Biological agents targeting interleukin-13 for atopic dermatitis

ABSTRACT

Introduction

Atopic dermatitis (AD) is a chronic inflammatory skin disease that is pathogenically driven by type-2 inflammation. Interleukin-13 (IL-13) plays a central role in AD pathogenesis, as confirmed by the clinical efficacy of agents that selectively block IL-13, although their therapeutic value and place-in-therapy are incompletely defined.

Areas covered

This review article aimed to describe preclinical and clinical data regarding selective IL-13 inhibitors investigated in AD. In particular, we discuss the clinical outcomes obtained with lebrikizumab and tralokinumab, which are in a more advanced phase of development.

Expert opinion

Biological agents that neutralize IL-13 have demonstrated clinical benefits in treating AD with excellent safety profiles. Robust clinical evidence exists in support of tralokinumab, which underwent phase III trials, met the predefined primary endpoints, and is approaching the market. In contrast, clinical trial testing for lebrikizumab needs to be completed to fully assess its therapeutic potential.

PLAIN LANGUAGE SUMMARY

Selective interleukin-13 (IL-13) inhibitors have shown clinical efficacy against AD, suggesting that IL-13 plays a central in AD pathogenesis. However, the therapeutic value and place-in-therapy of IL-13 inhibitors are not fully defined. This review articledescribed strengths and limitations of different anti-IL-13 agents used to treat AD that might be useful in driving treatment decision.

KEYWORDS:

• ASLAN004
• atopic dermatitis
• interleukin 13
• lebrikizumab
• tralokinumab

Article highlights

• IL-13 is a key cytokine involved in the pathogenesis of AD.

• Therapeutic agents selectively targeting IL-13, namely lebrikizumab and tralokinumab, have demonstrated clinical efficacy against AD with an excellent safety profile.

• Lebrikizumab is entering a phase III clinical program.

• Tralokinumab completed phase III trials and is entering the market.

Declaration of Interests

A Chiricozzi served as advisory board member and consultant and has received fees and speaker’s honoraria or has participated in clinical trials for AbbVie, Almirall, Leo Pharma, Lilly, Janssen, Novartis, Sanofi Genzyme, Pfizer, and Incyte. P Gisondi has been a consultant and/or speaker for Abbvie, Almirall, Amgen, Janssen, Leo-pharma, Eli Lilly, Novartis, Pierre Fabre, Sandoz, Sanofi and UCB. C De Simone reports consulting fees or honorarium from Abbvie, Amgen, Novartis, Celgene, Sanofi, UCB Pharma, Janssen, and Lilly and payment for lectures from Abbvie, Lilly, Novartis, UCB Pharma, and Celgene. G Caldarola reports consulting fees or honorarium and payment for lectures from Lilly and Novartis. K Peris has served on advisory board, received honoraria for lectures and/or research grants for Abbvie, Almirall, Lilly, Galderma, Leo Pharma, Pierre Fabre, Novartis, Sanofi, Sun Pharma, Janssen. G Girolomoni has been principal investigator in clinical trials sponsored by and/or and has received personal fees from AbbVie, Almirall, Amgen, Biogen, Boehringer-Ingelheim, Bristol-Meyers Squibb, Celgene, Eli-Lilly, Galderma, Leo Pharma, Novartis, Pfizer, Regeneron and Samsung. 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.