@article{abdcc6ac5dfd456dae2bc3d03dc08945,
title = "Dupilumab reduced impact of severe exacerbations on lung function in patients with moderate-to-severe type 2 asthma",
abstract = "Background: Severe asthma exacerbations increase the risk of accelerated lung function decline. This analysis examined the effect of dupilumab on forced expiratory volume in 1 s (FEV1) in patients with moderate-to-severe asthma and elevated type 2 biomarkers from phase 3 LIBERTY ASTHMA QUEST (NCT02414854). Methods: Changes from baseline in pre- and post-bronchodilator (BD) FEV1 and 5-item Asthma Control Questionnaire (ACQ-5) scores were assessed in patients with elevated type 2 biomarkers at baseline (type 2–150/25: eosinophils ≥150 cells/μl and/or fractional exhaled nitric oxide [FeNO] ≥25 ppb; type 2–300/25: eosinophils ≥300 cells/μl and/or FeNO ≥25 ppb), stratified as exacerbators (≥1 severe exacerbation during the study) or non-exacerbators. Results: In exacerbators and non-exacerbators, dupilumab increased pre-BD FEV1 by Week 2 vs placebo; differences were maintained to Week 52 (type 2–150/25: LS mean difference (LSMD) vs placebo: 0.17 L (95% CI: 0.10–0.24) and 0.17 L (0.12–0.23); type 2–300/25: 0.22 L (0.13–0.30) and 0.21 L (0.15–0.28)), in exacerbators and non-exacerbators, respectively (p <.0001). Similar trends were seen for post-BD FEV1. Dupilumab vs placebo also showed significantly greater improvements in post-BD FEV1 0–42 days after first severe exacerbation in type 2–150/25 (LSMD vs placebo: 0.13 L [0.06–0.20]; p =.006) and type 2–300/25 (0.14 L [0.06–0.22]; p =.001) patients. ACQ-5 improvements were greater with dupilumab vs placebo in both groups. Conclusion: Dupilumab treatment led to improvements in lung function independent of exacerbations and appeared to reduce the impact of exacerbations on lung function in patients who experienced a severe exacerbation during the study.",
keywords = "FEV, dupilumab, severe exacerbations, type 2 biomarkers",
author = "Alberto Papi and Jonathan Corren and Mario Castro and Christian Domingo and Linda Rogers and Chapman, {Kenneth R.} and Jackson, {Daniel J.} and Nadia Daizadeh and Nami Pandit-Abid and Rebecca Gall and Jacob-Nara, {Juby A.} and Rowe, {Paul J.} and Yamo Deniz and Benjamin Ortiz",
note = "Funding Information: AP has received grants, personal fees, non‐financial support, and other funding from AstraZeneca, Boehringer Ingelheim, Chiesi Farmaceutici, GSK, Mundipharma GmbH, Teva Pharmaceuticals; reports personal fees and non‐financial support from Menarini, Novartis, Zambon; and grants from Sanofi. JC reports research grants, consultancy fees for AstraZeneca, Genentech, Novartis, Regeneron Pharmaceuticals, Inc., Sanofi; and has received speaker fees from AstraZeneca, Genentech, Novartis. MC has received research support from American Lung Association, AstraZeneca, GSK, NIH, Novartis, PCORI, Pulmatrix, Inc., Sanofi‐Aventis, Shionogi; is a consultant for Genentech, Novartis, Sanofi‐Aventis, Teva Pharmaceuticals; has received speaker fees from AstraZeneca, Genentech, GSK, Regeneron Pharmaceuticals, Inc., Sanofi, Teva Pharmaceuticals; and reports royalties from Elsevier. CD has received travel and speaker fees from ALK, Allergy Therapeutics, Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi Farmaceutici, Esteve, Ferrer Pharma, GSK, HAL Allergy Group, ImmunoTek, Menarini, Novartis, Pfizer, Sanofi‐Aventis, Stallergenes Greer PLC, Takeda, Teva Pharmaceuticals. LR reports research support from Lung Association, NIH, Sanofi; is a consultant for AstraZeneca, Genentech, Novartis, Sanofi; and has received payments for organizing educational events from AstraZeneca, Genentech. KRC has received grants and personal fees from AstraZeneca, Boehringer Ingelheim, CSL Behring, Genentech, Grifols Ltd., Kamada Ltd., Mereo BioPharma Group, Novartis, Roche, Sanofi; reports grants from Amgen, Baxter, GSK; and has received personal fees from CIHR‐GSK Research Chair in Respiratory Health Care Delivery, Merck, UHN. DJJ is a consultant for AstraZeneca, Boehringer Ingelheim, GSK, Novartis, Regeneron Pharmaceuticals, Inc., Sanofi, Vifor Pharma; and reports membership of the data and safety monitoring board for Pfizer. ND is a former employee of Sanofi and may hold stock and/or stock options in the company. NP, JAJ, and PJR are Sanofi employees and may hold stock and/or stock options in the company. RG, YD, and BO are employees and shareholders of Regeneron Pharmaceuticals, Inc. Funding Information: Research sponsored by Sanofi and Regeneron Pharmaceuticals, Inc. ClinicalTrials.gov Identifier: NCT02414854. Support for data analysis and statistics was provided by Armin Altincatal. Medical writing/editorial assistance was provided by Martina Fuchsberger, PhD, of Excerpta Medica, and was funded by Sanofi Genzyme and Regeneron Pharmaceuticals, Inc., according to the Good Publication Practice guideline. Open Access Funding provided by Universita degli Studi di Ferrara within the CRUI‐CARE Agreement. Open Access Funding provided by Universita degli Studi di Ferrara within the CRUI‐CARE Agreement. Publisher Copyright: {\textcopyright} 2022 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.",
year = "2023",
month = jan,
doi = "10.1111/all.15456",
language = "English",
volume = "78",
pages = "233--243",
journal = "Allergy: European Journal of Allergy and Clinical Immunology",
issn = "0105-4538",
publisher = "Wiley-Blackwell Publishing Ltd",
number = "1",
}