​​IPF is characterized by chronic inflammation, fibrosis, and aberrant wound-healing processes that progressively destroy lung architecture. Current therapies slow decline but do not halt or reverse disease progression. Our team identified small molecules capable of directly interfering with these processes, aiming not just to manage symptoms but to fundamentally change the course of disease.

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Preclinical Success: In rigorous preclinical studies, our promising therapeutic agents  demonstrated the ability to inhibit IPF progression by:

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• Reducing fibrotic tissue accumulation.

• Limiting chronic inflammation that drives lung scarring.

• Preserving lung structure and function in models of disease.

 

​Impact and Vision: Our NIH-funded translational IPF research highlights the versatility and translational strength of our discovery platform. By addressing the core processes of inflammation and fibrosis across multiple organs, our team is advancing therapies with broad implications for degenerative and inflammatory diseases. This achievement reinforces our core mission: to transform scientific discovery into interventions that protect patients’ healthspan and improve lives.