An Open-Label, Randomized Controlled Trial of Pramipexole Versus Escitalopram to Treat Major Depressive Disorder (MDD) and Comorbid MDD With Mild Neurocognitive Disorder (MND) in Persons With HIV

A phase II, randomized, open-label, two-arm clinical trial evaluating the safety and efficacy of pramipexole extended release (ER) versus escitalopram for the treatment of major depressive disorder (MDD) and comorbid MDD with mild neurocognitive disorder (MND) in persons with HIV (PWH). Participants will be assessed comprehensively and briefly at intercurrent visits to monitor for toxicity, response to therapy, and to assess for dose changes.
An optional sub-study to evaluate treatment impact on the cerebrospinal fluid (CSF) profile will be conducted in a subset of 36 participants.

开始日期2025-10-31

申办/合作机构

National Institute of Allergy & Infectious Diseases

[+1]

NCT07022405

/ Not yet recruiting临床2期IIT

Stratified Pharmacological Approaches for Regulating Circuit-Level Effects Study

This research study aims to understand how people with depression respond to the medication pramipexole and to determine whether clinical response differs depending on the function of specific circuits in the brain. The investigators hope to learn which circuits are involved in depression and how these circuits interact with pramipexole to affect mood, behavior, and cognition.
Eligible participants will undergo an 8-week treatment course of pramipexole followed by a 2-week down taper and follow up. The ultimate goal is to offer people experiencing depression a medication that is alternative to ones that may not have worked in the past and to apply the knowledge the investigators gain from investigating the brain circuits involved in depression to help personalize treatment.
The investigators invite anyone who has recently experienced symptoms of depression to participate. A prior diagnosis of depression is not required.

开始日期2025-08-01

申办/合作机构

Stanford University

[+1]

CTR20251664

/ Active, not recruiting临床1期

PKA透皮贴剂单次给药药代动力学对比研究

①评估广东红珊瑚药业有限公司提供的受试制剂PKA透皮贴剂单次给药1/2贴（规格：15.3mg/16.6cm2）和Boehringer Ingelheim International GmbH持证生产的对照制剂盐酸普拉克索缓释片多次给药（规格：0.375 mg；商品名：森福罗®/Sifrol®）的安全性及药代动力学特征。 ②评估PKA透皮贴剂与盐酸普拉克索缓释片的相对生物利用度。 ③评估PKA透皮贴剂的皮肤刺激性和黏附性。

开始日期2025-05-22

申办/合作机构

广东红珊瑚药业有限公司

100 项与盐酸普拉克索相关的临床结果

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100 项与盐酸普拉克索相关的转化医学

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100 项与盐酸普拉克索相关的专利（医药）

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1,989

项与盐酸普拉克索相关的文献（医药）

2026-01-01·EXPERIMENTAL NEUROLOGY

Pramipexole improves cognitive deficits and synaptic plasticity impairments in 3xTg-AD mice through enhancing autophagy

Article

作者: Cui, Chenglong ; Han, Feifei ; Tuo, Chunmei ; Sui, Xiaofan ; Jiao, Juanjuan ; Wu, Meina ; Cai, Hongyan

Autophagy dysfunction plays important roles in the pathogenesis of Alzheimer's disease (AD), and activation of autophagy might be a potential strategy in AD treatment. Although some autophagy inducers play beneficial roles in AD, no autophagy inducer has been available in AD clinical treatment due to lack of efficacy or obvious side effects. A recent study demonstrated that pramipexole (PPX) can activate autophagy in the brain without interfering with protein synthesis, thereby avoiding the side effects associated with prolonged use of an autophagy inducer. However, whether PPX can exert neuroprotective effects on AD and whether its potential mechanism is related to autophagy remains unclear. In the present study, the effects of PPX on the cognitive function of 3xTg-AD mice were observed using multiple behavioral tests, then synaptic plasticity was evaluated through in vivo hippocampal electrophysiological recordings and by measuring synaptic proteins, while Aβ and tau pathologies were detected using immunofluorescence staining and western blot. Finally, autophagy was detected and the potential target was predicted using bioinformatics analysis, qRT-PCR and molecular docking. Results demonstrated that PPX significantly improved cognitive deficits and hippocampal long-term potentiation (LTP) depression, increased the expression of PSD95, reduced Aβ deposition and tau hyperphosphorylation, activated autophagy by increasing LC3-II/LC3-I ratios and decreasing p62 levels, and restored Beclin1 expression. Bioinformatics analysis identified MAPK1 as a key target in PPX-ameliorated AD by enhancing autophagy. These findings suggest that PPX alleviates AD-related cognitive deficits and neuropathologies through increased autophagy, emphasising its potential as a disease-modifying therapeutic strategy for AD.

