SELtx™ is designed to flip the body back into a healing state. In ALS-model mice, the difference in motor function was visible — and it tracked the immune shift we're targeting in humans.
We compared motor function in SOD1-mutant ALS mice treated with SELtx™ against untreated controls. The treated mice kept running; the untreated mice could not. The improvement matched a measured M1-to-M2 phenotype switch.
Mice love treadmills — which made them a clear way to see whether motor function held up under ALS.
Mice carrying the mutated SOD1 gene lose motor control as the disease progresses and can't stay on the treadmill.
The same SOD1-mutant mice, treated with SELtx™, kept running — holding the function the disease normally takes.
The motor results correlated with an M1-to-M2 immune shift — the exact mechanism the platform is built to trigger.
Where untreated mice declined, treated mice held their motor function across the study. For a disease defined by losing movement, holding onto it is the outcome that matters most.
Illustrative of observed trends; treated mice maintained motor function while controls declined.
The immune shift was confirmed with established markers — TNF-α, CD206, and NOS1 — not assumed from behavior alone.
These results drive our path toward first-in-human trials — and beyond ALS.
See the roadmap