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Hong Kong, Oct 12, 2026 - (ACN Newswire) - The International Congress of Parkinson's Disease and Movement Disorders (MDS 2026) was held in Seoul, South Korea, from October 4 to 8, 2026. Micot Pharma (2335.HK) presented, for the first time in an electronic poster, nonclinical findings in Huntington's disease (HD) and Phase I clinical results in healthy volunteers for its independently developed drug candidate MT200605. Together with previously announced positive Phase II data in acute ischemic stroke (AIS), these findings are beginning to establish a development path for this small-molecule tropomyosin receptor kinase B (TrkB) agonist from acute brain injury to neurodegenerative diseases.On-site photo from the MDS 2026 CongressOrganized 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 CongressMT200605 Explores Disease-Modifying Potential in Huntington's Disease through Motor Improvement and Preservation of Brain StructureHuntington'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 that drug exposure increased with dose, with no appreciable accumulation after multiple doses and an overall predictable pharmacokinetic profile. These results provide a safety and pharmacokinetic foundation for subsequent clinical studies in patient populations.TrkB Signaling Provides a Basis for Extending Development from Acute Brain Injury to Neurodegenerative DiseasesA defining feature of MT200605's mechanism is its pharmacological modulation of the brain-derived neurotrophic factor (BDNF)/TrkB neurotrophic signaling pathway. This pathway contributes to neuronal survival, synaptic maintenance, and mitochondrial stability, providing an important biological basis for neuroprotection and the preservation of function.MT200605's pharmacological design reportedly combines agonism of the BDNF/TrkB pathway with attenuation of oxidative stress and relief of microcirculatory impairment caused by calcium ion-induced contraction of vascular smooth muscle. The development rationale is to explore more comprehensive neuroprotection by intervening in multiple components of the injury process.From a mechanistic perspective, targeting TrkB provides a rationale for extending MT200605's development into chronic neurodegenerative diseases. Although the pathogenic processes of stroke and Huntington's disease differ substantially, neuronal injury, loss of function, and insufficient neurotrophic support offer points of entry for research across diseases. The findings across multiple measures in the HD model provide new experimental support for this direction.Positive Phase II Stroke Results Show a Significant Reduction in Disability and Potential for Renal ProtectionMT200605 has completed a Phase II clinical trial in acute ischemic stroke. The multicenter, randomized, double-blind, placebo-controlled study enrolled 360 participants. The primary efficacy endpoint was the proportion of patients achieving a modified Rankin Scale (mRS) score of 0-1 at 90 days after stroke onset.Results disclosed by the company show that the proportions of patients achieving favorable functional outcomes in both the medium- and high-dose groups were higher than in the placebo group, demonstrating a treatment advantage rarely seen among drugs in this class. For the high-dose group, achieving an mRS score of 0-1 corresponded to an increase of more than 100% in the odds of functional recovery versus placebo, as reflected by the odds ratio (OR). In terms of clinical benefit, approximately one additional patient moved from "requiring assistance" to "being able to live largely independently" for every six patients treated. Over decades of neuroprotective drug development, agents demonstrating such a marked difference in functional outcomes versus placebo in a randomized controlled trial have been exceptionally rare. The difference between the high-dose group and placebo was statistically significant, and the study showed a clear dose-response relationship. The study also observed a trend toward early neurological recovery in the high-dose group, with no serious adverse events related to the investigational drug.For stroke-associated acute kidney injury (AKI), the study also observed a trend toward a dose-dependent reduction in incidence, providing exploratory clinical evidence for further research into the mechanism of "dual brain and kidney protection." The design rationale for this dual protection was validated in the Phase II trial: MT200605 significantly reduced disability and showed the potential to lower AKI incidence in patients with AIS in a dose-dependent manner. AKI incidence in the high-dose group was more than 80% lower than in the placebo group. This result addresses the existing therapeutic gap in preventing AKI in patients with AIS.Neurological Recovery and Combined Brain and Kidney Protection Offer the Potential to Fill a Therapeutic GapCurrently, no neuroprotective drug for AIS has a Class I recommendation supported by Level A evidence in Chinese clinical guidelines. Most marketed agents have Class II recommendations supported by Level B evidence.Mainstream neuroprotective drugs in China include