2026-01-01·JOURNAL OF AFFECTIVE DISORDERS

Efficacy and tolerability of pramipexole versus antidepressants for Parkinson's disease with depression: a meta-analysis of randomized controlled trials

Review

作者: Wei, Xue ; Gong, Siyin ; Browning, Michael ; Zhang, Yuqing ; Zhang, Xiong ; Xu, Fenghua ; Li, Jinfang ; Tang, Han

BACKGROUND:

Pramipexole is thought to exert antidepressant effects in patients with Parkinson's disease (PD) and depression, but its efficacy compared with typical antidepressants is unclear. This meta-analysis aims to directly compare the safety and efficacy of pramipexole and antidepressants for depression in PD patients.

METHODS:

Twelve electronic databases including Cochrane, PubMed, Embase, Web of Science, CINAHL, PsycINFO, ProQuest, Open Grey, CBM, The CNKI, Wan Fang Data and VIP, and two clinical trial registry websites were systematically searched up to December 30, 2024. The primary outcomes were severity of depression (change in depression rating scale) and tolerability (discontinuation for any reason at the end of treatment). Secondary outcomes included changes in motor symptoms and adverse effects. This study was registered in PROSPERO (reference number: CRD42024525826).

RESULTS:

A total of 12 randomized controlled trials involving 772 participants were included. There was no significant difference in the efficacy between pramipexole and antidepressants in the treatment of PD patients with depression (SMD -0.14,95 % CI -0.48 ∼ -0.21, P = 0.45) and they did not differ significantly in terms of tolerability (OR 0.78, 95 % CI 0.36-1.71, P = 0.54, I² = 26 %). Pramipexole significantly improved motor symptoms better (SMD -0.44, 95 % CI -0.82 ∼ -0.05, P = 0.03) and decreased the incidence of anorexia (P = 0.05), but had a similar risk of other adverse effects as antidepressants.

CONCLUSION:

Pramipexole has an antidepressant effect similar to typical antidepressants while improving motor symptoms in PD patients. Both of them are well tolerated, and may be associated with some common adverse effects, such as anorexia, nausea, and vomiting.

2025-12-01·JOURNAL OF AFFECTIVE DISORDERS

Cost-effectiveness of pramipexole in addition to mood stabilisers for patients with treatment-resistant bipolar depression: Economic evaluation of the PAX-BD randomised controlled trial

Article

作者: Helter, Timea ; Berger, Michael ; Geddes, John ; Hindmarch, Paul ; Fouweather, Tony ; Azim, Lumbini ; Simon, Judit ; Young, Allan H ; Courtney, Paul ; Morriss, Richard ; Stokes, Paul R A ; Weetman, Christopher ; Watson, Stuart ; Chadwick, Thomas ; McAllister-Williams, R Hamish

BACKGROUND:

People with bipolar disorders (BD) frequently experience depressive symptoms that do not respond to available treatment options. The resulting burden for people with BD and society is substantial. This study sought to explore the cost-effectiveness of pramipexole in combination with mood stabilisers for people with treatment-resistant bipolar disorder (TRBD).

METHODS:

We calculated mean incremental cost-effectiveness ratios (ICER) of pramipexole compared to placebo over 12 and 48 weeks from health and social care (NHS + PSS) and societal perspectives for 36 participants with TRBD. Quality-adjusted life years (QALY) were captured with the EQ-5D-5L as the primary outcome measure. We used capability well-being measures (ICECAP-A, OxCAP-MH) to assess the robustness of the results and multiple imputation and bootstrapping to address missing data and small sample size.

