New and Emerging Systemic Treatments for Atopic Dermatitis
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LEADING ARTICLE
New and Emerging Systemic Treatments for Atopic Dermatitis Megan Newsom1 · Arjun M. Bashyam1 · Esther A. Balogh1 · Steven R. Feldman1,2,3,4 · Lindsay C. Strowd1
© Springer Nature Switzerland AG 2020
Abstract Atopic dermatitis (AD) is a prevalent inflammatory skin condition that, depending on its severity, can cause enormous morbidity. Corticosteroids and systemic immunosuppression, traditionally standard of care for difficult-to-treat disease, have many undesirable side effects. The desire for targeted treatments along with an improved understanding of the pathophysio‑ logy of AD has spurred the development of novel treatments. In this article, we review promising new treatments and discuss how their targets—IL-13, IL-31, OX40 (CD134), and the Janus kinase family of proteins—participate in the pathogenesis of AD. We review the published phase II and III data for dupilumab, tralokinumab, lebrikizumab, nemolizumab, anti-OX40 antibody, baricitinib, abrocitinib, and upadacitinib. The introduction of new agents may offer new options, but it remains to be seen how narrow-acting agents, like single interleukin inhibitors, will compare in safety and efficacy to broad-acting agents such as JAK inhibitors.
Key Points
1 Introduction
Our better understanding of the pathophysiology of AD has resulted in an explosion of research into new immunotherapies for this patient population.
Atopic dermatitis (AD) is a common inflammatory skin disease characterized by pruritus and skin barrier dysfunction [1–3]. Current mainstay treatments include topical moisturizers, topical corticosteroids, topical calcineurin inhibitors, phototherapy, and systemic immunotherapies [4]. Moderateto-severe AD is often refractory to first-line topical treatments; while systemic immunosuppressants are efficacious, they have significant adverse effects [4]. The shortcomings of mainstay treatments prompted the development of targeted topical and systemic immunotherapies involving pathways directly responsible for AD. The US Food and Drug Administration (FDA) approved a topical phosphodiesterase-4 ( PDE4) inhibitor, crisaborole, in 2016 for mild-to-moderate AD and a monoclonal antibody, dupilumab, in 2017 for moderate to severe AD [5]. While the efficacy of dupilumab is considerable, the clinical success
Multiple new agents targeting IL-13, IL-31, OX40 (CD134), and Janus kinase proteins may be effective for AD.
* Megan Newsom [email protected] 1
Department of Dermatology, Center for Dermatology Research, Medical Center Boulevard, Wake Forest School of Medicine, Winston‑Salem, North Carolina, 27157‑1071, USA
2
Department of Pathology, Wake Forest School of Medicine, Winston‑Salem, NC, USA
3
Department of Social Sciences and Health Policy, Wake Forest School of Medicine, Winston‑Salem, NC, USA
4
Department of Dermatology, University of Southern Denmark, Odense, Denmark
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of crisaborole is less impressive. Additional new treatments are desirable, as AD is a heterogeneous disease with sever
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