On-site photo from the MDS 2026 Congress

Organized by the International Parkinson and Movement Disorder Society, the MDS Congress is one of the largest and most influential international scientific meetings in the field. The selection of MT200605's Huntington's disease research for presentation signals recognition by the international scientific community of its clinical value in neurodegenerative diseases.

For Micot Pharma, the significance of this appearance extends beyond the poster presentation itself. It brings MT200605's progress in clinical development for stroke into an international forum for scientific exchange on movement disorders and neurodegenerative diseases. It also gives the market a more complete view of the development program: animal-model findings and Phase I data in healthy volunteers are available for the HD program, Phase II topline results are available for AIS, and the TrkB mechanism provides the central link between research in acute brain injury and chronic neurodegenerative diseases.

On-site photo from the MDS 2026 Congress

MT200605 Explores Disease-Modifying Potential in Huntington's Disease through Motor Improvement and Preservation of Brain Structure

Huntington's disease is an inherited, progressive neurodegenerative disorder. Patients gradually develop chorea, cognitive decline, and psychiatric and behavioral disturbances, eventually becoming fully dependent on care. Current treatments primarily manage symptoms; no treatment can yet halt or reverse disease progression. Protecting neurons and preserving neurological function are therefore important areas of research.

The publicly available MDS 2026 abstract reports that MT200605 improved motor coordination and attenuated whole-brain, cortical, and striatal atrophy in transgenic HD mice. The study also found that levels of the striatal neuronal marker DARPP-32 were maintained and that aggregation of mutant huntingtin protein (mHTT) in the cortex was reduced. In vitro experiments showed activation of TrkB and downstream AKT signaling, as well as enhanced mitochondrial adenosine triphosphate (ATP) production in HD cells.

The value of these findings lies in the converging evidence from behavioral, imaging, and cellular pathology measures. Beyond improved motor performance, changes in brain atrophy and aggregation of the disease-causing protein provide a more concrete basis for investigating a potential disease-modifying effect.

The poster also presented results from a Phase I clinical study of MT200605 in healthy adults. The study used a single-center, randomized, double-blind, placebo-controlled design and comprised single ascending dose (SAD) and multiple ascending dose (MAD) stages.

No serious adverse events, deaths, or withdrawals due to adverse events were reported. Drug-related adverse events were all mild and self-limiting. Pharmacokinetic results showed th