Background
Adults over the age of 60 with symptoms of major depressive disorder are said to have late-life depression (LLD), a condition that usually decreases a person's quality of life and is associated with other risks like physical frailty and dementia. A common feature of more severe LLD is psychomotor slowing, where a person's ability to think and move are impaired. For example, they might not be able to walk or process information as quickly, and they might have problems with their working memory.
Psychomotor slowing in LLD might be the result of a problem with the way a person's body produces or responds to the neurotransmitter dopamine. The drug Levodopa (L-DOPA), which can replace missing dopamine in the brain, has been used to treat to treat Parkinson's disease for many decades, and it might also affect psychomotor slowing in LLD.
Methods
In this study, participants are adults aged 60 years or older with moderate to severe major depression. Participants undergo the "L-DOPA challenge"-a 2-week period where they receive a dose of L-DOPA once a day for the first week and a dose of L-DOPA twice a day for the second week. Before and after a participant completes the L-DOPA challenge, the study team assesses their depressive symptoms and psychomotor function. After the L-DOPA challenge, if a participant still shows signs of moderate or severe depression, they receive an antidepressant for 12 weeks.
Aims
The first aim of this study is to test the feasibility of the L-DOPA challenge-that is, whether most of the 50 participants recruited for this study will complete the L-DOPA challenge. For example, participants might have to withdraw if they can't make the daily visits to the research site to receive their L-DOPA medication, if they can't tolerate the medication's side effects, or if their depressive symptoms get significantly worse. Our hypothesis is that 80% of the participants will complete the L-DOPA challenge.
The second aim of the study is to see if L-DOPA affects participants' depressive symptoms, processing speed, and working memory. Our hypothesis is that L-DOPA response, measured as an improvement in gait speed, is associated with a decrease in depressive symptoms and an increase in processing speed and working memory.

开始日期2024-08-15

申办/合作机构

University of British Columbia

[+1]

NCT06365515

/ RecruitingN/AIIT

Dopamine and Reward Learning Across Hormonal Transition Phases

Hormonal transition periods during the menstrual cycle may predispose women to mental disorders. Hormonal fluctuations provide specific neuroendocrine conditions that modulate brain structure and function and these actions affect cognitive and emotional behaviors and affect energy and mood homeostasis. It is thought that these changes are driven by altered dopamine transmission. Here, the investigators aim to examine (1) how sex hormones and dopamine are linked and also (2) how hormonal changes affect motivation, mood, and energy homeostasis.
To this end, dopamine intervention will be tested on effort-based decision-making and motivational circuits in three hormonal stages (i.e., women in early-follicular phase (EF), women in mid-luteal phase (ML), and men). Additionally, the effects of hormonal status on metabolic indices will be tested, and its effects on mood fluctuations in a period of a month.
The investigator hypothesizes that women in EF cycle phase (1) have naturally less dopamine and show less effort, and (2) they show greater improvement in effort-based decision-making after Levodopa administration. The investigator has exploratory outcomes about (3) sex differences in reward-learning with and without Levodopa administration and explores if these differences correlate with elevated female sex hormone levels. Moreover, it is hypothesized that (4) hormonal fluctuations affect energy homeostasis, thus women in their EF cycle phase have higher energy expenditure and (5) they report more negative mood than in their mid-luteal (ML) cycle phase.

开始日期2024-05-01

申办/合作机构

Deutsche Forschungsgemeinschaft

[+1]

JPRN-UMIN000054201

/ RecruitingN/A

Low-dose L-DOPA treatment for drug-induced dystonia - Low-dose L-DOPA treatment for drug-induced dystonia

开始日期2024-04-18

申办/合作机构

Osaka Neurological Institute

100 项与左旋多巴相关的临床结果

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100 项与左旋多巴相关的转化医学

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100 项与左旋多巴相关的专利（医药）

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38,064

项与左旋多巴相关的文献（医药）

2025-06-01·EXPERIMENTAL NEUROLOGY

Activating Wnt1/β-Catenin signaling pathway to restore Otx2 expression in the dopaminergic neurons of ventral midbrain

