A Phase 1, Randomized, Double-blind, Placebo-controlled, Single and Multiple Ascending Dose Study to Investigate the Safety, Tolerability, and Pharmacokinetics of SNP318 in Healthy Adult Participants

SNP318 is developed to treat neurodegenerative diseases including Alzheimer's disease. In the current phase 1 study, the IP is tested in healthy volunteers, and the purpose is to investigate the safety, tolerability, and PK of single and multiple ascending oral doses of SNP318.

开始日期2023-03-20

申办/合作机构

赛神（上海）医药科技有限公司

NCT05638815 / CompletedN/A

An Observational Study to Explore the Role of Alpha-Synuclein-related Biomarkers in the Diagnosis and Disease Evaluation of Parkinson's Disease and Other Synucleinopathies

The study is a multi-center, observational study to evaluate the feasibility of α-synuclein-related biomarkers and imaging data in the disease diagnosis and prognosis evaluation in Synucleinopathies and healthy subjects.

开始日期2021-11-23

申办/合作机构

赛神（上海）医药科技有限公司

100 项与赛神（上海）医药科技有限公司相关的临床结果

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0 项与赛神（上海）医药科技有限公司相关的专利（医药）

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项与赛神（上海）医药科技有限公司相关的文献（医药）

2024-03-01·Molecular Psychiatry

ABCA7 deficiency causes neuronal dysregulation by altering mitochondrial lipid metabolism

Article

作者: Li, Zonghua ; Roy, Bhaskar ; Holm, Marie-Louise ; Jiang, Peizhou ; Parsons, Tammee M ; Lu, Wenyan ; Zhao, Jing ; Bu, Guojun ; Baker, Samantha K ; Kanekiyo, Takahisa ; Martens, Yuka A ; Wang, Ni ; Han, Xianlin ; Jiang, Yangying ; Ren, Yingxue ; Starling, Skylar C ; Bao, Hanmei ; Perkerson, Ralph B ; Kawatani, Keiji

AbstractABCA7 loss-of-function variants are associated with increased risk of Alzheimer’s disease (AD). Using ABCA7 knockout human iPSC models generated with CRISPR/Cas9, we investigated the impacts of ABCA7 deficiency on neuronal metabolism and function. Lipidomics revealed that mitochondria-related phospholipids, such as phosphatidylglycerol and cardiolipin were reduced in the ABCA7-deficient iPSC-derived cortical organoids. Consistently, ABCA7 deficiency-induced alterations of mitochondrial morphology accompanied by reduced ATP synthase activity and exacerbated oxidative damage in the organoids. Furthermore, ABCA7-deficient iPSC-derived neurons showed compromised mitochondrial respiration and excess ROS generation, as well as enlarged mitochondrial morphology compared to the isogenic controls. ABCA7 deficiency also decreased spontaneous synaptic firing and network formation in iPSC-derived neurons, in which the effects were rescued by supplementation with phosphatidylglycerol or NAD+ precursor, nicotinamide mononucleotide. Importantly, effects of ABCA7 deficiency on mitochondria morphology and synapses were recapitulated in synaptosomes isolated from the brain of neuron-specific Abca7 knockout mice. Together, our results provide evidence that ABCA7 loss-of-function contributes to AD risk by modulating mitochondria lipid metabolism.

2023-12-01·Alzheimer's & Dementia

Regulation of meningeal lymphatic function by APOE

作者: Martens, Yuka A ; Fryer, John D. ; Mesquita, Sandro Gabriel (Sandro Da Mesquita) Ferreira Da ; DELIVANOGLOU, NIKOLETA ; Todd, Kennedi ; Barber, Megan J ; Schrader, Racquelle ; Sanchez, Guadalupe ; Bu, Guojun ; Neves, Sofia Pereira ; Rego, Shanon

