NCFB is a common final pathway for a broad range of chronic airway insults. An interplay between neutrophil-driven inflammation, excess mucus production and airway plugging, and chronic infection leads over time to lung damage. This interplay is often referred to as the “vicious vortex” of NCFB. Patients with NCFB suffer from chronic cough, sputum production and shortness of breath and experience frequent exacerbations, which can lead to even further lung damage. No agents are approved in the US for the treatment of NCFB, although agents are in development that target the neutrophil-driven inflammation aspect of the vicious vortex. An urgent unmet need exists for agents that can target all relevant aspects of NCFB and potentially reverse existing lung damage.

IPF is a chronic, progressive lung disease associated with high morbidity and mortality. Although the exact cause is unknown, various factors cause repeated injury to the lung that trigger abnormal wound healing and life-threatening scarring. IPF has a very poor prognosis with an average life expectancy of only 3-5 years after diagnosis. Current therapies such as pirfenidone and nintedanib slow the progression of IPF, but do not reverse existing lung damage. Therefore, a urgent unmet need exists for therapies that can reverse lung fibrosis and scarring and improve lung function, quality of life and survival.

In in vitro models of IPF, ELD607 potently blocks the production of pro-fibrotic biomarkers in fibroblasts from both normal human lung and patients with IPF. In animal models of chronic IPF, ELD607 has shown an unprecedented reversal of lung fibrosis and scarring. Therefore, ELD607 has the unique potential to reverse existing lung damage and improve lung function, quality of life and survival in patients with IPF.