Article

作者: Zheng, Canbing ; Lin, Xian ; Ye, Tonglin ; Duan, Jinhai ; Gong, Zhuo ; Cao, AnQi ; Liu, Hao ; He, Yongqian ; Shen, Danyang ; He, Shuaiying ; Cen, Qikai ; Li, Zhao ; Zhu, Shunyan

Parkinson's disease (PD) is the world's second most prevalent neurodegenerative disease. Currently, aside from levodopa, there are no other effective drugs clinically available to slow its progression. Otx2 plays a critical role in the differentiation of midbrain dopaminergic neurons (mDANs) during midbrain development. However, in adulthood, Otx2 is primarily expressed in the ventral tegmental area (VTA)-ventral part, and mDANs in the dorsal part of the VTA and the substantia nigra pars compacta (SNc) show no Otx2 expression. Research indicates that Otx2 is essential not only for the development of mDANs but also for their protection against the toxicity of MPTP and rotenone. Consequently, Otx2 is a potential clinical target for mDANs protection. Identifying the upstream mechanism that regulates Otx2 expression is crucial to restoring its expression in the SNc and enhancing its levels in the entire ventral midbrain mDANs. In this study, we have demonstrated the safety of Otx2 overexpression in vitro by using adeno-associate virus (AAV) and explored the feasibility of promoting Otx2 expression through the Wnt/β-Catenin signaling pathway using various drugs, a miR-34 mimic, and an inhibitor. Our results showed that Otx2 overexpression via AAV in the SNc is relatively safe, and CHIR99021 can induce Otx2 expression in mouse mDANs, thereby, alleviating PD-liked motor symptoms induced by MPTP. These findings suggest that modulating Otx2 expression through the Wnt/β-Catenin signaling pathway holds a therapeutic approach for Parkinson's disease.

2025-06-01·BIOMATERIALS

Gelatin-DOPA-knob/fibrinogen hydrogel inspired by fibrin polymerization and mussel adhesion for rapid and robust hemostatic sealing

Article

作者: Yu, Lisha ; Ding, Yuan ; Liu, Zhaodi ; Wang, Weilin ; Ding, Yihang ; Mao, Zhengwei

Tissue adhesives have attracted significant interest in the field of hemostasis. However, challenges including weak tissue adhesion, inadequate biocompatibility, and instability limit their clinical applications. Here, we have developed a gelatin-DOPA-knob/fibrinogen hydrogel inspired by the fibrin polymerization and mussel adhesion, resulting in a biocompatible bioadhesive with outstanding adhesion performance and great storage stability. This strategy involves modifying gelatin with knob peptides and catechol groups inducing crosslinking with fibrinogen to form a hydrogel via knob-hole interactions, and enhancing interfacial adhesion performance by interacting with the blood-covered tissue through catechol groups and knob peptides. This hydrogel exhibits rapid gelation, enhanced mechanical strength and adhesion properties, compared to the commonly used fibrin glue in surgery. The hydrogel significantly reduces the time required to hemostasis and the amount of blood loss in severe hemorrhage models. It ensures superior hemostatic efficacy, excellent biocompatibility, and long-term storage stability, which holds significant promise in medical settings.

2025-06-01·Neural Regeneration Research

Role of the globus pallidus in motor and non-motor symptoms of Parkinson’s disease

Article

作者: Zhu, Huixian ; Qi, Zengxin ; Chen, Liang ; Yuan, Wangrui ; Jiang, Yimiao ; Shen, Kangli ; Liu, Ruiqi ; Lou, Weiwei ; Fang, Chenxin ; Cao, Xin ; Jiang, Yifan ; Zhuang, Qianxing

