According to data from a Phase IIa study evaluating AstraZenaca’s novel investigational monoclonal antibody benralizumab in patients with COPD, the drug did not reduce the acute exacerbation rate compared with placebo in the overall patient population but did demonstrate clinically significant improvements in lung function in the overall population.

The results were published in The Lancet Respiratory Medicine and presented at ERS 2014. The study, conducted by MedImmune, the company’s global biologics research and development arm, evaluated the safety and efficacy of benralizumab in 101 adults with moderate-to-severe COPD and experiencing at least one acute exacerbation requiring oral corticosteroids, antibiotics, or hospitalization in the past year.

The study indicated that benralizumab reduced COPD exacerbations and improved other symptoms of COPD in certain patient groups. Patients treated with benralizumab who had higher baseline levels of eosinophils in their blood showed greater improvements in COPD symptoms, including exacerbation rate, lung function and disease-specific health status as measured by the Saint George’s Respiratory Questionnaire-COPD (SGRQ-C) versus placebo-treated subjects.

There was a higher incidence of serious treatment-emergent adverse events (TEAEs) in the benralizumab group compared with placebo (14 vs 9). Overall, TEAEs were similar across treatment and placebo groups.

Benralizumab is an anti-interleukin-5 receptor alpha monoclonal antibody that depletes blood and sputum eosinophils, a type of white blood cell. Elevated levels of eosinophils are associated with the cause and severity of COPD attacks, as well as asthma and asthma exacerbations. Eosinophilic airway inflammation is believed to be present in between 20 and 30 percent of the 210 million people who suffer from COPD worldwide.

“Benralizumab is the first biological agent to show marked reduction in eosinophilic inflammation and beneficial effects in COPD, indicating a potential new way to treat patients with severe COPD symptoms,” said lead investigator Professor Christopher Brightling, University of Leicester, Glenfield Hospital, Department of Respiratory Medicine. “The strength of these results reinforces the further development of this molecule for COPD.”