AbstractBackgroundThe meningeal layers form a unique interface between the central nervous and peripheral immune systems. The lymphatic vasculature that is present in the meningeal dura and drains cerebrospinal fluid (CSF) becomes dysregulated during aging and in models of neurodegenerative disorders such as Alzheimer’s disease (AD). Apolipoprotein E (APOE), and the isoform APOE4 in particular, increases the risk for late‐onset sporadic AD. However, it is still poorly understood whether changes in meningeal lymphatic morphology and drainage are mediating the deleterious effects of APOE4 expression. In the present study, we investigate the effects of human APOE3 or APOE4 on meningeal lymphatic function and immunity.MethodWe evaluated the morphology of lymphatic vessels in dural whole mounts of age‐matched wild type, Apoe‐KO, APOE3, and APOE4 mice at 2‐3, and 11‐12 months. This assessment was performed in both male and female mice. The drainage function of meningeal lymphatics is being assessed in the same mice by in vivo imaging of CSF‐derived fluorescent tracers into the deep cervical lymph nodes. We have also performed RNAscope and protein measurements using murine meningeal tissue to investigate the main cellular source(s) of Apoe, and single‐cell RNA sequencing to explore the cell‐specific transcriptomic signatures linked to the changes in meningeal lymphatic function.ResultLymphatic vessel length is increased in 11‐12‐month‐old APOE4 male mice, when compared to their APOE3 counterparts. Interestingly, the same was not detected in female mice. Dural myeloid cells, expressing Itgam (encoding for CD11b), are the main source of Apoe mRNA transcripts, and one of the main sources of apoE protein in the brain dura mater. APOE4 expression and age markedly alter the transcriptional profile of meningeal myeloid cells, which show overexpression of lysosomal, antigen presentation, and complement genes.ConclusionAPOE4 expression leads to a sex‐dependent meningeal lymphatic vascular remodeling, which is associated with an exacerbated activation of meningeal macrophages. In future studies, we will test whether the changes in meningeal lymphatics observed in mice expressing APOE4 are mediated by myeloid cell derived APOE.

2023-08-01·Trends in Molecular Medicine

Pushing the boundaries of brain organoids to study Alzheimer’s disease

Review

作者: Shi, Yanhong ; Bu, Guojun ; Cerneckis, Jonas

Progression of Alzheimer's disease (AD) entails deterioration or aberrant function of multiple brain cell types, eventually leading to neurodegeneration and cognitive decline. Defining how complex cell-cell interactions become dysregulated in AD requires novel human cell-based in vitro platforms that could recapitulate the intricate cytoarchitecture and cell diversity of the human brain. Brain organoids (BOs) are 3D self-organizing tissues that partially resemble the human brain architecture and can recapitulate AD-relevant pathology. In this review, we highlight the versatile applications of different types of BOs to model AD pathogenesis, including amyloid-β and tau aggregation, neuroinflammation, myelin breakdown, vascular dysfunction, and other phenotypes, as well as to accelerate therapeutic development for AD.