The globus pallidus plays a pivotal role in the basal ganglia circuit. Parkinson’s disease is characterized by degeneration of dopamine-producing cells in the substantia nigra, which leads to dopamine deficiency in the brain that subsequently manifests as various motor and non-motor symptoms. This review aims to summarize the involvement of the globus pallidus in both motor and non-motor manifestations of Parkinson’s disease. The firing activities of parvalbumin neurons in the medial globus pallidus, including both the firing rate and pattern, exhibit strong correlations with the bradykinesia and rigidity associated with Parkinson’s disease. Increased beta oscillations, which are highly correlated with bradykinesia and rigidity, are regulated by the lateral globus pallidus. Furthermore, bradykinesia and rigidity are strongly linked to the loss of dopaminergic projections within the cortical-basal ganglia-thalamocortical loop. Resting tremors are attributed to the transmission of pathological signals from the basal ganglia through the motor cortex to the cerebellum-ventral intermediate nucleus circuit. The cortico–striato–pallidal loop is responsible for mediating pallidi-associated sleep disorders. Medication and deep brain stimulation are the primary therapeutic strategies addressing the globus pallidus in Parkinson’s disease. Medication is the primary treatment for motor symptoms in the early stages of Parkinson’s disease, while deep brain stimulation has been clinically proven to be effective in alleviating symptoms in patients with advanced Parkinson’s disease, particularly for the movement disorders caused by levodopa. Deep brain stimulation targeting the globus pallidus internus can improve motor function in patients with tremor-dominant and non-tremor-dominant Parkinson’s disease, while deep brain stimulation targeting the globus pallidus externus can alter the temporal pattern of neural activity throughout the basal ganglia–thalamus network. Therefore, the composition of the globus pallidus neurons, the neurotransmitters that act on them, their electrical activity, and the neural circuits they form can guide the search for new multi-target drugs to treat Parkinson’s disease in clinical practice. Examining the potential intra-nuclear and neural circuit mechanisms of deep brain stimulation associated with the globus pallidus can facilitate the management of both motor and non-motor symptoms while minimizing the side effects caused by deep brain stimulation.

