Robert Tarran

last updated 4/16/2018

Robert Tarran

Associate Professor at University of North Carolina

500 Finley Golf Course Road, Chapel Hill, North Carolina, United States
HQ Phone:
(919) 962-2349

General Information


Scientific Founder - Spyryx Biosciences Inc

Key Regulator - ENaC

Assistant Professor, Cystic Fibrosis and Pulmonary Research and Treatment Center - professor , Cystic Fibrosis/Pulmonary Research & Treatment Center


B.Sc.University of Leeds , UK


Ph.D.University of Newcastle upon Tyne , UK

Ph.D.University of North Carolina School of Medicine

PhDUniversity of North Carolina at Chapel Hill Award Year

PhD - Physiology , Newcastle University


Advisory and Steering Committees - FDA

Recent News  

People With Asthma Are Missing An Airway 'Muscle Relaxer'

Robert Tarran, associate professor of medicine and a member of the UNC Marsico Lung Institute, linked the protein to cystic fibrosis.
"People have been studying SPLUNC1 and its role in the context of other diseases, such as cystic fibrosis and lung cancer, but we believe that we are the group to identify its role in asthma," Tarran says. Epithelial cells that line airways produce the SPLUNC1 protein. "We found that this protein, which is actually turned off by excessive inflammation, is needed to cause the muscle to relax. It's essentially a muscle-relaxing factor that's missing from asthma patients. It's something that normally acts as a brake," Tarran says. A potential therapy for asthma would be to replenish either the whole protein or part of the protein, which could be delivered via a nebulizer or inhaler. "Most of the asthma therapies people use are inhalers, which have been around for decades. There have only been a few new asthma medications in the past 10 or 20 years, and they're still being evaluated," says Tarran.

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BOARD OF DIRECTORS - Spyryx Biosciences

Robert Tarran, PhD
Director Dr. Tarran is the scientific founder of Spyryx Biosciences, based on his discovery of the SPLUNC1/ENaC regulatory pathway in the respiratory tract. He is an Associate Professor at UNC-Chapel Hill in the Department of Cell Biology and Physiology, a member of the Lineberger Cancer Center, and a member of the Cystic Fibrosis and Pulmonary Diseases Research and Treatment Center. Additionally, he is the founder and Director of UNC's NIH/FDA-funded Tobacco Center of Regulatory Science. Dr. Tarran has served on advisory and steering committees for the FDA and the Cystic Fibrosis Foundation. Dr. Tarran's research interests have centered on the role of ion channels in chronic lung diseases such as CF, COPD, and asthma. He has studied this field for more than 20 years and is widely published, including his work on SPLUNC1 as a key regulator of ENaC and airway hydration and its dysfunction in CF airways. He was also a member of the team that discovered airway surface liquid (ASL) dehydration to be one of the most significant defects in the CF airway and a target for therapeutic intervention. During his career, Dr. Tarran has significantly contributed to the establishment of confocal assessment of ASL height as a method for studying airway epithelial function. Dr. Tarran received his BSc (hons) from The University of Leeds, UK. His PhD in Physiology was awarded at Newcastle University. Prior to joining the faculty at UNC-Chapel Hill, he completed post-doctoral research in ion channel physiology at University of California-Berkley and at UNC-Chapel Hill.

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Awardees and Abstracts | AAFRP

Until recently, little was known about this protein, but work by Dr. Tarran and others has revealed that SPLUNC1 is important in maintaing watery airway fluid with minimal inflammation.
This helps keep normal lungs free from mucus. In cystic fibrosis, SPLUNC1 is non-functional, leading to thickened secretions and problems clearing infections. In preliminary studies, Dr. Tarran finds that SPLUNC1 is reduced in the sputum of patients with allergic asthma as well as in the nasal secretions of patients with allergic rhinitis. In a mouse model of asthma, he finds that treatment of mice with SPLUNC1 prevents airway constriction, even when it is given after allergy and inflammation are well established - evidence that loss of SPLUNC1 is not simply a result of asthma but is, instead, a cause. He proposes to define the mechanisms by which SPLUNC1 is reduced in asthma and the mechanisms by which SPLUNC1 blocks asthma symptoms. Dr. Tarran's proposal is unusual in that a natural product is shown to be a potential therapy for asthma, recalling the findings of Jonathan Stamler (2003 AAF Awardee) that the natural small molecule GSNO suppresses asthma. Dr. Tarran's studies will elucidate the best mechanisms for sustaining SPLUNC1 in asthma Scientific Abstract Robert Tarran, Ph.D. - 2014 Scholar Award University of North Carolina at Chapel Hill Does SPLUNC1 Deficiency Lead to Airways Hyperresponsiveness in Asthma?

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