New Hope for ARDS May Be on the Horizon

A drug-like molecule developed by researchers at the University of Illinois Chicago has been found effective in preventing fluid from leaking from the blood vessels in the lungs and improving lung function in mice with acute respiratory distress syndrome (ARDS).

The discovery stemmed from previous research by the team, which identified a protein called EB3 that activates calcium signals in blood vessel cells, triggering leakage. The new molecule, dubbed VT-109, inhibits EB3. When mice who developed ARDS due to multiple causes, ranging from sepsis to SARS-CoV-2, were treated with VT-109, the balance of fluid was restored, and lung compliance improved.  

“One dose of the drug in mice in 24 hours completely restores lung compliance to its normal healthy baseline,” said study author Yulia Komarova.

VT-109 also helped control immune cells, such as neutrophils, that can promote inflammation, and, perhaps most importantly, the treatment worked whether it was used soon after the onset of ARDS or later in the disease process.

Additional experiments showed that VT-109 activates a cellular factor called FOXM1, which in turn kicks off the regeneration and repair effects that help heal the diseased lungs. The researchers plan to conduct additional testing on the molecule to determine its safety and will then launch clinical trials with clinicians at Oregon Health Sciences University.

The study was supported by a $5.86 million grant from the Office of the Assistant Secretary of Defense for Health Affairs and published by Signal Transduction and Targeted Therapy. 

Highlighted in RC Buzz, May 11, 2026