项与赛神（上海）医药科技有限公司相关的新闻（医药）

2024-04-12

·GBIHealth

帕金森：新疗法已在路上

帕金森病（Parkinson's disease，简称PD）帕金森病是仅次于阿尔茨海默病（AD）的第二大神经退行性疾病，于1817年由James Parkinson医生最早描述其症状，并以他的名字命名。作为常见的中老年神经系统退行性疾病，临床表现为震颤、肌强直、姿势平衡障碍等运动症状和睡眠障碍、自主神经功能障碍、认知和精神障碍等非运动症状，中晚期阶段常伴有运动并发症，严重影响患者的生活质量。变，万物随阳气上升而萌芽生长。 “ 据统计，全球范围内约有1000多万名患者饱受帕金森病的困扰。而我国的帕金森病患者人数预计将从2005年的199万人上升到2030年的近500万人，几乎占到全球帕金森病患病人数的一半。”发病机制帕金森的主要病理变化发生在中脑黑质腹侧的致密部，该区含有大量多巴胺神经元，患者致密部神经元大量死亡，有的甚至丧失高达70%的神经元，导致多巴胺的缺乏以及动作、边缘系统等神经回路的故障。二十世纪60年代研究发现，多巴胺前体化合物左旋多巴对帕金森症有治疗效果，直到今天仍是治疗帕金森的主力药物。然而，多巴胺制剂只能缓解帕金森症状，治标不治本，且副作用较大。后续研究发现，大脑黑质的病变与α-突触核蛋白有关，这种蛋白异常积聚，形成纤维蛋白沉淀并最终导致神经细胞死亡。α-突触核蛋白是可溶性蛋白，导致其异常聚集通常伴随着免疫激活、神经炎症、线粒体功能障碍以及溶酶体和内体功能的改变。研究者发现，这些病理过程与基因密切相关。比如，具有PRKN基因突变和主要线粒体功能障碍的患者表现出一种受限的细胞丧失模式，主要局限在黑质纹状体系统中，没有典型散发性帕金森病中所见的广泛病理和非运动特征。相反，具有SNCA或GBA突变，且α-突触核蛋白病理明显的患者在早期表现出非运动特征，包括自主神经功能障碍和痴呆，可能反映了全身和大脑中的广泛病理。这些风险基因不一定与α-突触核蛋白的病理直接相关。目前已经确定七个基因作为单基因病因，其中四个导致晚发性、常染色体显性遗传疾病（即LRRK2、CHCHD2、VPS35和SNCA），三个导致早发性、常染色体隐性遗传疾病（即PARKIN、DJ1和PINK1）。第八个基因GBA的变异是帕金森病的最常见遗传风险因素。未来有望开发出针对专门靶点的治疗药物。主要治疗思路流程除多巴胺制剂之外，儿茶酚-氧位-甲基转移酶抑制剂以及单胺氧化酶B型抑制剂也是帕金森的常用药物。根据《2020年中国帕金森病治疗指南》，对早发型、晚发型帕金森病，根据主要症状的不同选择不同的治疗方案（图1）。图1.患者用药选择流程图参考来源：《2020年中国帕金森病治疗指南》；DAs：多巴胺受体激动剂；MAO-BI：单胺氧化酶B型抑制剂；COMTI：儿茶酚-O-甲级转移酶抑制剂2020年指南继续强调了多学科治疗： ①坚持综合治疗，应对帕金森病的运动症状和非运动症状采取全面综合治疗；②强调多学科治疗模式，药物治疗仍为首选，并结合手术、运动与康复、心理干预等多种治疗手段；同时，提倡在临床条件允许的情况下，组建神经内科、功能神经外科、神经心理、康复乃至社区全科医生等多学科的医生团队；③明确全程管理，目前的治疗仍以改善症状为主，不能阻止病情的发展，治疗不仅立足当前，而且需长期管理，以达到长期获益。常见药物与在研新药根据传统治疗分类和在中国获批的药品，帕金森治疗药物主要有以下几种。复方左旋多巴：恩他卡朋双多巴、多巴丝肼多巴胺受体激动剂（DAs）：溴隐亭、培高利特（已撤市）、吡贝地尔、甲磺酸-a-二氢麦角隐亭、普拉克索、罗匹尼罗和罗替高汀儿茶酚-O-甲级转移酶抑制剂（COMTI）：托卡朋和恩他卡朋单胺氧化酶B型抑制剂（MAO-BI）：雷沙吉兰和司来吉兰抗胆碱药：苯甲托品、苯海索以及苯海拉明去甲肾上腺素前体：屈昔多巴神经保护剂：单唾液酸四己糖神经节苷脂钠此外，还有左旋多巴和卡比多巴，其中卡比多巴需与左旋多巴联用。