Nikhil Prasad Fact checked by:Thailand Medical News Team Jun 28, 2026 1 hour, 11 minutes ago
Medical News: Existing narcolepsy medication shows surprising ability to reduce lung inflammation and scarring
Researchers from the Department of Physiology, College of Medicine, Ewha Womans University, Seoul, Republic of Korea, and the Department of Thoracic & Cardiovascular Surgery, College of Medicine, Ewha Womans University, Seoul, Republic of Korea, have uncovered an unexpected new use for the wakefulness-promoting drug solriamfetol. Their research suggests that the medication, currently prescribed for excessive daytime sleepiness in people with narcolepsy, may also help combat lung inflammation and fibrosis by targeting a key enzyme involved in disease progression.
Researchers discovered that the narcolepsy drug solriamfetol may dramatically reduce lung inflammation and
scarring by blocking adenosine deaminase.
Idiopathic pulmonary fibrosis (IPF) is a chronic disease in which scar tissue gradually replaces healthy lung tissue, making breathing increasingly difficult. Although treatments exist, they only slow disease progression, creating an urgent need for better therapeutic options.
Drug dramatically reduced inflammation and lung damage
Using both human lung fibroblast cells and a mouse model of pulmonary fibrosis, the researchers investigated whether solriamfetol could influence the inflammatory and scarring processes responsible for IPF.
The results were encouraging. Mice treated with solriamfetol showed significantly fewer inflammatory immune cells entering the lungs. The treatment also reduced inflammatory molecules, improved lung structure, and lessened damage to delicate air sacs. Animals receiving the higher dose experienced the greatest improvements, suggesting that the drug's benefits are dose dependent.
Researchers also found that the medication reduced the production of inflammatory cytokines that normally fuel tissue injury, producing effects comparable to well-known anti-inflammatory medications in laboratory experiments.
Less scar tissue and healthier lung cells
One of the most important findings involved fibrosis itself. Solriamfetol significantly lowered collagen accumulation within lung tissue. Excess collagen is responsible for the stiff scar tissue that prevents lungs from expanding properly.
The drug also reduced levels of alpha-smooth muscle actin, a marker of activated myofibroblasts. These specialized cells are largely responsible for producing scar tissue during pulmonary fibrosis. By preventing fibroblasts from transforming into these highly active scar-forming cells, solriamfetol effectively interrupted one of the disease's major driving forces.
Researchers additionally observed reductions in several fibrosis-associated proteins and genes, suggesting the treatment acts across multiple biological pathways instead of targeting only one process.
A completely different way the drug may work
Perhaps the most surprising discovery involved the enzyme adenosine deaminase (ADA). Rather than acting solely through its known effects on dopamine and norepinephrine, solriamfetol directly suppressed ADA activity and reduce
d ADA expression.
Because ADA normally breaks down adenosine, blocking the enzyme allowed adenosine levels to rise. Increased adenosine activated protective A2A and A2B receptors, restoring important cellular signaling involving cyclic AMP and Epac proteins that had become impaired during fibrosis.
This
Medical News report highlights that restoring these signaling pathways appeared to switch off several disease-promoting mechanisms simultaneously. The researchers also found that blocking either adenosine receptor largely eliminated the protective effects, confirming that this pathway plays a central role in the drug's newly discovered activity.
Further experiments showed that solriamfetol also inhibited KCa3.1 potassium channels, which are known to promote both inflammation and fibrosis. Suppressing these channels may provide another explanation for the drug's broad anti-fibrotic effects.
Could an approved medicine be repurposed?
Since solriamfetol is already an approved medication for sleep disorders, repurposing it for pulmonary fibrosis could potentially shorten future development timelines if additional research confirms its safety and effectiveness in humans.
However, the researchers caution that these findings are based mainly on laboratory experiments and animal studies. Clinical trials involving patients with idiopathic pulmonary fibrosis will still be required before the drug can be considered a treatment option.
Conclusion
The study provides compelling evidence that solriamfetol may possess powerful anti-inflammatory and anti-fibrotic properties that extend far beyond its current role as a wakefulness-promoting medicine. By inhibiting adenosine deaminase, restoring protective adenosine signaling, reducing immune cell infiltration, limiting collagen deposition, preventing activation of scar-forming cells, and suppressing multiple fibrosis-related pathways, the drug demonstrated remarkable therapeutic potential in preclinical models. Although human studies are still needed, these findings open an exciting new avenue for repurposing an existing medication to treat one of the most devastating chronic lung diseases.
The study findings were published in the peer reviewed journal: Therapeutics.
https://www.mdpi.com/2813-9909/3/3/15
For the latest on preventing, treating or slowing lung fibrosis, keep on logging to Thailand
Medical News.
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https://www.thailandmedical.news/news/u-s--fda-greenlights-jascayd-as-breakthrough-drug-for-lung-fibrosis
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