Idiopathic Pulmonary Fibrosis (IPF) Clinical Trials

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic interstitial lung disease of unknown etiology characterized by progressive replacement of normal lung tissue with fibrotic scar tissue. This fibrosis impairs gas exchange, leading to progressive hypoxemia and dyspnea, primarily with exertion initially but progressing to dyspnea at rest. The disease demonstrates typical/usual interstitial pneumonia (UIP) pattern on imaging and histology.

The most common symptoms of Idiopathic Pulmonary Fibrosis include Progressive shortness of breath, initially with exertion, Persistent dry cough, Fatigue and weakness, Chest discomfort, Clubbing of fingers and toes, among others. About 100,000 people in the U.S., with 30,000 to 40,000 new cases a year (MedlinePlus Genetics). Symptoms can range from mild to severe and may vary between individuals.

Trial Friend lists all active clinical trials for Idiopathic Pulmonary Fibrosis from ClinicalTrials.gov, with eligibility criteria translated into plain English. Patients can filter by trial phase and recruitment status, search by location, and use the Match Me tool to score trials against their profile. Three antifibrotic medications are FDA approved for IPF: pirfenidone (Esbriet and generics), nintedanib (Ofev, with generics approved in April 2026) and nerandomilast (Jascayd, approved October 7, 2025), which was tested both on its own and alongside either of the other two. Each slows the loss of lung function rather than reversing scarring.

Yes. As of October 21, 2026, 3 FDA-approved medicines have a current label that names Idiopathic Pulmonary Fibrosis: Esbriet (pirfenidone), first approved in 2014; Jascayd (nerandomilast), first approved in 2025; and Ofev (nintedanib), first approved in 2014. Corticosteroids and immune globulins count once each.

The exact cause of Idiopathic Pulmonary Fibrosis is not fully understood. It is not caused by a single gene; inherited variants raise risk, and immune, environmental or other triggers are thought to set it off. Sporadic IPF has no diagnostic gene test; in the minority of familial cases, telomere-gene variants (TERT, TERC and others) are found in about 15%, so testing is relevant mainly with a family history. About 100,000 people in the U.S., with 30,000 to 40,000 new cases a year (MedlinePlus Genetics). Research is ongoing to better understand the disease mechanism.

No single gene test diagnoses Idiopathic Pulmonary Fibrosis. The diagnosis rests on clinical findings and laboratory or imaging results; genetic variants shift risk rather than cause the disease. Sporadic IPF has no diagnostic gene test; in the minority of familial cases, telomere-gene variants (TERT, TERC and others) are found in about 15%, so testing is relevant mainly with a family history.

Some trials collect genetic samples for research or check specific risk markers. The Genetic Testing section of this page shows any tests listed in the NIH Genetic Testing Registry, which for this condition are usually research or risk-marker tests rather than diagnostic ones.

Eligibility for Idiopathic Pulmonary Fibrosis clinical trials depends on factors like age, diagnosis, treatment history, and overall health. Each trial sets its own inclusion and exclusion criteria. Trial Friend translates these requirements from medical language into plain English so patients can review them more easily. The Match Me tool can score your profile against active trials to help identify studies that may be a fit.

Participating in a Idiopathic Pulmonary Fibrosis clinical trial typically involves scheduled visits, medical tests, and close monitoring by a research team. Depending on the study phase, you may receive an investigational treatment, a placebo, or the current standard of care. Trials may last from a few weeks to several years. Study participation is voluntary, and you can withdraw at any time.