An overview of new and emerging antibody therapies for moderate-severe atopic dermatitis in adults

特应性皮炎 医学 杜皮鲁玛 单克隆抗体 临床试验 皮肤病科 免疫学 单克隆 抗体 病理
作者
Vincenzo Picone,Ylenia Vallone,Cataldo Patruno,M. Napolitano
出处
期刊:Expert Review of Clinical Pharmacology [Informa]
卷期号:16 (12): 1239-1248
标识
DOI:10.1080/17512433.2023.2292615
摘要

ABSTRACTIntroduction A comprehensive review of the English-language medical literature was performed searching for on-going and closed clinical trials concerning new and emerging monoclonal antibody therapies for moderate-to-severe atopic dermatitis in adults.Areas covered Atopic dermatitis is a chronic inflammatory cutaneous disease with a complex pathogenesis. In the last years, numerous advances in understanding the atopic dermatitis pathogenesis allowed to obtain several therapeutic options, such as numerous monoclonal antibodies. Some monoclonal antibodies, such as dupilumab (anti-IL-4 Rα) and tralokinumab (anti-IL13) are already approved for the treatment of moderate-to-severe atopic dermatitis, and numerous articles in the literature have demonstrated their efficacy and safety. As there are numerous drugs under investigation, this review focuses on emerging monoclonal antibodies therapies.Expert opinion There are numerous monoclonal antibodies under investigation that may be approved in the near future for the treatment of atopic dermatitis. Data from phase 2b and phase III clinical trials in moderate-to-severe atopic dermatitis in adults indicate that these drugs have a promising efficacy and safety profile. Monoclonal antibodies currently under investigation will be available in the coming years to enrich the therapeutic choice of new alternatives that are valid both in terms of efficacy and safety.KEYWORDS: Adult atopic dermatitisemerging monoclonal antibodiesLebrikizumabGBR 830AmlitelimabRocatinlimabEtokimabTezepelumabBermekimabDisclaimerAs a service to authors and researchers we are providing this version of an accepted manuscript (AM). Copyediting, typesetting, and review of the resulting proofs will be undertaken on this manuscript before final publication of the Version of Record (VoR). During production and pre-press, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal relate to these versions also. Article highlightsAtopic dermatitis (AD) is a chronic inflammatory cutaneous disease that can occurs in childhood and may resolve before adulthood or be present with a chronic relapsing course until adulthood (persistent AD). It can also occur in adulthood (adult-onset AD).Numerous factors play an important role in the pathogenesis of atopic dermatitis.Inflammation in AD is mainly caused by cells of innate and adaptive immune system and by numerous chemokines and cytokines produced by them, such as IL-4, IL-13, IL-22, IL-31 and IL-17. They are the target of numerous monoclonal antibodies already approved or under investigation for the treatment of moderate-to-severe atopic dermatitis.The emerging monoclonal antibodies discussed in this review targets IL-13, OX40-OX40L, IL-33, thymic stromal lymphopoietin, IL-1 and in the future some of them will probably be valid therapeutic alternatives for atopic dermatitis, both in terms of efficacy and safety.Data about new emerging therapies efficacy and adverse events recorded in phase 2b and phase III clinical trials have been discussed.Declaration of interestM Napolitano acted as speaker, consultant and advisory board member for Sanofi, Abbvie, Leo Pharma, Novartis and Eli Lilly. 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 disclosuresPeer reviewers on this manuscript have no relevant financial or other relationships to disclose.Figure 1: Illustration of the multiple immune pathways and targets for monoclonal antibodies in atopic dermatitis.Display full sizeAdditional informationFundingThis paper was not funded.
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