帕金森领域进展较慢，从2010年至今，美国FDA批准的能用于缓解帕金森症状的新分子实体仅4款：Acadia Pharma 的5-羟色胺2A受体反向激动剂酒石酸匹莫范色林、US WorldMeds的沙非酰胺、协和发酵麒麟的A2A受体拮抗剂伊曲茶碱以及第三代强效COMTI奥匹卡朋。奥匹卡朋已有复星医药引进中国，目前正在进行临床试验。在国内进行开发的帕金森药品见下表。来源：GBI SOURCE新兴技术干细胞衍生药物治疗帕金森成为一条新的探索帕金森治疗的路径。继拜耳BlueRock之后，睿健医药成为国际第二家、国内首家提交帕金森领域多能干细胞衍生药物临床申请的公司。2022年4月28日，国家药监局受理了睿健医药自主研发的帕金森管线人源多巴胺能前体细胞注射液NouvNeu001的IND申请。临床前数据显示，通过睿健医药自研的高效化学小分子诱导功能细胞再生技术，NouvNeu001 移植入体内后可高效转化为成熟多巴胺能神经元，分泌多巴胺递质，并与体内原有神经元形成神经连接，产生综合性的治疗功能，改善帕金森症状。这类前体细胞除了能够分泌多巴胺这类递质之外，还可进一步分泌多种蛋白及小核酸来改善帕金森病灶，为移植到脑部的细胞发挥作用提供良好的“土壤”环境。企业交易活动国内对帕金森病的研究对比国际略显落后，因此一些企业开始引进海外的产品和技术。2018年1月，万邦生化（母公司复星医药）与葡萄牙公司BIAL达成合作，在中国大陆独家销售代理其帕金森病治疗药物奥吡卡朋；2020年10月，日本药企Kissei Pharmaceutical宣布已与中国生物医药公司AffaMed Therapeutics就其帕金森在研新药KDT-3594达成许可协议，Affamed Therapeutics将获得在大中华区（包括中国大陆、香港、澳门和台湾地区）和东南亚六国（包括新加坡，马来西亚，泰国，印尼，越南和菲律宾）开发和商业化KDT-3594（DAs）的独家权利;2021年4月，赛神医药与礼来达合作，获得在大中华区开发和商业化针对帕金森病α-突触核蛋白靶向疗法的权利；2022年3月，上海中泽医药与美国公司 Digestome Therapeutics达成合作，获得后者DGX-001在大中华市场的独家权利。DGX-001是一种全球首创口服治疗药物，可用于治疗精神分裂症的阴性症状和认知障碍，以及帕金森病的非运动症状；2022年3月，翼思生物与德国史达德大药厂（STADA Arzneimittel AG）子公司Brtiannia Pharmaceuticals Ltd签署了一项许可协议，获得在中国大陆、香港和澳门开发和商业其皮下注射阿扑吗啡用于帕金森病的独家权利；2023年5月，畅溪制药与美国公司Acorda Therapeutics达成合作，引进后者INBRIJA（左旋多巴吸入粉雾剂）在大中华地区（中国大陆及港澳台地区）的权利。INBRIJA已在美国和欧盟获批上市，用于正在接受左旋多巴-多巴脱羧酶抑制剂治疗的成年帕金森病患者，其在关闭期（OFF episodes）的间歇性治疗；2024年1月，斯坦福大学与先声药业达成合作研究协议，将共同推动一项神经系统领域的探索性研究，为帕金森患者研发创新疗法。帕金森发现至今，目前虽有多种可以缓解症状的疗法，但还没有一种能够延缓疾病进展或治愈疾病。未来，开发这一疾病更理想的治疗方法依然是医学领域的重要目标之一。\ | /★联系我们投稿 | 发稿 | 媒体合作▶ sylvia.hua@generalbiologic.com数据库 | 咨询服务 | 资讯追踪▶ 点击左下“阅读原文”完成表单填写点击阅读原文立即订阅相关报告

