Coya Therapeutics hits its 100th ALS trial enrollment and publishes new preclinical data, both pointing to the same immune-cell mechanism.
Two pieces of news came out of Coya Therapeutics in a span of a week, and taken together they tell a more complete story than either one does alone. One came from a mouse study, newly published research showing an experimental drug combination calming brain inflammation [1]. The other came from an actual clinical trial: patient number 100, enrolled and moving through a Phase 2/3 study in ALS [2].
Different stages of drug development entirely, but the same idea sits underneath both, get the immune system’s regulatory cells working properly again, and neurodegenerative disease might actually respond differently than it has so far.
A milestone in the clinic
The clinical update landed first, chronologically the more recent of the two. Coya announced that the 100th participant has now been enrolled in its ongoing Phase 2/3 ALSTARS trial, testing a drug called COYA 302 in patients with amyotrophic lateral sclerosis. Around 120 people are being split into three roughly even groups, receiving one of two dosing regimens or a placebo, for 24 blinded weeks. Those who complete that stretch move into a 24-week extension, where COYA 302 patients keep going and placebo patients get switched to one of the active doses, generating up to 48 weeks of data by the end.
The main thing being tracked is the ALSFRS-R, a scale that measures how well someone can still walk, speak, swallow and breathe, compared between baseline and week 24.
“Enrollment of the 100th participant in the ALSTARS trial represents a critical milestone for Coya and brings us closer to completing this important Phase 2/3 study,” said Fred Grossman, DO, FAPA, president and chief medical officer of Coya. “Our current screening and enrollment rates have been consistent, and we project that all 120 participants will be enrolled in the upcoming weeks and on target for a topline readout in early Q2 2027.”
COYA 302 combines low-dose interleukin-2, which boosts the activity of regulatory T cells, or Tregs, with a second compound called CTLA-4 Ig, aimed at calming the inflammatory immune cells that run unchecked when Tregs stop doing their job. It’s already been granted FDA Fast Track designation, a status reserved for therapies targeting serious conditions with real unmet need, which doesn’t guarantee approval but does mean more frequent contact with regulators along the way.
ALS patients lose roughly a point a month on that ALSFRS-R scale, on average, and 20% to 30% die within two years of diagnosis even with the treatments currently available. About 90% of cases show up with no family history at all.
“We are deeply grateful to the patients, caregivers, investigators, and clinical site teams whose participation and commitment continue to make the ALSTARS trial possible,” Grossman said. “We look forward to topline data and believe that, if positive, COYA 302 has the potential to significantly alter the course of this devastating disease and offer new hope to people living with ALS and their families.”
The same biology, tested a different way
A week earlier, Coya had put out a different kind of update, this one from the lab rather than the clinic. The company published preclinical results for a related combination, COYA 303, pairing that same low-dose IL-2 with a GLP-1 receptor agonist, the drug class behind Ozempic and Wegovy.
The study, run in mice engineered to show the kind of chronic, low-grade brain inflammation seen in neurodegenerative disease, found that each drug did something useful on its own: the GLP-1 compound calmed overactive inflammatory cells, while the low-dose IL-2 boosted Treg numbers and stability, but the combination did more than either managed alone.
In blood samples, it cut two well-known inflammatory markers while raising several tied to healthy Treg function. Inside the brain itself, in both the cortex and hippocampus, it lowered inflammatory markers while raising ones linked to a more protective, repair-oriented kind of immune cell.
“We are encouraged by these preclinical findings, which we believe demonstrate the therapeutic potential of immunomodulatory combinations for the treatment of serious neurodegenerative diseases characterized by sustained inflammation,” Grossman said of that study. “These results continue to reinforce our belief that complex neurodegenerative diseases like amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer’s disease (AD) are best addressed through a combination approach.”
The work was carried out by Dr Stanley Appel and Dr Aaron Thome at Houston Methodist Neurological Institute and published in the International Journal of Molecular Sciences.
Why the mouse data still matters
It’s worth being clear-eyed about what stage each piece of news actually represents. COYA 303 is mouse data, not human data, and Coya says as much itself: more work is needed before anyone can say how well it translates to actual patients. COYA 302, on the other hand, is already more than halfway enrolled in real people.
What connects them isn’t the drugs themselves, which pair low-dose IL-2 with two different second compounds, but the underlying bet Coya has built its entire pipeline around: that dysfunctional Tregs, and the unchecked inflammation that follows, sit underneath a whole cluster of neurodegenerative diseases rather than any one of them individually.
That’s a meaningfully different approach than developing a drug for a single disease and hoping it holds up. Immune dysregulation and chronic low-grade inflammation are among the more consistently cited hallmarks of an aging brain, and a therapy built around fixing that mechanism is the kind of platform bet longevity researchers have increasingly gravitated toward. Whether it actually works is still an open question on both fronts.
The ALSTARS trial is expected to finish enrolling within the coming weeks, with topline data due in early Q2 2027, which is when the more interesting question – whether any of this changes what happens to an actual ALS patient – finally starts getting an answer.
[1] https://ir.coyatherapeutics.com/news/news-details/2026/Coya-Therapeutics-Announces-Publication-of-Preclinical-Study-Demonstrating-Combination-Immunomodulatory-Effects-of-COYA-303-in-a-Well-Established-Model-of-Peripheral-and-CNS-Inflammation/default.aspx
[2] https://ir.coyatherapeutics.com/news/news-details/2026/Coya-Therapeutics-Announces-Enrollment-of-100th-Participant-in-Phase-23-ALSTARS-Trial-of-COYA-302-for-the-Treatment-of-ALS/default.aspx