butylphthalide, edaravone, and edaravone dexborneol. Their mechanisms are generally limited to blocking injury through one or two targets, without a mechanistic design that simultaneously promotes neural repair, and none has demonstrated a statistically significant difference in long-term functional outcomes such as those measured by the mRS.Butylphthalide has a research foundation in neuroprotection involving multiple targets. The randomized BAST trial enrolled 1,216 patients with acute ischemic stroke who received intravenous thrombolysis and/or endovascular treatment. Favorable functional outcomes at 90 days were achieved by 56.7% of patients in the butylphthalide group and 44.0% in the placebo group. The endpoint used different mRS thresholds according to baseline stroke severity, providing evidence for combining neuroprotection with reperfusion treatment.Edaravone's principal pharmacological action is free radical scavenging, while edaravone dexborneol extends antioxidant and anti-inflammatory intervention through a combination formulation. In the Phase III TASTE study involving 1,165 patients, the proportions achieving an mRS score of ≤1 at 90 days were 67.18% in the edaravone dexborneol group and 58.97% in the edaravone group. Edaravone dexborneol was superior to edaravone, with a statistically significant difference.The research indicates that MT200605's differentiation should not be reduced to a simple numerical comparison of efficacy with existing agents. The more relevant question to follow is whether the TrkB neurotrophic pathway can translate the functional outcome signals observed in patients with AIS into clinical benefits in chronic neurodegenerative diseases. As a first-in-class (FIC) investigational drug, MT200605 has completed clinical proof of concept. Its effect size far exceeds that of other neuroprotective agents, and it has the potential to become the first treatment in this field to receive high-level recommendations as a first-line option in both Chinese and international clinical guidelines.Another "silent killer" can emerge following stroke: acute kidney injury (AKI).Approximately 19% of patients with AIS develop AKI, and the risk of in-hospital death among patients with AKI is around two to three times that of patients without AKI. Product labeling for approved mainstream neuroprotective drugs advises caution or contraindicates use in patients with impaired renal function or severe renal failure. As a result, precisely those stroke patients facing a higher risk of death are excluded from treatment.A further reason to follow MT200605 is that, alongside the positive signals for 90-day functional outcomes in the AIS Phase II trial, the company has disclosed a new area of investigation: renal protection after stroke. According to Micot Pharma's announcement, AKI incidence in the high-dose group was approximately 80% lower than with placebo in the Phase II data. This means that MT200605 is currently the world's only investigational neuroprotective drug with the potential to specifically prevent and treat post-stroke AKI, and the only agent in this class that could potentially be approved and used with a "renal protection" claim in its labeling.MT200605's ability to protect both the brain and kidneys is closely linked to its distinctive mechanism of action.TrkB receptors are expressed not only in brain tissue but also in renal podocytes, renal tubular epithelial cells, and the juxtaglomerular apparatus. Their activation can stabilize the podocyte cytoskeleton, inhibit renal tubular epithelial cell apoptosis by counteracting endoplasmic reticulum stress through PI3K/AKT signaling, and activate antioxidant defenses through the nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), an important target of neuroprotective drugs.A single molecule protects two organs affected by stroke. The protective pathways in the brain and kidneys share the core PI3K/AKT signaling cascade, disrupting at its origin the vicious cycle of brain injury leading to AKI, worsening renal function, and further aggravation of brain injury.The MDS presentation and AIS Phase II topline results are therefore complementary. The former expands MT200605's international scientific visibility and the scope of its HD research, while the latter provides a translational foundation in patient functional outcomes. For a biopharmaceutical company focused on innovative medicines, a development program built around one mechanism, multiple disease settings, and progressively accumulating evidence at different levels often has greater scope for expansion than an early-stage narrative centered on a single indication.ConclusionIn the near term, MDS 2026 has given Micot Pharma an international platform to present its research in movement disorders. Over the medium to long term, the program's value as a platform will depend on whether the company can continue to use verifiable clinical data to translate the potential of the TrkB mechanism across different disease settings into benefits for patients. For the capital markets, this is the central rationale for continuing to follow MT200605's development.


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