核酸药物

2023-11-30

·PRNewswire

SciNeuro completes dosing in its Phase 1 clinical trial of SNP318, an oral therapeutic for Alzheimer's disease and other neurodegenerative diseases

SNP318, a novel, small molecule, orally administered, brain penetrant lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor, was well-tolerated in the Phase 1 study. Inhibition of Lp-PLA2 improves integrity of blood-brain barrier (BBB), that has previously resulted in clinical benefit in Alzheimer's disease (AD)1. SNP318 Phase 2 study is planned for 2024. ROCKVILLE, Md., Nov. 30, 2023 /PRNewswire/ -- SciNeuro Pharmaceuticals, a clinical stage biotech company focused on developing treatments for neurodegenerative diseases, particularly Alzheimer's Disease (AD) and Parkinson's Disease (PD), today announced the completion of dosing in its Phase 1, randomized, double-blind, placebo-controlled, single and multiple ascending dose study. The trial was designed to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of the company's lead clinical asset, SNP318, in healthy participants. Administration of SNP318 was well-tolerated with a favorable exposure, strong target engagement, and excellent safety profile. Additionally, the CNS penetrance and food effects were investigated separately. These results support further development with once daily dosing. A Phase 2 study to assess clinical benefits of SNP318 in stratified AD patients is planned for 2024 as the next step to continue its global development. "We are delighted to see the scheduled conclusion and informative outcomes of a well planned and executed SNP318 Phase 1 study, thanks to the SciNeuro clinical and translation teams," said Min Li, Ph.D., founder and CEO of SciNeuro Pharmaceuticals. "These results represent a significant step forward in our efforts to further clinical development of SNP318. Our very special gratitude also extends to all the trial participants and dedicated clinical team in Australia. We look forward to continuing our work by addressing neurovascular deficits common among AD to improve the patients' lives affected by these devastating conditions." Topline Phase 1 study data summary SNP318 was safe and well-tolerated with no serious adverse events (SAEs) observed. Pharmacokinetics and pharmacodynamics data revealed excellent oral exposure supporting for once-daily dosing. SNP318 has outstanding distribution in the cerebrospinal fluid (CSF) to achieve complete target inhibition in a clinical setting for both peripheral and CNS tissues. AD and Vascular Pathology More than 80% AD patients exhibit vascular pathology, a key driver of cognitive decline. While etiology is heterogenous, vascular lesion alone suffices to cause dementia commonly known as vascular dementia. Vascular dementia and AD have considerable overlap. Studying Late-Onset Alzheimer's Disease (LOAD) by following both patients and healthy subjects indicated intra-brain vascular dysfunction is an early and predominant disease development event preceding or independent of amyloid pathology. About Lp-PLA2 Lp-PLA2 is a phospholipase secreted primarily by inflammatory cells, including peripheral and CNS cells. Lp-PLA2 hydrolyzes oxidized phospholipids, producing lysophosphatidylcholine (LysoPC) and other potent proinflammatory factors. LysoPC is a key mediator of inflammatory stress on brain microvascular endothelial cells resulting in vascular pathology including vessel leakage and other BBB damage. About SNP318 SNP318 is a potent Lp-PLA2 inhibitor that dampens vascular inflammation, a common pathological feature of multiple neurodegenerative diseases. SNP318 is the only CNS-penetrant Lp-PLA2 inhibitor in clinical development that has been specifically optimized for the treatment of CNS disorders. Therefore, SNP318, independent from anti-amyloid strategy, has the potential to become a new AD therapy. About SciNeuro Pharmaceuticals SciNeuro Pharmaceuticals is a clinical-stage biotechnology company focused on developing groundbreaking therapies for neurodegenerative diseases. Since its founding in 2020, SciNeuro has built a portfolio of pipeline programs staged from discovery to clinical development by addressing three key disease-driving mechanisms of neurodegeneration – neurovascular inflammation, proteinopathy, and immune response. The company aims to develop disease-modifying treatment options for Alzheimer's disease, Parkinson's disease, and other devastating CNS diseases. For more information, please visit . Reference: Maher-Edwards G, De'Ath J, Barnett C, Lavrov A, Lockhart A. A 24-week study to evaluate the effect of rilapladib on cognition and cerebrospinal fluid biomarkers of Alzheimer's disease. Alzheimers Dement (N Y). 2015 Jun 30;1(2):131-140. doi: 10.1016/j.trci.2015.06.003. PMID: 29854933; PMCID: PMC5975052. SciNeuro Media Contact Jessie Yang [email protected] SOURCE SciNeuro Pharmaceuticals