645

项与左旋多巴相关的新闻（医药）

2025-03-26

·CPHI制药在线

重磅突破！人福医药多巴丝肼片获批上市，治疗帕金森病

关注并星标CPHI制药在线在医药创新的赛场上，每一次关键药品的获批都如同闪耀的里程碑，照亮患者康复的希望之路，也重塑着行业的竞争格局。近期，人福医药旗下控股子公司武汉人福药业成功研发的多巴丝肼片正式获得国家药监局《药品注册证书》，这一消息瞬间在医药圈引发震动，宛如一颗投入平静湖面的巨石，激起层层波澜。帕金森患者的漫长等待与曙光初现帕金森病，这一全球第二大神经退行性疾病，正无情地侵扰着无数患者的生活。在我国，已有超过300万的患者深受其苦，随着老龄化趋势的加剧，患病群体还在不断扩大。帕金森病的典型症状，如震颤、僵直和运动迟缓等，严重降低患者的生活质量，让他们在日常活动中困难重重。多巴丝肼是治疗帕金森病及症状性帕金森综合症的"黄金药物"，其巧妙地将左旋多巴与苄丝肼组合，能够有效缓解帕金森病的核心症状，为患者的生活带来极大改善。原研多巴丝肼由罗氏研发，最早于1973年在瑞士上市，1993年在国内获批。值得一提的是，多巴丝肼片在国内已完成原研地产化。国内多巴丝肼片市场长期被罗氏垄断，据米内网数据，2022年、2023年多巴丝肼片的销售额均在10亿元以上，其中公立医院终端（城市公立医院+县级公立医院）为销售主阵地，零售药店终端（城市实体药店+网上药店）以及公立基层医疗终端（城市社区中心+乡镇卫生院）的销售额也在1亿元以上。这一数据不仅反映出市场对巴丝肼片的巨大需求，也凸显了国产替代的迫切性。据不完全统计，此前国内浙江花园药业、浙江华海药业、北京福元医药、石家庄四药、重庆圣华曦药业已先后获得多巴丝肼片仿制药生产批件，其中浙江花园药业于2023年12月拿下了多巴丝肼片的国内首仿+首家过评。此外，除片剂外，多巴丝肼制剂还有胶囊剂型，其中多巴丝肼胶囊已有多家企业取得仿制药生产批件。不过多巴丝肼胶囊只占整个多巴丝肼市场份额的0.52%，罗氏的多巴丝肼片占据超99%市场份额。高效研发，实力铸就辉煌人福医药早在多年前就敏锐捕捉到帕金森病治疗领域的未被满足的临床需求，开启了对相关药物的探索。人福医药多巴丝肼片的研发过程面临着诸多挑战，如在药物合成工艺上，需要不断优化以提高纯度、稳定性和产量；在临床试验阶段，要严格按照规范招募合适的帕金森病患者作为受试者，密切监测药物的安全性和有效性数据，收集患者反馈。 2023年10月，人福医药多巴丝肼片的研发进入关键冲刺阶段，其上市许可申请获CDE受理。2025年3月，人福医药的多巴丝肼片获批。不足两年的获批速度与人福医药在研发上的持续投入和创新体系建设密不可分。其专业的研发团队，凭借着深厚的专业知识和丰富的经验，攻克了一个又一个技术难题。在研发过程中，严格遵循国际标准进行临床试验，确保药品的安全性和有效性。多巴丝肼片获批后将委托子公司宜昌人福生产。而宜昌人福在原料药和制剂生产方面拥有成熟的技术和丰富的经验，具备强大的产能。这将确保人福医药的多巴丝肼片能够快速实现规模化供应，及时满足市场需求，让患者能够尽快用上这款国产新药。机遇与挑战并存，理性看待发展据米内网数据，2024上半年在中国公立医疗机构终端，人福医药是神经系统药物（化+生）市场的TOP1集团（一级），其神经系统药物TOP20产品中有16个产品销售额有正增长，其中盐酸安非他酮缓释片、盐酸安非他酮缓释片(Ⅱ)、注射用磷丙泊酚二钠的增长率均达三位数，潜力惊人。多巴丝肼片的获批，有望成为其神经管线的新引擎，推动公司迈向新的高峰。不过，人福医药的多巴丝肼片也面临着诸多挑战，市场竞争加剧的风险不容忽视。随着国产多巴丝肼片的上市，其他国内药企也会跟进仿制。据不完全统计，国内超10家企业的多巴丝肼片已经申请上市。此外，政策的不确定性也是一大挑战。集采政策虽然能够让更多患者受益，但也可能会对药品的利润空间产生影响，如何在保证市场份额的同时维持合理的利润，是人福医药需要面对的问题。此外，公司的合规风险也需要投资者关注。2024年10月，人福医药曾因涉嫌信披违规被证监会立案调查，这一事件的后续进展将对公司的发展产生一定影响。投资者需要理性看待人福医药在多巴丝肼片上市后的发展，权衡其中的机遇与风险。总结人福医药此次多巴丝肼片的获批，不仅是技术实力的有力证明，更是国产药企突围的生动缩影。对于帕金森患者而言，更实惠、更优质的用药选择即将成为现实；对于投资者来说，在看到巨大机遇的同时，也需谨慎评估风险。未来，人福医药的多巴丝肼片在市场上究竟会有怎样的表现？让我们共同拭目以待，期待它在帕金森治疗领域书写新的辉煌篇章，为更多患者带来健康与希望。 END 2025金笔奖征文活动开启，来投稿吧！领取CPHI & PMEC China 2025展会门票智药研习社直播预告来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com ▼更多制药资讯，请关注CPHI制药在线▼ 点击阅读原文，进入智药研习社~

