Coya's ALS Drug Hits 100 Trial Enrollees While New Mouse Data Backs the Same Immune Mechanism

ALS remains one of the most devastating neurodegenerative diseases, killing 20–30% of patients within two years of diagnosis and offering few effective treatments. Coya Therapeutics is betting that the key to changing that trajectory lies in the immune system — specifically in regulatory T cells, or Tregs, which normally keep damaging brain inflammation in check but fail to do so in ALS patients.

The company's Phase 2/3 ALSTARS trial just passed a meaningful benchmark: 100 patients enrolled out of a planned 120. The trial tests COYA 302, a combination of low-dose interleukin-2 (IL-2), which amplifies Treg activity, and CTLA-4 Ig, which suppresses overactive inflammatory immune cells. Participants are randomized into three groups for 24 blinded weeks, with the primary endpoint being change on the ALSFRS-R — a functional scale tracking walking, speaking, swallowing, and breathing. Topline results are projected for early Q2 2027, and the drug already holds FDA Fast Track designation.

A week before that enrollment announcement, Coya published preclinical findings for COYA 303, a related but distinct combination pairing the same low-dose IL-2 with a GLP-1 receptor agonist — the same drug class as Ozempic. In mice engineered to exhibit chronic low-grade neuroinflammation, each agent had modest standalone effects, but the combination reduced two established inflammatory blood markers while raising several Treg-associated markers. Inside brain tissue — both cortex and hippocampus — the combination produced measurable anti-inflammatory changes beyond what either drug achieved alone.

The convergence of clinic and lab data around a single mechanism is notable. Both programs point to immune dysregulation, particularly Treg dysfunction, as a driver of neurodegeneration — a framework increasingly supported across ALS and other brain diseases.

Caveats remain significant. The COYA 303 findings are from mice, not humans, and mouse models of neuroinflammation have a mixed track record in predicting clinical success. The ALSTARS trial is still enrolling, and efficacy data will not arrive until 2027. Until then, these findings are promising signals rather than confirmed breakthroughs.