenesis. Nevertheless, this biologic does not work for everyone, highlighting the need for a more precise approach to address the unique immune fingerprints of each AD subset. Ultimately targeted therapeutics will complement our understanding of the AD molecular map and help push AD management into an era of personalized medicine.

KEYWORDS:

• Atopic dermatitis
• biologics
• dupilumab
• lebrikizumab
• tralokinumab
• nemolizumab
• fezakinumab
• tezepelumab
• secukinumab
• etokimab

Article highlights

• Approval of dupilumab, the first biologic to be used in AD, has opened the door for the therapeutic development of other targeted treatments

• There is differential activation of the Th2, Th1, Th17 and Th22 cytokine pathways depending on the AD phenotype (e.g. depending on age or ethnicity), underscoring the heterogeneous nature of this disease

• Clinical trials of biologics that target these different immune axes will ultimately contribute to the evolving understanding of AD pathogenesis and shift AD treatment into an era of personalized medicine

This box summarizes key points contained in the article.

Declaration of interest

E Guttman-Yassky is an employee of Mount Sinai and has received research funds (grants paid to the institution) from: Abbvie, Celgene, Eli Lilly, Janssen, Medimmune/Astra Zeneca, Novartis, Pfizer, Regeneron, Vitae, Glenmark, Galderma, Asana, Innovaderm, Dermira, UCB. E Guttman-Yassky is also a consultant for Sanofi Aventis, Regeneron, Stiefel/GlaxoSmithKline, MedImmune, Celgene, Anacor, AnaptysBio, Dermira, Galderma, Glenmark, Novartis, Pfizer, Vitae, Leo Pharma, Abbvie, Eli Lilly, Kyowa, Mitsubishi Tanabe, Asana Biosciences, and Promius. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.

Additional information

Funding

This paper was not funded.