IL-23 inhibition for chronic inflammatory disease.
| Autor: | Jairath V; Departments of Medicine, Division of Gastroenterology, Western University, Ontario, ON, Canada., Acosta Felquer ML; Rheumatology Unit, Internal Medicine Service, Hospital Italiano de Buenos Aires and Instituto Universitario Hospital Italiano de Buenos Aires, Buenos Aires, Argentina., Jaihyun Cho R; Department of Dermatology, University of California, San Francisco, CA, USA. Electronic address: raymond.cho@ucsf.edu. |
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| Jazyk: | angličtina |
| Zdroj: | Lancet (London, England) [Lancet] 2024 Oct 26; Vol. 404 (10463), pp. 1679-1692. |
| DOI: | 10.1016/S0140-6736(24)01750-1 |
| Abstrakt: | Biological monoclonal antibody drugs inhibit overactive cytokine signalling that drives chronic inflammatory disease in different organ systems. In the last 10 years, interleukin (IL)-23 inhibitors have attained an important position in the treatment of psoriatic skin and joint disease as well as inflammatory bowel diseases. Addressing an upstream pathological mechanism shared between these disorders, this drug class has high efficacy rates and a durable response that extends dosing intervals up to 3 months. Pooled clinical trial data show objective disease improvement for more than 70% of patients with psoriasis and up to 50% of patients with inflammatory bowel disease. The first antibody inhibitor for IL-23A targeted a p40 subunit shared with IL-12. Subsequently, even greater improvement was established for inhibitors of the p19 protein unique to IL-23A. IL-23 p19 inhibitors elicit clinical response in both bio-naive and bio-exposed patients and show superiority to tumour necrosis factor α inhibitors in plaque psoriasis. Reported differences in efficacy between p19 inhibitors suggest that individual drug action might be modulated by antibody affinity. Although long-term safety data are accumulating, rates of serious adverse events and infections for interleukin (IL)-23 inhibitors are similar to the rates for placebo across approved indications. Competing Interests: Declaration of interests VJ received research funding from Celgene/BMS, Pfizer, AbbVie, Boehringer Ingelheim, Eli Lilly, Janssen, Takeda, Gilead Sciences, and Tigenix; and declares receiving compensation from AbbVie, Alimentiv, Amgen, Anokion, Applied Strategic, Arena Pharmaceuticals, Asahi Kasei Pharma, Asieris, AstraZeneca, BioJamp, Celgene/BMS, Celltrion, Eli Lilly, Ferring, F. Hoffman-La Roche, Flagship Pioneering, Fresenius Kabi, Fusion MD Network, Galapagos, Genentech, Gilead, GlaxoSmithKline, Janssen, Knightslab, Organon (Merck), Landos BioPharma, McKesson, Metacrine, Mylan, Pandion, Pendopharm, Pfizer, Prometheus, Protagonist Therapeutics, Reistone Biopharma, Roche, Sandoz, Second Genome, Sorriso, Takeda, Teva, Topivert, Ventyx Biosciences, Viatris, and Vividion Therapeutics. MLAF received research fundings from PANLAR, Novartis, and Janssen; and received compensation from Asoforma and Janssen. RJC received research funding from Sun Pharma, Leo Pharma, Bristol Myers Squibb, Regeneron, and Janssen. (Crown Copyright © 2024 Published by Elsevier Ltd. All rights reserved, including those for text and data mining, AI training, and similar technologies.) |
| Databáze: | MEDLINE |
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