Efficacy of Tezepelumab in Patients with Severe, Uncontrolled Asthma with and without Nasal Polyposis: A

asthma biomarkers nasal polyps sinusitis tezepelumab thymic stromal lymphopoietin

Journal

Journal of asthma and allergy
ISSN: 1178-6965
Titre abrégé: J Asthma Allergy
Pays: New Zealand
ID NLM: 101543450

Informations de publication

Date de publication:
2021
Historique:
received: 09 11 2020
accepted: 06 01 2021
entrez: 11 2 2021
pubmed: 12 2 2021
medline: 12 2 2021
Statut: epublish

Résumé

Tezepelumab is a human monoclonal antibody that blocks thymic stromal lymphopoietin, an epithelial cytokine implicated in asthma pathogenesis, from binding to its heterodimeric receptor. In the phase 2b PATHWAY study, tezepelumab significantly reduced annualized asthma exacerbation rates (AAERs) versus placebo, irrespective of baseline disease characteristics, and improved lung function and symptom control, in adults with severe, uncontrolled asthma. This In this At baseline, NP+ patients had higher blood eosinophil counts, higher FeNO levels and higher serum IL-5 and IL-13 levels than NP- patients. Tezepelumab 210 mg reduced the AAER versus placebo to a similar extent in both NP+ and NP- patients (NP+, 75% [95% confidence interval (CI): 15, 93], n=23; NP-, 73% [95% CI: 47, 86], n=112). Patients treated with tezepelumab 210 mg demonstrated greater reductions in blood eosinophil count and levels of FeNO, IL-5 and IL-13 than placebo-treated patients, irrespective of NP status. Tezepelumab reduced exacerbations and reduced type 2 inflammatory biomarkers in patients with and those without NP, supporting its efficacy in a broad population of patients with severe asthma.

Sections du résumé

BACKGROUND BACKGROUND
Tezepelumab is a human monoclonal antibody that blocks thymic stromal lymphopoietin, an epithelial cytokine implicated in asthma pathogenesis, from binding to its heterodimeric receptor. In the phase 2b PATHWAY study, tezepelumab significantly reduced annualized asthma exacerbation rates (AAERs) versus placebo, irrespective of baseline disease characteristics, and improved lung function and symptom control, in adults with severe, uncontrolled asthma. This
METHODS METHODS
In this
RESULTS RESULTS
At baseline, NP+ patients had higher blood eosinophil counts, higher FeNO levels and higher serum IL-5 and IL-13 levels than NP- patients. Tezepelumab 210 mg reduced the AAER versus placebo to a similar extent in both NP+ and NP- patients (NP+, 75% [95% confidence interval (CI): 15, 93], n=23; NP-, 73% [95% CI: 47, 86], n=112). Patients treated with tezepelumab 210 mg demonstrated greater reductions in blood eosinophil count and levels of FeNO, IL-5 and IL-13 than placebo-treated patients, irrespective of NP status.
DISCUSSION CONCLUSIONS
Tezepelumab reduced exacerbations and reduced type 2 inflammatory biomarkers in patients with and those without NP, supporting its efficacy in a broad population of patients with severe asthma.

Identifiants

pubmed: 33568920
doi: 10.2147/JAA.S288260
pii: 288260
pmc: PMC7868291
doi:

Types de publication

Journal Article

Langues

eng

Pagination

91-99

Informations de copyright

© 2021 Emson et al.

Déclaration de conflit d'intérêts

CE, KS, ÅH and GC are employees of AstraZeneca and may have stock options in AstraZeneca. JC received grants from AstraZeneca during the conduct of the study, and has received grants and personal fees from Genentech, personal fees from Teva Pharmaceuticals, grants from Sanofi and personal fees from Vectura Group outside of the submitted work. JRP is an employee of Amgen Inc., and holds stock and stock options in Amgen Inc. JRP has patents US20180296669A1 and WO201819479A1, Treatment of Asthma with Anti-TSLP Antibody, pending. The authors report no other conflicts of interest in this work.

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Auteurs

Claire Emson (C)

Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA.

Jonathan Corren (J)

David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA, USA.

Kinga Sałapa (K)

Biometrics, Late-Stage Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Warsaw, Poland.

Åsa Hellqvist (Å)

Biometrics, Late-Stage Development, Respiratory and Immunology, AstraZeneca, Gothenburg, Sweden.

Jane R Parnes (JR)

Amgen, Thousand Oaks, CA, USA.

Gene Colice (G)

Late-Stage Development Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA.

Classifications MeSH