Joe Arron

We have sWe have shown that subsets of asthma patients exhibit activity of diverse pathways including various inflammatory cytokines, mast cells, and neuroinflammation. We developed non-invasive biomarkers of these asthma subtypes and discovered mechanistically differentiated candidate therapeutics that are being tested in clinical studies.

Idiopathic pulmonary fibrosis (IPF) is a devastating progressive interstitial lung disease with a worse prognosis than most cancers. We have characterized the activity of therapeutically targetable pathways in primary lung tissue from IPF patients. This work has led to the discovery of several targets currently in preclinical and clinical development as well as blood biomarkers that can identify patients at risk of rapid disease progression and monitor response to targeted therapies. We are particularly excited about the potential to promote regenerative processes so that instead of just slowing disease progression, we might someday be able to reverse pathology and regain function.

Taking advantage of the samples and phenotypic data available from the well-characterized patients enrolled in our clinical trials, we are performing genetic studies and developing sophisticated preclinical models to discover new disease mechanisms and therapeutic targets in respiratory diseases. This represents a great example of the feed-forward virtuous cycle of translational research in drug discovery and drug development as we move back and forth between bench and bedside.

• Stanford University School of Medicine, Postdoctoral scholar – 2006
• Weill Medical College of Cornell University, M.D. – 2003
• The Rockefeller University, Ph.D. – 2002
• Princeton University, A.B. – 1996