MT200605入选MDS 2026:全球首创TrkB激动剂亮相运动障碍国际学术年会
MICOT
点击蓝字 关注我们

Slide to view different languages
滑动查看不同语言
2026年10月4日至8日,国际帕金森与运动障碍学会(MDS)2026年国际大会将于韩国首尔举行,麦科奥特自主研发的全球首创MT200605在亨廷顿病研究成果已正式入选本届会议,并将以壁报(Poster)形式面向全球学界发布。
MDS国际大会由国际帕金森与运动障碍学会主办,涵盖帕金森病、亨廷顿病、肌张力障碍、共济失调等全部运动障碍疾病谱系,是全球该领域学术门槛最高的年度集会。

注:图片来源于大会官方海报,侵删
亨廷顿病:亟待疾病修饰疗法的罕见病
亨廷顿病被称为史上最残酷的遗传病,是一种常染色体显性遗传的神经退行性疾病,由HTT基因CAG重复扩增导致突变亨廷顿蛋白(mHTT)异常聚集,引发集运动障碍、认知衰退及精神异常症状于一体的“三重打击”疾病。患者发病后中位生存期约15-20年,美国约有4.1万名有症状患者,全球患者总数约40万人。目前尚无获批的疾病修饰疗法,现有治疗仅限症状管理。
MT200605: 双机制协同
作为全球首个进入临床阶段的TrkB受体激动剂及抗氧自由基药物,MT200605的作用机制区别于当前亨廷顿病管线中主流的亨廷顿蛋白(HTT)沉默或清除策略:
01
TrkB受体激动: 直接激活TrkB受体,重启脑源性神经营养因子(BDNF)下游信号通路,促进神经元存活、突触可塑性与线粒体ATP合成,直接对抗亨廷顿病中BDNF/TrkB通路功能下调导致的神经元退化。
02
抗氧化保护: 发挥抗氧化和清除氧自由基的作用,减少神经细胞死亡。
临床前研究显示,MT200605在亨廷顿病模型中通过激活TrkB信号、保护神经元健康、减少mHTT聚集,展现出神经保护效应;I期临床数据则证实了其在健康受试者中的安全性与可预测的PK特征。
临床推进:孤儿药认证,中美双报并行
MT200605已完成美国I期临床(亨廷顿病方向),安全性良好,PK特征支持后续开发。2026年3月,MT200605获FDA孤儿药资格认证,为后续临床开发、市场独占期及监管沟通提供政策支撑。
此外,该分子在缺血性脑卒中适应症的中国II期临床已于2026年3月完成全部360例受试者入组,形成多适应症并行的开发格局。
MICOT

The International Congress of Parkinson’s Disease and Movement Disorders® 2026, organized by the International Parkinson and Movement Disorder Society (MDS), will be held in Seoul, Korea. MT200605, a first-in-class candidate independently developed by Micot, has been officially accepted for presentation at this year’s Congress for its research findings in Huntington’s disease and will be presented to the global academic community as a poster presentation.
Organized by the International Parkinson and Movement Disorder Society, the MDS International Congress covers the full spectrum of movement disorders, including Parkinson’s disease, Huntington’s disease, dystonia, and ataxia. It is one of the world’s leading annual academic congresses in the field.

Note: Images are from the official poster of the conference. For infringement, please contact us for removal.
Huntington’s Disease: A Rare Neurodegenerative Disorder in Urgent Need of Disease-Modifying Therapies
Huntington’s disease is often regarded as one of the most devastating inherited disorders. It is an autosomal dominant neurodegenerative disease caused by CAG repeat expansion in the HTT gene, leading to abnormal aggregation of mutant huntingtin protein (mHTT). The disease imposes a “triple burden” of motor dysfunction, cognitive decline, and psychiatric manifestations.
After onset, median survival is approximately 15–20 years. In the United States, approximately 41,000 people have symptomatic Huntington’s disease, while the global patient population is estimated at around 400,000. To date, no disease-modifying therapy has been approved, and existing treatments remain limited to symptom management.
MT200605: Dual Mechanism Synergy
MT200605 is the world’s first clinical-stage TrkB receptor agonist with antioxidant/free radical-scavenging activity. Its mechanism of action differs from the mainstream huntingtin protein (HTT) silencing or clearance strategies currently pursued in Huntington’s disease pipelines, establishing a distinct and potentially complementary position in the disease’s therapeutic development landscape:
01
TrkB receptor agonism: MT200605 directly activates the TrkB receptor and reactivates downstream brain-derived neurotrophic factor (BDNF) signaling, promoting neuronal survival, synaptic plasticity, and mitochondrial ATP synthesis. This directly counteracts neuronal degeneration associated with functional downregulation of the BDNF/TrkB pathway in Huntington’s disease.
02
Antioxidant protection: MT200605 exerts antioxidant and free radical-scavenging effects, thereby reducing neuronal cell death.
Preclinical studies have shown that MT200605 delivers neuroprotective effects in Huntington’s disease models by activating TrkB signaling, preserving neuronal health, and reducing mHTT aggregation. Phase I clinical data have further confirmed its safety and predictable PK profile in healthy subjects.
Clinical Development: Orphan Drug Designation and Parallel Development in China and the United States
MT200605 has completed a Phase I clinical trial in the United States for Huntington’s disease, demonstrating a favorable safety profile and a PK profile supportive of further clinical development. In March 2026, MT200605 received Orphan Drug Designation from the U.S. Food and Drug Administration (FDA), providing policy support for subsequent clinical development, potential market exclusivity upon approval, and regulatory interactions.
In addition, for the ischemic stroke indication, the molecule completed enrollment of 360 subjects in a Phase II clinical trial in China in March 2026, establishing a parallel multi-indication development strategy.
MICOT

详情
奋斗为本、求是创新、协作共赢