上市批准

2025-03-18

·neurolixis.com

18 March 2025 - Neurolixis Publishes Positive Phase 2A Trial Results for NLX-112 in Parkinson’s Disease

Neurolixis today announced the publication of the results from its successful Phase 2A proof-of-concept clinical trial of NLX-112 (befiradol) in Parkinson’s disease. The findings, published in the prestigious journal 𝘔𝘰𝘷𝘦𝘮𝘦𝘯𝘵 𝘋𝘪𝘴𝘰𝘳𝘥𝘦𝘳𝘴, highlight NLX-112’s potential as a first-in-class, non-dopaminergic therapy with dual efficacy in addressing both levodopa-induced dyskinesia (LID) and motor impairment in Parkinson’s patients. The randomized, double-blind, placebo-controlled trial, supported by The Michael J. Fox Foundation and Parkinson’s UK, evaluated NLX-112 in patients with troubling LID. The study successfully met its primary endpoint of safety and tolerability, as well as its secondary endpoint of significantly reducing LID. Notably, NLX-112 also demonstrated anti-parkinsonian effects, significantly improving motor function in study participants. See the full publication (Open Access): 𝗡𝗟𝗫-𝟭𝟭𝟮 𝗿𝗮𝗻𝗱𝗼𝗺𝗶𝘇𝗲𝗱 𝗣𝗵𝟮𝗔 𝘁𝗿𝗶𝗮𝗹: 𝘀𝗮𝗳𝗲𝘁𝘆, 𝘁𝗼𝗹𝗲𝗿𝗮𝗯𝗶𝗹𝗶𝘁𝘆, 𝗮𝗻𝘁𝗶-𝗱𝘆𝘀𝗸𝗶𝗻𝗲𝘁𝗶𝗰 𝗮𝗻𝗱 𝗮𝗻𝘁𝗶-𝗽𝗮𝗿𝗸𝗶𝗻𝘀𝗼𝗻𝗶𝗮𝗻 𝗲𝗳𝗳𝗶𝗰𝗮𝗰𝘆. 𝘔𝘰𝘷𝘦𝘮𝘦𝘯𝘵 𝘋𝘪𝘴𝘰𝘳𝘥𝘦𝘳𝘴, 2025 (https://doi.org/10.1002/mds.30175) 𝗔 𝗡𝗼𝘃𝗲𝗹 𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺 𝗼𝗳 𝗔𝗰𝘁𝗶𝗼𝗻: Unlike current Parkinson’s treatments that target the dopamine system, NLX-112 acts on the serotonin (5-HT) system, as a highly selective full activator of 5-HT1A receptors. This unique mechanism differentiates NLX-112 from previous serotonergic drugs and is believed to underlie its dual efficacy in reducing dyskinesia and improving motor function. The promising results from this Phase 2A trial support further development of NLX-112 as a transformative therapy for movement disorders. Neurolixis is actively planning next steps in the clinical development program to advance NLX-112 toward potential regulatory approval. 𝗔𝗯𝗼𝘂𝘁 𝗣𝗮𝗿𝗸𝗶𝗻𝘀𝗼𝗻’𝘀 𝗗𝗶𝘀𝗲𝗮𝘀𝗲 𝗮𝗻𝗱 𝗥𝗲𝗹𝗮𝘁𝗲𝗱 𝗠𝗼𝘃𝗲𝗺𝗲𝗻𝘁 𝗗𝗶𝘀𝗼𝗿𝗱𝗲𝗿𝘀: Parkinson’s disease is the second most common neurodegenerative disorder, affecting over 10 million people worldwide. Levodopa, the mainstay treatment for Parkinson’s, often leads to debilitating dyskinesias (involuntary movements) after prolonged use. Up to 80% of patients develop LID within ten years of levodopa therapy. Current treatments for LID, such as amantadine, are limited by side effects and variable efficacy, underscoring the need for new therapeutic options. As well as Parkinson’s disease, other disorders also involve dysfunction in the basal ganglia, a brain region critical for coordinating movement. Such disorders include spinocerebellar ataxia, Huntington’s disease, essential tremor and dystonia, and lead symptoms such as tremors, rigidity, and impaired motor control.

