Dupilumab pharmacokinetics and effect on type 2 biomarkers in children with moderate-to-severe asthma.


Journal

Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
ISSN: 1534-4436
Titre abrégé: Ann Allergy Asthma Immunol
Pays: United States
ID NLM: 9503580

Informations de publication

Date de publication:
07 2023
Historique:
received: 31 10 2022
revised: 14 03 2023
accepted: 14 03 2023
medline: 4 7 2023
pubmed: 24 3 2023
entrez: 23 3 2023
Statut: ppublish

Résumé

Type 2 inflammation is common in children with asthma. Dupilumab, a human antibody, blocks the signaling of interleukin -4 and -13, key and central drivers of type 2 inflammation. In the LIBERTY ASTHMA VOYAGE (NCT02948959) study, dupilumab reduced severe asthma exacerbations and improved lung function in children aged 6 to 11 years with uncontrolled, moderate-to-severe asthma. To assess the pharmacokinetics of dupilumab and type 2 biomarker changes in children with type 2 asthma in VOYAGE. Patients were randomized to dupilumab 100 mg (≤30 kg) or 200 mg (>30 kg) or placebo every 2 weeks for 52 weeks. Dupilumab concentrations and changes in type 2 biomarkers were assessed at each visit. Dupilumab concentrations in serum reached a steady state by week 12, with mean concentrations of 51.2 mg/L and 79.4 mg/L in children receiving dupilumab 100 mg every 2 weeks and 200 mg every 2 weeks, respectively (therapeutic range in adults and adolescents: 29-80 mg/L). Reductions in type 2 biomarkers were comparable between regimens, and greater in patients treated with dupilumab vs placebo. In children treated with dupilumab 100 mg and 200 mg every 2 weeks, the median percent changes (Q1-Q3) from baseline at week 52 were, respectively, -78.6% (-86.3 to -69.80) and -78.6% (-84.9 to -70.1) for serum total immunoglobulin E, -53.6% (-66.4 to -34.6) and -43.7% (-58.6 to -28.5) for thymus and activation-regulated chemokine; -25.7% (-60.0 to 27.6) and -33.3% (-60.6 to 16.6) for blood eosinophils, and -47.7% (-73.8 to 18.9) and -55.6% (-73.6 to -20.0) for fractional exhaled nitric oxide. Weight-tiered dose regimens achieved mean concentrations within the dupilumab therapeutic range. The median decreases in type 2 biomarker levels were similar between dose regimens. ClinicalTrials.gov Identifier: NCT02948959.

Sections du résumé

BACKGROUND
Type 2 inflammation is common in children with asthma. Dupilumab, a human antibody, blocks the signaling of interleukin -4 and -13, key and central drivers of type 2 inflammation. In the LIBERTY ASTHMA VOYAGE (NCT02948959) study, dupilumab reduced severe asthma exacerbations and improved lung function in children aged 6 to 11 years with uncontrolled, moderate-to-severe asthma.
OBJECTIVE
To assess the pharmacokinetics of dupilumab and type 2 biomarker changes in children with type 2 asthma in VOYAGE.
METHODS
Patients were randomized to dupilumab 100 mg (≤30 kg) or 200 mg (>30 kg) or placebo every 2 weeks for 52 weeks. Dupilumab concentrations and changes in type 2 biomarkers were assessed at each visit.
RESULTS
Dupilumab concentrations in serum reached a steady state by week 12, with mean concentrations of 51.2 mg/L and 79.4 mg/L in children receiving dupilumab 100 mg every 2 weeks and 200 mg every 2 weeks, respectively (therapeutic range in adults and adolescents: 29-80 mg/L). Reductions in type 2 biomarkers were comparable between regimens, and greater in patients treated with dupilumab vs placebo. In children treated with dupilumab 100 mg and 200 mg every 2 weeks, the median percent changes (Q1-Q3) from baseline at week 52 were, respectively, -78.6% (-86.3 to -69.80) and -78.6% (-84.9 to -70.1) for serum total immunoglobulin E, -53.6% (-66.4 to -34.6) and -43.7% (-58.6 to -28.5) for thymus and activation-regulated chemokine; -25.7% (-60.0 to 27.6) and -33.3% (-60.6 to 16.6) for blood eosinophils, and -47.7% (-73.8 to 18.9) and -55.6% (-73.6 to -20.0) for fractional exhaled nitric oxide.
CONCLUSION
Weight-tiered dose regimens achieved mean concentrations within the dupilumab therapeutic range. The median decreases in type 2 biomarker levels were similar between dose regimens.
TRIAL REGISTRATION
ClinicalTrials.gov Identifier: NCT02948959.

Identifiants

pubmed: 36958470
pii: S1081-1206(23)00180-1
doi: 10.1016/j.anai.2023.03.014
pii:
doi:

Substances chimiques

dupilumab 420K487FSG
Antibodies, Monoclonal 0
Biomarkers 0

Banques de données

ClinicalTrials.gov
['NCT02948959', 'NCT02948959']

Types de publication

Randomized Controlled Trial Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

44-51.e4

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Daniel J Jackson (DJ)

Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin. Electronic address: djj@medicine.wisc.edu.

Leonard B Bacharier (LB)

Division of Allergy, Immunology and Pulmonary Medicine, Monroe Carell Jr Children's Hospital at Vanderbilt University Medical Center, Nashville, Tennessee.

Wanda Phipatanakul (W)

Department of Allergy and Immunology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.

Lawrence Sher (L)

Peninsula Research Associates, Rolling Hills Estates, California.

Christian Domingo (C)

Pulmonary Service, Corporació Sanitària Parc Taulí, Sabadell, Autonomous University of Barcelona (UAB), Barcelona, Spain.

Nikolaos Papadopoulos (N)

Allergy Department, Second Pediatric Clinic, University of Athens, Greece.

Brian Modena (B)

Department of Allergy and Immunology, Modena Allergy & Asthma, La Jolla, California.

Ning Li (N)

Department of Immunology, Sanofi, Beijing, People's Republic of China.

Changming Xia (C)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

Mohamed A Kamal (MA)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

Myles Dillon (M)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

Kelley Wolfe (K)

Department of Immunology, Sanofi, Bridgewater, New Jersey.

Rebecca Gall (R)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

Nikhil Amin (N)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

Leda P Mannent (LP)

Department of Immunology, Sanofi, Chilly-Mazarin, France.

Elizabeth Laws (E)

Department of Immunology, Sanofi, Bridgewater, New Jersey.

Paul J Rowe (PJ)

Department of Immunology, Sanofi, Bridgewater, New Jersey.

Juby A Jacob-Nara (JA)

Department of Immunology, Sanofi, Bridgewater, New Jersey.

Yamo Deniz (Y)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

David J Lederer (DJ)

Department of Immunology, Regeneron Pharmaceuticals Inc, Tarrytown, New York.

Megan Hardin (M)

Department of Immunology, Sanofi, Cambridge, Massachusetts.

Christine Xu (C)

Department of Immunology, Sanofi, Bridgewater, New Jersey.

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