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Review

Biologics targeting IL-5, IL-4 or IL-13 for the treatment of asthma – an update

Pages 143-149 | Received 24 May 2016, Accepted 20 Jul 2016, Published online: 02 Aug 2016
 

ABSTRACT

Introduction: The development of monoclonal antibody-based biologics targeted at inhibition of the Th2 cytokines IL-4, IL-5 and IL-13 represent potentially effective treatments for patients with the glucocorticoid refractory eosinophilic asthma phenotype.

Areas covered: Asthma exhibits marked heterogeneity both clinically and at the molecular phenotypic level, requiring specifically targeted treatments to block the key pathways of the disease. It is becoming apparent that significant clinical effects with anti-cytokine-based biologic therapies are more likely in carefully selected patient populations that take asthma phenotypes into account. The development of reproducible and straightforward discriminatory biomarkers may aid identification of those patients most likely to benefit from treatment with these expensive interventions. This narrative review is based on English-language original articles in PubMed or Med-Line that reported significant clinical findings published in the last two years on the evidence demonstrating the effectiveness or otherwise of the targeting of IL-4, IL-5, or IL-13 in carefully selected patients with severe refractory asthma.

Expert commentary: The use of a baseline peripheral blood eosinophilia as a simple reproducible biomarker to identify patients with particular sub-phenotypes of asthma to guide the effective use of biologic therapy represents a significant step forward.

Declaration of interest

The author has no 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. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

This paper was not funded.

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