临床2期临床结果

2025-03-09

·医学新视点

每日口服一次！新药显著改善帕金森病患者运动障碍

▎药明康德内容团队编辑 Celon Pharma公司近日宣布，其PDE10A抑制剂CPL’36的2期临床试验取得积极结果。该药为一种每日一次的创新口服药物，用于治疗帕金森病患者中左旋多巴诱导的运动障碍（LID）。该研究达到了主要终点及多个次要终点，CPL’36在所有衡量帕金森病LID治疗改善的量表上均显示出强力且一致的疗效，效果具有临床意义。该2期临床试验为一项多国、多中心、随机、安慰剂对照试验，在105例伴有LID的帕金森病成年患者中进行。CPL’36以20 mg或40 mg两种剂量每日一次口服给药，并按照1：1：1的比例设置安慰剂对照，治疗期为4周。患者病情基线严重程度为中重度至重度，他们的统一运动障碍评分量表（UDysRS）评分约为45分。在第4周，与安慰剂组相比，20 mg剂量组UDysRS总分改善12.30分（p<0.001），而40 mg剂量组改善13.58分（p<0.001）。CPL’36治疗还与大多数次要终点的改善相关，包括UDysRS客观子量表，在CPL’36组中自治疗第7天起均显示出统计学显著性。该药物耐受性良好，绝大多数严重不良事件发生在安慰剂组（安慰剂组8.8%，20 mg组0%，40 mg组5.7%）。因治疗相关的突发不良事件而导致停药的比例分别为安慰剂组2.9%、20 mg组11.1%和40 mg组8.6%。CPL’36组中最常见的不良事件为嗜睡，程度为轻至中度。试验中未报告死亡事件，在40 mg组报告了一例中度房颤的严重不良事件。推荐阅读《自然-医学》：针对帕金森病“病根”，新药有效延缓甚至逆转运动功能下降《自然-医学》：帕金森病症状改善50%，新一代“大脑起搏器”更精准帕金森病如何治疗更有效？《柳叶刀》：这5类非口服疗法值得关注！《柳叶刀》子刊25年追踪研究：中年肥胖和“三高”，痴呆风险升高？参考资料： [1] Strong Proof-of-Concept Data from Phase 2 Trial of PDE10A Inhibitor (CPL’36), a Novel Once-Daily Treatment of Levodopa-Induced Dyskinesia in Parkinson’s Disease. Retrieved March 5, 2025, from https://www.globenewswire.com/news-release/2025/03/04/3036951/0/en/Strong-Proof-of-Concept-Data-from-Phase-2-Trial-of-PDE10A-Inhibitor-CPL-36-a-Novel-Once-Daily-Treatment-of-Levodopa-Induced-Dyskinesia-in-Parkinson-s-Disease.html 免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：本文来自药明康德内容团队，欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「药明康德」微信公众号回复“转载”，获取转载须知。分享，点赞，在看，传递医学新知

临床结果临床研究

100 项与左旋多巴相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D00059	左旋多巴	N04BA01	DB01235

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
帕金森病	美国	Hoffmann-La Roche, Inc.	1970-06-04
帕金森病	美国	Shire Development LLC	1970-06-04

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
运动失调	临床3期	美国	AbbVie, Inc.	2009-06-01
运动失调	临床3期	德国	AbbVie, Inc.	2009-06-01
运动失调	临床3期	新西兰	AbbVie, Inc.	2009-06-01
哮喘	临床1期	美国	Acorda Therapeutics, Inc.	2015-12-01
吸烟	临床1期	美国	Acorda Therapeutics, Inc.	2015-12-01

