Joe Arron

We have shown that subsets of asthma patients exhibit excessive type 2 or type 17 airway inflammation and we developed non-invasive biomarkers of these asthma subtypes. These biomarkers are being tested to see if they can identify which patients may be appropriate candidates for several experimental drugs in clinical studies. We are currently working to identify additional mechanisms of disease, candidate therapeutic targets, and biomarkers in other asthma subtypes.

Idiopathic pulmonary fibrosis (IPF) is a devastating progressive lung disease with a worse prognosis than most cancers. We have characterized the activity of several therapeutically targetable pathways in lung tissue from IPF patients and discovered blood biomarkers that are being used to identify patients at risk of rapid disease progression, patients most likely to respond to specific therapies, and monitor the biological consequences of therapeutic interventions in clinical studies.

Taking advantage of the samples and phenotypic data available from the well-characterized patients enrolled in our clinical trials, we are performing genetic studies 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