Researchers are developing a promising approach to detecting patients at risk of interstitial lung disease (ILD), an increasingly common condition that is a leading reason for lung transplants. The approach could accelerate the development of new and better treatments with more tolerable side effects than existing options.

For the nearly 3 million patients with idiopathic pulmonary fibrosis (IPF), what typically starts as shortness of  breath can rapidly worsen into a suffocating inability to breathe, often leading to a dangerous elevation in pulmonary artery pressure, related heart attacks or fatal respiratory failure within three to five years of diagnosis. USC physician-scientists Denis Evseenko and Toby Maher hope to offer these patients a better prognosis by developing a regenerative drug to block the cells that promote fibrosis, or scarring, in the lungs, with support from a five-year $3.2 million grant from the National Institute on Aging, part of the National Institutes of Health (NIH). Evseenko has already developed two drug-like molecules designed to stop immune cells and small blood vessels from initiating the cellular stress response that triggers inflammation and fibrosis. By blocking inflammation and fibrosis, these drug-like molecules promote a healthier environment conducive to regeneration. To develop these drug candidates for IPF, Evseenko is teaming up with Maher, who is a professor of clinical medicine and director of interstitial lung Disease at the Keck School of Medicine. An experienced pulmonologist recently recruited to the USC Hastings Center for Pulmonary Research, Maher has a biorepository of patient lung specimens and has been involved in more than 100 clinical trials for IPF and other fibrotic lung diseases. Through their collaboration, the team will test the safety and therapeutic potential of the two drug-like molecules in animals and human cells, and develop the most effective one into an oral pill—ideally ready for human clinical trials by the time the grant concludes in five years.