RESULTS:

We found that pramipexole is dominantly more effective and cost-saving from the NHS + PSS perspective with 86 % probability of being cost-effective at £30,000/QALY gained over 12 weeks and 93 % over 48 weeks. From the societal perspective, pramipexole was more effective but also more expensive with lower probability of cost-effectiveness (36 % over 12 weeks and 48 % over 48 weeks). Uncertainty around the mean ICERs was substantial due to the small sample size.

LIMITATIONS:

The PAX-BD trial was conducted during the COVID-19 pandemic and terminated early, resulting in a limited generalizability of resource use outside the pandemic context and a small sample size.

CONCLUSIONS:

Pramipexole is a cost-effective treatment option for TRBD from the NHS + PSS perspective, with statistically significant increases in health-related quality of life and capability well-being over extended periods.

118

项与盐酸普拉克索相关的新闻（医药）

2025-10-23

·三优生物医药

三优十周年｜神经系统疾病治疗进展

作者：金汉卿美工：何国红罗真真排版：马超 01 引言延长预期寿命可谓人类公共卫生领域最伟大的成就之一。然而，寿命的增长也伴随与年龄相关的神经系统疾病 (Neurological disorders) 负担不断攀升。神经系统疾病是指发生于中枢或周围神经系统、以感觉、意识、运动等功能受损为主要表现的一类疾病，整体呈现低病死率、高致残率的特点。就在2025年10月14日，世界卫生组织发布了新的《全球神经病学状况报告》1，报告显示神经系统疾病目前影响着全球40%以上的人口——超过30亿人，造成4.35亿伤残调整生命年 (DALY) ，使其成为全球疾病与残疾的主要原因。37种神经系统疾病共导致1180万人死亡、1.62亿年残疾生活年与2.72亿年寿命损失。本文聚焦若干神经系统疾病的治疗前沿，旨在为行业专业人士提供可操作的靶点开发参考。 ▲ 图1：影响神经系统疾病的全球负担2 02 阿尔兹海默病阿尔茨海默病 (Alzheimer’s disease, AD) 是一种以进行性认知障碍为核心表现的中枢神经系统退行性疾病。其病理特征包括淀粉样β (Aβ) 斑块沉积与Tau蛋白异常磷酸化/神经原纤维缠结，并常伴随神经炎症与突触功能障碍。近年，基于脑脊液/影像的病理分层逐步延伸至血液标志物 (如血浆p tau217) ，为早期识别与入组提供更可及的工具。 ▲ 图2：阿尔茨海默病的病理机制3 目前的治疗以对症药物 (胆碱酯酶抑制剂与NMDA受体拮抗剂) 和在早期人群中使用的疾病修饰疗法为主。抗Aβ单抗方面，lecanemab (Leqembi) 已在2023年获FDA批准，而donanemab (Kisunla) 也于2024年获FDA批准用于早期症状性AD (MCI/轻度痴呆) 并按月静脉给药。临床实践通常需要影像/体液证据确认Aβ阳性，并在治疗过程中进行MRI监测以管理ARIA。 • 药物前沿进展聚焦三条主线：抗Aβ策略升级：已上市抗体在早期人群显示减缓进展的临床获益。为实现更高的皮层暴露，罗氏开发Brainshuttle技术，通过偶联可结合转铁蛋白受体 (TfR) 的模块，显著提高穿透BBB能力与脑内分布。抗Tau与联合方案：多款抗Tau通路药物推进中。尽管单药结果不积极，但与Aβ清除形成序贯/联合方案，有望影响下游神经退行改变。炎症抑制与精准分层：围绕神经炎症的多靶点布局逐步成形。例如选择性中和可溶性TNF的XPro™/XPro1595：II期MINDFuL总体未达主要终点，但在炎症生物标志物富集的早期AD亚组出现认知、行为与生物学端点的获益信号，且安全性良好，提示“炎症表型分层”的精准用药方向。 ▲ 图3：阿尔茨海默病的在研药物靶点汇总 03 帕金森病帕金森病 (Parkinson’s disease, PD) 是一种影响中枢神经系统、以运动系统受累为主的慢性神经退行性疾病，症状通常缓慢进展。静止性震颤、肌强直、运动迟缓与步态异常常见于早期，也可伴随认知与行为改变。病理学上，以黑质多巴胺能神经元丢失及细胞内α‑突触核蛋白聚集为特征；早期退变多局限于腹外侧黑质，随病程推进而扩展。路易体主要由聚集的α‑突触核蛋白组成，病变通常自脑干胆碱能/单胺能神经元与嗅觉系统起始，随后累及边缘系统和新皮质。 ▲ 图4：帕金森病的病理机制4 现行治疗方面，左旋多巴及多巴胺替代治疗仍为金标准。早期可用左旋多巴单药，或联合多巴胺激动剂 (如罗匹尼罗、普拉克索、罗替戈汀) 及MAO‑B抑制剂 (如司来吉兰、雷沙吉兰) 。与早期左旋多巴单药相比，早期启用多巴胺激动剂对长期残疾与生活质量并无显著优势。对出现“开-关”波动者，常通过缩短左旋多巴给药间隔，联合COMT抑制剂 (恩他卡朋、阿匹卡朋) 和/或MAO-B抑制剂 (司来吉兰、雷沙吉兰、沙芬酰胺、唑尼沙胺) ，并调增多巴胺激动剂；若出现异动症，可加用金刚烷胺；部分合适人群可考虑设备辅助治疗以缩短“关”期并改善运动障碍。 • 药物/技术前沿主要包括：靶向α‑突触核蛋白的被动免疫：临床前可改善病理与行为。两项大型早期PD试验 (SPARK/cinpanemab与PASADENA/prasinezumab) 虽未达主要终点，PASADENA显示运动进展减缓趋势。基于2b期PADOVA及其OLE与PASADENA长随，罗氏已推进prasinezumab进入III期。 LRRK2降解/抑制策略：LRRK2为公认关键靶点。2025年10月8日，Arvinas公布ARV‑102 (LRRK2降解剂) I期积极数据，显示良好的脑脊液暴露与显著的靶蛋白下调 (外周>90%，脑脊液>50%) ，并伴随pRab10与尿BMP等下游生物标志物降低。基因治疗：AAV2‑GAD向丘脑底核递送在晚期PD中证实安全并带来治疗侧改善；AAV2‑AADC在壳核过表达可增强左旋多巴转化，6个月UPDRS (用药/停药) 约三成改善且用药剂量下降，但4年随访提示临床收益逐步回归基线，提示需进一步优化递送与联合策略。 ▲ 图5：帕金森病的在研药物靶点汇总 04 中风中风 (Stroke，脑卒中) 包括缺血性与出血性两大类，其中以缺血性为主。其发病机制中，缺血造成的级联反应涉及多种中枢神经系统细胞：在缺血核心，神经元发生形态改变，细胞体与轴突消失；小胶质细胞、星形胶质细胞亦随之发生反应性改变。缺血后BBB通透性增加，多种免疫细胞 (白细胞、单核细胞、巨噬细胞) 浸润病灶区，释放神经毒性或神经营养因子，对受损脑组织产生既可能保护亦可能有害的影响。 ▲ 图6：脑卒中的病理机制5 现行治疗策略强调“急性再灌注+二级预防”两端发力。针对急性期，发病4.5小时内静脉溶栓仍为基础。除阿替普酶外，多项指南与综述支持替奈普酶 (TNK) 0.25 mg/kg在部分场景作为替代选择；对大血管闭塞患者，借助灌注成像选择性入组，机械取栓时间窗可拓至6–24小时。针对二级预防，小卒中/高危TIA人群的短期双联抗血小板 (阿司匹林+氯吡格雷) 获益主要集中在起始后21天内；合并房颤者以口服抗凝 (优选DOACs) 为一线，无法长期抗凝者可考虑左心耳封堵 (LAAO) 作为替代或补充方案。 • 药物/技术前沿主要体现在：靶向药： 1. glenzocimab (抗GPVI) 旨在在降低血栓形成的同时控制出血风险； 2. 3K3A‑APC兼具神经与血管保护，早期研究显示良好安全性与出血相关指标改善信号； 3. nerinetide (PSD‑95抑制肽) 总体结论中性，但在未合用tPA或特定流程亚群显现潜在获益，提示存在人群与流程依赖性。细胞与基因治疗： 1. SB623 (基因改造间充质基质细胞) 用于慢性期功能重建显示上肢运动量表改善且安全性良好； 2. MultiStem (同种异体MAPC) 在18–36小时给药窗内安全可行，关键III期验证持续； 3. AAV递送 (如VEGF/神经营养因子/抗炎因子) 临床前证据积极，但跨BBB的安全与递送效率仍是转化瓶颈。 ▲ 图7：脑卒中的在研药物靶点汇总 05 其他神经系统疾病及治疗前沿除AD、PD与中风外，神经系统疾病还包括多发性硬化 (MS)、视神经脊髓炎谱系疾病 (NMOSD) 、肌萎缩侧索硬化 (ALS)、重症肌无力 (gMG) 、偏头痛等。随着靶向药与技术平台的演进，越来越多的创新疗法为不同疾病带来新的治疗希望： NMOSD：已有三条机制获批——补体C5抑制剂 (依库珠单抗/拉夫珠单抗) 、抗CD19 (伊妥珠单抗/inebilizumab) 、抗IL‑6R (沙妥利珠单抗/satralizumab) 。偏头痛：中枢敏化与CGRP通路为关键机制。美国头痛学会已将CGRP疗法 (艾伦单抗/芙马珠单抗/加拉单抗/艾普替单抗) 纳入一线预防选项。 gMG：FcRn拮抗剂 (efgartigimod、rozanolixizumab) 与补体C5抑制剂 (eculizumab、ravulizumab) 确立了分子靶向治疗范式，显著改善症状、加速缓解。 • 基因疗法亦加速进入临床：亨廷顿病 (HD)：等位基因选择性ASO (WVE‑003) 实现突变HTT下调且安全性可接受；AMT‑130 (AAV‑miHTT) I/II期长随提示疾病进展减缓信号。难治性癫痫：ASO上调SCN1A (zorevunersen/STK‑001) 在早期研究显示发作频率下降与行为/认知改善信号；基因调控疗法ETX101 (AAV9) 在SCN1A+德拉维特综合征进入I/II期；抑制性中间神经元细胞疗法NRTX‑1001在成人MTLE一期呈现发作显著降低与良好耐受性。脊髓性肌萎缩 (SMA)：已建立三大治疗支柱——ASO (nusinersen) 、基因疗法 (AAV9‑SMN1，onasemnogene abeparvovec) 与口服小分子剪接调节剂 (risdiplam) 。 06 神经系统疾病治疗总结神经系统疾病呈“低病死、高致残”特征，已成全球疾病负担首因。治疗正由对症控制走向“疾病修饰+精准分层”。阿尔茨海默病方面，抗Aβ单抗 (lecanemab、donanemab) 在早期人群证实减缓进展，血液标志物与穿越BBB的递送技术 (如Brainshuttle) 加速落地，抗Tau与抗炎 (如选择性中和可溶性TNF) 成为重要补充。帕金森病仍以多巴胺替代为基石，但围绕α-突触核蛋白的免疫、LRRK2抑制/降解与基因治疗正在逼近关键验证。中风治疗两端发力：急性期强调再灌注 (TNK与晚窗机械取栓) ，二级预防重视分型与个体化 (短期DAPT、DOACs、LAAO) 。除AD/PD/中风外，NMOSD、gMG、偏头痛已形成明确分子靶向范式；HD、癫痫、SMA等病种的基因/细胞疗法进展迅速。 • 针对神经系统疾病的未来治疗方向将聚焦于： ① 跨BBB递送与长效化——TfR介导、脑内暴露定量学、皮下长效制剂； ② 基因治疗——AAV/ASO精准调控与免疫规避，提升持续表达与安全窗； ③ AOC药物——抗体-寡核苷酸偶联，实现细胞/区域特异输送与基因沉默、上调或剪接校正，为难治性癫痫、遗传性运动障碍等提供新解。 