Benralizumab for the add-on maintenance treatment of patients with severe asthma aged 12 years and older with an eosinophilic phenotype

ABSTRACT

Introduction: Asthma is an airway disease characterized by airway inflammation. It is associated with significant morbidity, mortality, and costs to the health-care system and society. Eosinophils and interleukin-5 (IL-5) play a key role in the inflammatory response in T-helper 2-high asthma. IL-5 is pivotal for eosinophil development, maturation, and survival in tissues. Asthma severity has been related to both airway and peripheral blood eosinophilia.

Areas covered: In this review, we present the pharmacokinetics and pharmacodynamics of benralizumab in addition to efficacy and safety data in the treatment of severe eosinophilic asthma.

Expert commentary: Benralizumab is a potent biologic targeting the IL-5 receptor on eosinophils and basophils leading to depletion of target cells in peripheral blood and tissues. It is effective in reducing asthma exacerbations and has an oral corticosteroid-sparing effect in the treatment of asthma patients who are not controlled with medium-to-high-dose inhaled corticosteroids and long-acting beta agonists. The side effect profile is similar to placebo with the most reported adverse events being nasopharyngitis and worsened asthma in the pivotal trials. Its long-term safety is currently under investigation.

KEYWORDS:

• Benralizumab
• IL-5
• biologics
• asthma
• MEDI-563

Declaration of Interest

JM FitzGerald discloses advisory board/membership to GSK, AstraZeneca, BI, Novartis, Teva, ALK and Pfizer and peer reviewed funding from CIHR, Allergan, BC Lung Association, Canadian Lung Association. He has also received research funding from GSK, AstraZeneca, Amgen, Johnson and Johnson, Sanofi and Novartis all paid directly to the University of British Columbia as well as unrestricted grants from GSK and Merck. He is also an advisor to the BC Ministry of Health and discloses receiving honoraria from AstraZeneca, BI, Novartis Pfizer and Merck. K Al Efraij’s fellowship is funded by AstraZeneca and was also supported in part by an unrestricted educational grant from TEVA. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Additional information

Funding

This manuscript was not funded.