Do We Really Need to Keep Redesigning β2-Agonists for the Management of Asthma?

ISSN: 1875-5704 (Online)
ISSN: 1567-2018 (Print)


Volume 11, 6 Issues, 2014


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Editor-in-Chief:
Istvan Toth
School of Pharmacy,University of Queensland
Brisbane, 4072
Australia


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Do We Really Need to Keep Redesigning β2-Agonists for the Management of Asthma?

Author(s): David VAN LY and Brian G. G. OLIVER

Affiliation: School of Medical & Molecular Biosciences, University of Technology Sydney, Building 4, Level 6, City Campus, PO Box 123 Broadway NSW 2007 Australia

Abstract

There is an enormous drive to refine therapeutic designs and delivery systems, but in this review we ask is this always the right direction? We choose to play devil's advocate, and argue that refining drug design is not always needed, and what is actually needed is a greater understanding of the biology of the disease. Here we focus upon asthma and the β2 agonist group of bronchodilators as an example of how a class of therapeutic has developed and continues to be developmentally refined. In this review we define viral-induced exacerbations as the greatest cause of lung attacks and the most crucial time β2 agonist therapy are needed. We explore the reasons why β2 agonist therapy fail in patients with rhinovirus-induced exacerbations, and predict that current or future “more potently engineered” β2 agonist therapies will continue to fail in this subset of asthmatic population. We justify our prediction by coming back to the biology of the cause of disease and suggest the need for “more research” into alternative therapies instead for this population of asthmatic patients

Keywords: β2-agonists, Desensitization, Exacerbations, Leukotrienes, Prostaglandins, Rhinovirus

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Article Details

Volume: 11
First Page: 1
Last Page: 7
Page Count: 7
DOI: 10.2174/1567201811666140606112918
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