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


EAN2024	N/A	帕金森病	-	Inhaled levodopa	窪鹹鬱襯遞壓淵憲憲網(窪鏇淵蓋壓網醖壓築構) = reported by 12 (66.7%) patients 顧顧構壓鹽製顧淵範網 (襯獵觸選鑰鬱蓋選繭範 ) 更多	-	2024-06-28
S2.007 (AAN2024)	N/A	激活PI3K-δ综合征	-	Carbidopa-levodopa enteral suspension (CLES)	壓鏇襯淵餘衊衊糧鹽餘(廠淵膚範鬱簾膚鏇願鹽) = 齋廠夢鑰積築糧餘獵顧鹹鏇願艱衊淵築壓網膚 (願遞淵願網夢夢鏇糧鏇 )	不佳	2024-04-09
				Surgical Device-aided Therapies (DATs) (Deep brain stimulation (DBS))	壓鏇襯淵餘衊衊糧鹽餘(廠淵膚範鬱簾膚鏇願鹽) = 醖蓋膚糧簾蓋獵壓觸餘鹹鏇願艱衊淵築壓網膚 (願遞淵願網夢夢鏇糧鏇 )
MDS2023	N/A	-	110	LD/DCI	襯壓鏇夢鹽網衊夢窪餘(蓋窪觸構廠選獵網齋窪) = 蓋膚鹹憲選夢淵艱顧醖願積醖積膚築餘網範製 (夢範範齋築選膚鬱構簾 ) 更多	积极	2023-08-27
				LD/DCI+COMT-I	襯壓鏇夢鹽網衊夢窪餘(蓋窪觸構廠選獵網齋窪) = 願選淵遞遞範壓範醖鬱願積醖積膚築餘網範製 (夢範範齋築選膚鬱構簾 ) 更多
PD MED early disease randomisation (MDS2023)	N/A	帕金森病	1,593	Levodopa-sparing therapy (dopamine agonist or monoamine oxidase B inhibitor)	願選獵蓋觸構窪範窪鏇(鑰餘繭壓簾範簾製獵廠): P-Value = 0.84 更多	积极	2023-08-27
				Levodopa alone
INVEST study (MDS2023)	N/A	帕金森病	-	Continuous intrajejunal levodopa infusion (CILI)	構獵選壓積選範製構襯(夢簾範構鏇簾艱衊觸壓) = 餘築鑰膚簾顧選鏇壓鑰鹹壓襯網壓顧積積構製 (蓋築鏇鬱觸鏇鏇遞鑰蓋, -2.9 ~ 11.0)	-	2023-08-27
Parkinson’s Progression Markers Initiative (PPMI) (MDS2023)	N/A	帕金森病	428	levodopa	鑰壓積鹽艱窪餘顧遞網(蓋鏇艱窪廠選簾醖鬱鹽) = 網壓範鑰觸餘願鑰憲夢餘觸艱壓製廠鏇鏇衊獵 (齋製淵顧選糧糧構選網 )	-	2023-08-27
				levodopa	鑰壓積鹽艱窪餘顧遞網(蓋鏇艱窪廠選簾醖鬱鹽) = 範淵壓餘醖遞鏇遞製衊餘觸艱壓製廠鏇鏇衊獵 (齋製淵顧選糧糧構選網 )
MDS2023	N/A	肌张力障碍	-	Pre-levodopa administration	艱網觸繭觸糧繭網築選(膚淵齋構鹽願製願觸鹹) = 繭夢築膚遞鏇鑰構鏇構鏇積顧衊築淵鬱膚襯鏇 (餘顧餘壓鬱襯鏇製製廠 )	-	2023-08-27
				Post-levodopa administration	艱網觸繭觸糧繭網築選(膚淵齋構鹽願製願觸鹹) = 觸艱築觸積鬱糧蓋膚蓋鏇積顧衊築淵鬱膚襯鏇 (餘顧餘壓鬱襯鏇製製廠 )
MDS2023	N/A	帕金森病	3	Levodopa intake	窪願鹹襯遞網鹽願網製(襯鏇顧憲衊齋醖廠蓋艱) = 積製製網夢醖鏇選願糧鬱艱膚壓鏇遞觸積繭醖 (衊鹽鹽網鹽鬱膚築窪製, 57.2)	积极	2023-08-27
MDS2023	N/A	帕金森病	-	Levodopa/Benserazide	衊艱蓋醖壓艱淵鑰憲壓(膚範顧築獵遞範鬱壓簾) = 蓋鹽廠積顧網遞糧糧繭窪築餘選膚範鹽膚鬱選 (憲鏇蓋夢製繭膚齋憲壓 )	不佳	2023-08-27
				Placebo	衊艱蓋醖壓艱淵鑰憲壓(膚範顧築獵遞範鬱壓簾) = 網淵齋夢願淵觸鹹窪遞窪築餘選膚範鹽膚鬱選 (憲鏇蓋夢製繭膚齋憲壓 )