Fresh data, fresh air for asthma

WRITTEN BY

Bing Yao, Ph.D

Asthma is one of those conditions that the general population doesn’t give much thought to. But, talk to anyone with a severe form of this disease—up to 10 percent of 300 million asthmatics worldwide —and you’ll hear horror stories that will wrench your heart.

This is why developing innovation-driven targeted therapies is a core component of our respiratory strategy. We’re following the science to help identify which subsets of patients are most likely to respond to specific respiratory therapies.

At this year’s annual meeting of the American Thoracic Society (ATS), we’re introducing new data about two investigational biologics—benralizumab and tralokinumab—for severe forms of asthma. Both are part of our personalized healthcare approach that we’re exploring for asthma.

These two drugs attack different, but equally ruthless types of asthma: one that is driven by eosinophils, a type of white blood cell that is a key target in inflammatory respiratory diseases such as asthma and Chronic Obstructive Pulmonary Disorder (COPD); and the other that involves a separate asthmatic pathway involving the cytokine interleukin-13 (IL-13).

At the end of last year, we were able to share that we’ve progressed benralizumab into Phase III trials for severe asthma. The Phase IIb research we’ll discuss at ATS further supports this. Benralizumab has a unique mode of action as it binds to the interleukin-5 receptor alpha (IL-5Rα) on eosinophils and subsequently depletes them.

We’ll also discuss our research into the effects of benralizumab in patients with COPD characterized by higher baseline eosinophils. Scientific literature supports that elevated eosinophil levels are associated with the cause and severity of asthma and asthma exacerbations, as well as COPD exacerbations.

In addition, we’ll talk about the science behind tralokinumab and our Phase II data for this biologic. This includes our studies into blocking the IL-13 pathway to determine its effect against a number of key measures of asthma control such as exacerbations (asthma attacks), pulmonary function and asthma symptoms. Based on the results of the Phase II studies, we plan to study whether patients with elevated levels of certain IL-13-related biomarkers in the blood will gain any benefits from chronic tralokinumab therapy.

While this may sound complicated, what it comes down to, in part, is helping the respiratory community understand the biology, phenotypes and new drug combinations that are being scrutinized to determine their ability to contribute to step-changes in clinical outcomes for patients in the future. We know asthma is heterogeneous, which is why our focus is on the development of personalized therapeutics. And, we’re following the science that supports the evolution of this type of personalized healthcare with the hope of transforming how respiratory diseases are managed.

We’ll be confirming more about benralizumab as we continue its current Phase III program, and we anticipate tralokinumab moving in to Phase III development later this year, as well as moving benralizumab into Phase III for COPD. There are a number of abstracts at the ATS meeting that represent our respiratory portfolio, and we’re very much looking forward to presenting them in more details.

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