Sanyou 10th Anniversary: Therapeutic Advances in Neurological Disorders 01 Introduction Extending life expectancy is one of humanity’s greatest public-health achievements. Yet longer lives come with a steadily rising burden of age-related neurological disorders. Neurological disorders—conditions of the central or peripheral nervous system characterized primarily by impairments of sensation, consciousness, and movement—generally have low case-fatality but high disability rates. On October 14, 2025, the World Health Organization released a new Global Status Report on Neurology1, estimating that neurological disorders currently affect over 40% of the world’s population—more than 3 billion people—and account for 435 million disability-adjusted life years (DALYs), making them the leading cause of disease and disability worldwide. Across 37 neurological conditions, there were 11.8 million deaths, 162 million years lived with disability, and 272 million years of life lost. This article highlights therapeutic frontiers across selected neurological diseases to provide actionable target ideas for R&D professionals. ▲ Fig. 1 Global burden of conditions affecting the nervous system2 02 Alzheimer’s Disease Alzheimer’s disease (AD) is a progressive, degenerative disorder of the central nervous system whose core clinical feature is cognitive decline. Pathology includes extracellular amyloid-β (Aβ) plaque deposition and abnormal phosphorylation of tau protein/neurofibrillary tangles, often accompanied by neuroinflammation and synaptic dysfunction. In recent years, pathology-based stratification via CSF/imaging has extended to blood biomarkers (e.g., plasma p-tau217), providing more accessible tools for early identification and trial enrollment. ▲ Fig. 2 Pathology of Alzheimer’s disease3 • Current therapies Management combines symptomatic agents (cholinesterase inhibitors and the NMDA receptor antagonist memantine) with disease-modifying therapy initiated in early-symptomatic populations. Among anti-Aβ monoclonal antibodies, lecanemab (Leqembi) received traditional FDA approval in 2023 with labeling that emphasizes ARIA risk and APOE ε4 stratification; donanemab (Kisunla) was approved in 2024 for early symptomatic AD (MCI/mild dementia) and is administered as monthly IV infusions. In clinical practice, Aβ positivity is typically confirmed by imaging or fluid biomarkers, and MRI monitoring is used during treatment to manage ARIA. • Frontline R&D themes Upgrading anti-Aβ strategies. Marketed antibodies show clinically meaningful slowing in early-stage populations. To achieve higher cortical exposure, Roche is developing Brainshuttle