临床1期临床2期

2023-08-11

·药智网

屡获全球突破！国内帕金森新药在研进展如何？

“无法治愈，不可逆转”，帕金森病虽然发现至今已有200余年，但目前依然是一种无法治愈的“绝症”。据调查显示，当前全球有1%-2%的65岁以上人群患有帕金森病，我国65岁以上人群的帕金森病患病率为1.7%，当前我国大约有帕金森患者300万人，但随着我国老龄化逐渐加剧，预计2030年我国帕金森患者将达到490万人。由于我国老龄化日趋严重，我国对于治疗帕金森药物的研发已经刻不容缓。幸运的是，近期国内药企在帕金森领域接连取得突破。01全球首款创新微球制剂，上市申请获受理近日，绿叶制药宣布其在研药物注射用罗替高汀缓释微球（LY03003）上市申请已被中国药监局受理，并纳入优先审评。注射用罗替高汀缓释微球（LY03003）适应症为帕金森病，LY03003是当前范围内全球首个用于治疗帕金森病的长效缓释微球制剂，该药物每周仅注射一次即可，是全球首个可以一周内持续产生多巴胺能刺激的药物。LY03003肌肉注射后显示出了显著的缓释制剂特性，7天内可持续并稳定的释放药物。此外，由于该药物浓度变化范围较小，所以产生的不良反应也相应减弱，一定程度上提高了患者的依从性。LY03003的上市申请基于其临床1期与临床3期试验结果，结果显示，LY03003是一种安全、有效的治疗帕金森的药物，能全面、持续的改善帕金森患病人群的症状，从而提高病人的生活质量。除LY03003的上市申请已被中国药监局受理外，近年来也有多款治疗帕金森的1类新药获批上市，下表1为笔者通过药智数据所整理的近10年获批用于治疗帕金森的1类新药信息。除LY03003外，国内帕金森领域接连取得突破。沙芬酰胺国内第一款即将获批的治疗帕金森的进口1类新药即沙芬酰胺，沙芬酰胺已于2022年04月27日在国内进行了NDA申请，预计今年即可获批上市。沙芬酰胺是一种针对MAOB的选择性抑制剂，其临床研究发现，沙芬酰胺可使“开启”期明显延长，而“关闭”期明显缩短。该药物曾被誉为是美国治疗帕金森病的重要里程碑，该药若能成功在我国获批上市，对于我国的帕金森患者也是意义重大。表1 近10年全球获批的帕金森1类新药数据来源：药智数据奥匹卡朋国内第二款即将获批的治疗帕金森的进口1类新药即奥匹卡朋，奥匹卡朋的NDA申请已于2021年03月10日获受理，但据药智数据显示，该药物至今还未获批。奥匹卡朋由Bial制药所研发，后授权给日本小野制药开发，用于治疗帕金森症，该药物于2016年在德国获批，2020年在美国获批。根据新闻稿报道，奥匹卡朋是第一种也是唯一一种获批的每日一次COMT抑制剂，可以有效减少帕金森患者的“关闭”时间，增加帕金森患者的“开启”时间，并且不会出现运动障碍。02全球首个，帕金森患者或迎来治愈曙光？近日，国家药监局正式批准了睿健医药帕金森新药NouvNeu001的IND申请，这是当前全球首个用于治疗帕金森病进入临床阶段的基于化学诱导的通用型细胞治疗产品。其实自90年代以来，国际上就一直在研究帕金森患者是否可以使用细胞替代疗法进行治疗，但进展一直比较缓慢。FDA于2021年1月才批准了第一个IND药物，即BlueRock的ESCs衍生药物MSK-DA01，该药物已于2023年6月28日完成临床1期试验，并取得了良好的临床效果。如今我国在帕金森领域也有了自己的药物进入了IND阶段，并且从已完成的药理药效试验和安全性试验结果来看，NouvNeu001的起效速度优于MSK-DA01。使用NouvNeu001治疗4周后，行为学功能即可得到了极大恢复，同时多项生理生化指标也得到了显著提升，而MSK-DA01需要在给药十二周后才可起效。细胞疗法近年来频频在各大疾病领域取得重大突破，如今在这种前沿的治疗技术加持下，帕金森这一疾病已经具有了可逆转的可能，或许多年以后帕金森完全治愈也将不再是幻想。除近期NouvNeu001获批临床外，国内其余帕金森新药研发状况如何？下表2为笔者通过药智数据所查询到的当前处于临床阶段的用于治疗帕金森病的1类新药。