Preclinical Evaluation Of New Antifibrotics In Corona Mouse Virus-Induced Fibrosis Model

By Nagendra Ningaraj, Ph.D., MBA, CCRP Sr. Director, Scientific Affairs

According to the Pulmonary Fibrosis Foundation (PFF), there are approximately 200 types of interstitial lung diseases (ILDs), all of which involve varying degrees of lung inflammation, scarring (fibrosis), and impaired oxygen exchange. Among these, Idiopathic Pulmonary Fibrosis (IPF) is one of the most common and severe forms, marked by progressive and irreversible scarring of lung tissue. Major contributing factors to IPF include exposure to airborne pollutants, radiation therapy, certain medications, genetic predispositions, and autoimmune conditions. With no known cure, IPF typically leads to death within 3 to 5 years of diagnosis.

Similarly, Nonalcoholic Steatohepatitis (NASH), a serious form of fatty liver disease caused by inflammation and fat accumulation in the liver, is another increasingly prevalent fibrotic condition. Currently, the only approved antifibrotic drugs—pirfenidone and nintedanib—are available for treatment, but neither is capable of halting disease progression. This underscores the urgent need for innovative and effective antifibrotic therapies, supported by clinically relevant, IND-enabling preclinical models for robust evaluation.

Emerging research has also linked SARS-CoV-2 infection to the development of lung fibrosis through multiple signaling pathways, including the activation of TGF-β. In response to this growing concern, Aragen has developed a specialized coronavirus-induced mouse model to study lung fibrosis. This model is part of Aragen’s comprehensive platform of 17 validated fibrosis models, which span key organ systems such as lung, liver, kidney, skin (scleroderma), NASH-induced fibrosis, and biliary fibrosis. Our scientists bring extensive experience in preclinical IPF research, including the use of the coronavirus-induced fibrosis model, to evaluate the efficacy of novel antifibrotic drug candidates.