Abstract
Allergic disease prevalence has increased globally with the subset of type 2 inflammatory diseases playing a substantial role. Type 2 inflammatory diseases may differ in clinical presentation, but they exhibit shared pathophysiology that is targeted by the unique pharmacology of dupilumab. Dupilumab binds to the interleukin (IL)-4 receptor alpha subunit (IL-4Rα) that blocks IL-4 and IL-13 signaling, two key drivers of type 2 inflammation. Herein, we review the mechanism of action and pharmacology of dupilumab, and the clinical evidence that led to the regulatory approvals of dupilumab for the treatment of numerous type 2 inflammatory diseases: atopic dermatitis, asthma, chronic rhinosinusitis with nasal polyposis, eosinophilic esophagitis, and prurigo nodularis.
© 2024 Regeneron Pharmaceuticals, Inc and Sanofi. Clinical and Translational Science published by Wiley Periodicals LLC on behalf of American Society for Clinical Pharmacology and Therapeutics.
MeSH terms
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Antibodies, Monoclonal, Humanized* / pharmacology
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Antibodies, Monoclonal, Humanized* / therapeutic use
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Asthma / drug therapy
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Asthma / immunology
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Dermatitis, Atopic* / drug therapy
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Dermatitis, Atopic* / immunology
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Eosinophilic Esophagitis / drug therapy
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Eosinophilic Esophagitis / immunology
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Humans
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Interleukin-13* / antagonists & inhibitors
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Interleukin-13* / immunology
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Interleukin-13* / metabolism
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Interleukin-4 / antagonists & inhibitors
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Interleukin-4 / metabolism
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Interleukin-4 Receptor alpha Subunit* / antagonists & inhibitors
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Interleukin-4 Receptor alpha Subunit* / metabolism
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Nasal Polyps / drug therapy
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Nasal Polyps / immunology
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Prurigo / drug therapy
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Signal Transduction / drug effects
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Sinusitis / drug therapy
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Sinusitis / immunology
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Translational Research, Biomedical*
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Translational Science, Biomedical
Substances
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dupilumab
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Antibodies, Monoclonal, Humanized
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Interleukin-4 Receptor alpha Subunit
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Interleukin-13
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Interleukin-4
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IL4R protein, human
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IL4 protein, human