从中可以看出，目前获批临床的新药多以化药为主，生物制品仅有两款，除前文提到的NouvNeu001外，还有一款就是赛神（上海）医药的SNP201注射液，该药物也是近期刚获批临床。表2 国内临床阶段治疗帕金森的1类新药数据来源：药智数据SNP201注射液为一款α-突触核蛋白抑制剂，而α-突触核蛋白在神经元突触活性及胞内转运过程中发挥重要作用，与帕金森疾病密切相关的Lewis小体就是由α-突触核蛋白纤维化聚集而成的。对病人而言，减少α-突触核蛋白有望延缓或阻止帕金森的发病情况。03国内患帕金森人群持续增长，药物市场不断扩容据《中国帕金森病疾病负担变化趋势分析及预测》数据显示，2019年全世界的帕金森病患者已达到850万人左右，其中我国占据约284万人，占比33.37%，据世界首位。并且随着人口老龄化进程的加快，预计到2030年，我国帕金森病患者人数将达490万，占全球帕金森病患者总数的一半左右，这将对中国经济和医疗卫生体系带来沉重的负担。据头豹统计，我国2015年帕金森病药物市场规模为15.6亿元，2019年市场规模增长至27.1亿元，年复合增长率达到了14.9%。由于未来帕金森患者数量将会不断增多，这将带动药物治疗的需求，帕金森药物市场将持续扩容。此外，根据Global Health Data统计，当前全球患有帕金森病的人群已突破一千万，而2020年全球的帕金森用药市场规模也达到了45.64亿美元，预计2026年市场规模可达59.34亿美元，年均复合增长率为4.68%。由此可见，无论是国内还是全球范围内，帕金森药物市场都具有一定规模。尤其是国内，老龄化持续加重，帕金森药物年复合增长率近15%，都预示着国内帕金森药物市场将快速的扩增。04小结帕金森病是仅次于阿尔茨海默病的第二大神经退行性疾病，并且随着老龄化的加剧，帕金森的患病率也在随之增高，并且当前不可治愈。而细胞疗法的出现让人眼前一亮，似乎帕金森病也出现了被逆转的可能。也期待未来出现新的治疗手段，为帕金森患者带来新的曙光。参考文献[1]https://www.luye.cn/lvye/view.php?id=1659[2]https://mp.weixin.qq.com/s/jrt5SSBmx6LrrSgMTSNzFQ[3]https://mp.weixin.qq.com/s/20W10-OI2fZbaVGfEPubKw[4]《中国帕金森病疾病负担变化趋势分析及预测》.[5]http://www.neurocrine.com/assets/Neurocrine-Biosciences-Announces-FDA-Approval-of-Once-Daily-ONGENTYS%C2%AE-opicapone-as-an-Add-On-Treatment-for-Patients-with-Parkinson%E2%80%99s-Disease-Experiencing-%E2%80%9COff%E2%80%9D-Episodes-.pdf声明：本内容为作者独立观点，不代表药智网立场。如需转载，请务必注明文章作者和来源。对本文有异议或投诉，请联系maxuelian@yaozh.com。责任编辑 | 八角转载开白 | 马老师 18996384680（同微信）商务合作 | 张武龙 13368443108（同微信）阅读原文，是受欢迎的文章哦

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药物(靶点)	适应症	全球最高研发状态

GSK-2647544 ( Lp-PLA2 )	阿尔茨海默症更多	临床1期
SNP-318 ( Lp-PLA2 )	阿尔茨海默症更多	临床1期
SNP-201 ( α-synuclein )	帕金森病更多	临床申请批准
SNP-210 ( TDP43 )	肌萎缩侧索硬化更多	临床前
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