Omalizumab for severe asthma: toward personalized treatment based on biomarker profile and clinical history

Abstract

Asthma is a heterogeneous syndrome with numerous underlining molecular and inflammatory mechanisms contributing to the wide spectrum of clinical phenotypes. Multiple therapies targeting severe asthma with type 2 (T2) high inflammation are or soon will be available. T2 high inflammation is defined as inflammation associated with atopy or eosinophilia or an increase in cytokines associated with T-helper 2 lymphocytes. Omalizumab is a humanized anti-IgE monoclonal antibody and the first biologic therapy approved for moderate–severe allergic asthma. Despite the specificity of biologic therapies like omalizumab, clinical response is variable, with approximately 50% of treated patients achieving the primary outcome. A prior identification of the ideal candidate for therapy would improve patient outcomes and optimize the use of health care resources. As the number of biologic therapies for asthma increases, the goal is identification of biomarkers or clinical phenotypes likely to respond to a specific therapy. This review focuses on potential biomarkers and clinical history that may identify responders to omalizumab therapy for asthma.

Keywords:

• severe persistent asthma
• asthma phenotype and endotype
• T2 high inflammation
• omalizumab
• asthma biomarkers
• eosinophils
• fractional exhaled nitric oxide
• IgE

Disclosure

DKL has received research support (paid to University) from Genentech/Roche and AstraZeneca, consultant fees from AstraZeneca, speakers’ bureau fees from AstraZeneca, Genentech/Roche, Meda, Novartis, and Teva, and fees for legal opinions on drug allergy, metal allergy, radiocontrast reaction, and asthma death. The authors report no other conflicts of interest in this work.