New approaches in Immunology are advancing pulmonary fibrosis research to elevate the standard of care for patients.
Updated: August 6, 2026
Breathing is something most people rarely have to think about — until it becomes difficult. For people living with pulmonary fibrosis, breathing is always top of mind. Fibrosis, the thickening and excessive buildup of scar tissue in the lungs, can turn everyday activities into physical challenges, highlighting the need for new approaches that address the disease earlier and more effectively.
Pulmonary fibrosis is a chronic, life-threatening interstitial lung disease (ILD) that occurs when lung tissue becomes irreversibly damaged and scarred, impacting how the lungs function. Idiopathic pulmonary fibrosis (IPF) is a disease of unknown cause and is the most common type of progressive fibrosing ILD, with approximately 1.4 million people living with IPF globally. Progressive pulmonary fibrosis (PPF) includes patients with non-idiopathic forms of ILD. This includes systemic autoimmune rheumatic disease-associated interstitial lung diseases (SARD-ILD), such as rheumatoid-related lung fibrosis and scleroderma-related lung fibrosis, and other types, such as environmental lung fibrosis, which is caused by exposure to dust or chemicals.
Bristol Myers Squibb is leveraging deep expertise in drug discovery and disease biology to investigate potential treatments for pulmonary fibrosis to improve patients’ quality of life.
Pulmonary fibrosis is a devastating illness, often leaving patients physically impaired and making it difficult to perform simple activities due to persistent daily symptoms like chronic cough, extreme breathlessness and severe fatigue. Many patients living with IPF and PPF require continuous supplemental oxygen to ease the burden of normal breathing.
Early diagnosis is challenging and misdiagnosis often leads to treatment delays, which leaves patients burdened by symptoms and seeking answers and relief for long periods. IPF and PPF have lower survival rates than many cancers, and patients must navigate treatment difficulties alongside feelings of fear, depression and isolation.
Currently approved pulmonary fibrosis treatments can slow the decline of lung function; however, they show inconsistent quality of life benefits and may present tolerability challenges. As a result, many patients face difficult tradeoffs at diagnosis and as their condition worsens. There is an urgent need for well-tolerated therapies that can be used alone or with existing options to stabilize, prevent and/or reverse disease progression to help patients live longer while preserving their daily function and overall quality of life.
We have been researching therapies for patients with pulmonary fibrosis for more than a decade and are currently investigating potential therapies in both IPF and PPF.
Our research approach begins not at the point where fibrosis is visible, but at the origin of disease biology, where epithelial cell injury and dysfunctional repair first emerge. By examining these upstream drivers rather than solely the downstream fibrosis, we aim to identify the early events that contribute to disease progression. In doing so, we can uncover how interconnected systems, such as cellular dysfunction, signaling breakdowns and failed repair, shape how the disease spreads and becomes irreversible. This insight allows us to rethink where, not just how, intervention can have the greatest patient impact.
Fibrosis can develop in virtually any organ. It occurs when the body’s normal healing process is dysregulated and is a consequence of earlier disease processes and subtle, repeated biological disruptions. Our goal is to correct that dysfunction so fibrosis doesn’t occur.
Lysophosphatidic acid (LPA) is a signaling molecule that interacts with LPA receptors to mediate wound healing in response to an injury. Elevated LPA levels and increased activation of lysophosphatidic acid receptor 1 (LPA1) have been implicated in three key drivers of fibrosis in conditions such as pulmonary fibrosis, including faulty epithelial cell repair, inflammation/vascular leakage and fibroblast expansion.
Approaches targeting LPA1 may be used alongside established pulmonary fibrosis treatments with different mechanisms of action or in combination with immunosuppressive medications for other conditions.
Learn more about Bristol Myers Squibb's commitment to developing new treatments for immune-mediated diseases with our research on the LPA1 receptor and its role in IPF and PPF.
Fueled by our deep understanding of the immune system built on more than 20 years of experience, we are driven to deliver life-changing medicines that elevate new standards of care – not only to advance science, but to help people breathe more easily, stay active longer and feel more like themselves in the moments that matter.
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