Boehringer Ingelheim and Weill Cornell Medicine are again working together to identify treatment approaches to chronic obstructive pulmonary disease (COPD) that might halt or even reverse lung tissue damage.
Their three-year collaboration will build on Weill Cornell’s experience with chronic airway diseases and Boehringer Ingelheim’s expertise in developing therapies for respiratory conditions.
“Our continuous search for molecular drivers of chronic obstructive airway diseases has revealed novel repair mechanisms that warrant further investigation of their potential as therapeutic approaches,” Ronald G. Crystal, lead investigator in the project and Weill Cornell’s chairman of genetic medicine, said in a press release. “We will … focus on promising therapeutic concepts with the potential to slow down or halt progressive airway damage in patients with COPD.”
The two also worked together to identify treatments and biomarkers for inflammatory bowel disease (IBD) in an agreement that began in 2015.
“The new collaboration is an excellent example of our unique partnering approach and our focus on early innovation, underscoring our ambition to develop the next generation of medical treatments for patients with COPD,” said Clive R. Wood, senior corporate vice president of Boehringer Ingelheim’s discovery research.
There is no cure for COPD, and treatment options focus mainly on bronchodilation, symptom reduction and preventing flares that cause the disease to worsen.
Chronic lower respiratory diseases, like COPD, are the third leading cause of death in the United States, according to a 2014 Centers for Disease Control and Prevention (CDC) report.
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The largest study to date examining risk factors for lung disease showed that people at high genetic risk for developing COPD can cut that risk in half if they stop smoking in early adulthood.
The study examined 24 million genetic variants and concluded that those with the highest risk are 3.7 times more likely to develop COPD than those in the lowest risk group. Smoking further aggravates the risk, so much so that more than two-thirds of smokers in the high-risk group are likely to develop the condition.
Since COPD does not exclusively affect smokers, and not all smokers develop the condition, the research team focused especially on understanding how a person’s genetic makeup affects risk in smokers and non-smokers separately.