technology by coupling to transferrin receptor (TfR)–binding modules, markedly improving BBB penetration and brain distribution. Anti-tau and combination/sequencing. Multiple programs targeting tau pathways are advancing. Although monotherapy results have been mixed, pairing with Aβ clearance in sequential/combination regimens may modulate downstream neurodegeneration. Inflammation control with precise stratification. A growing multi-target portfolio focuses on neuroinflammation. For example, selective neutralization of soluble TNF with XPro™/XPro1595 missed the primary endpoint in the phase II MINDFuL study overall, but showed signals of benefit across cognitive, behavioral, and biomarker endpoints in an inflammation-enriched early-AD subgroup with good safety—supporting “inflammatory phenotype stratification” for precision use. ▲ Fig. 3 Drug targets under development for Alzheimer’s disease 03 Parkinson’s Disease Parkinson’s disease (PD) is a chronic neurodegenerative disorder primarily affecting the motor system with typically slow progression. Early features include resting tremor, rigidity, bradykinesia, and gait disturbance, often with cognitive/behavioral changes. Pathology features loss of dopaminergic neurons in the substantia nigra and intracellular α-synuclein aggregation; early degeneration is often localized to the ventrolateral substantia nigra and expands with disease. Lewy bodies are mainly composed of aggregated α-synuclein, with lesions commonly starting in brainstem cholinergic/monoaminergic neurons and the olfactory system, then involving limbic structures and neocortex. ▲ Fig. 4 Pathology of Parkinson’s disease4 • Current therapies There is no established disease-modifying therapy. Levodopa and dopamine replacement remain the gold standard. Early treatment can be levodopa monotherapy or combined with dopamine agonists (e.g., ropinirole, pramipexole, rotigotine) and MAO-B inhibitors (e.g., selegiline, rasagiline). Compared with early levodopa monotherapy, starting dopamine agonists early shows no clear advantage for long-term disability or quality of life. For “on–off” fluctuations, clinicians often shorten levodopa dosing intervals, add COMT inhibitors (entacapone, opicapone) and/or MAO-B inhibitors (selegiline, rasagiline, safinamide, zonisamide), and titrate dopamine agonists; amantadine may be added for dyskinesia. Device-aided therapies can be considered in selected patients to reduce “off” time and improve motor complications. • Frontline R&D themes Passive immunotherapy against α-synuclein. Preclinical data show improvements in pathology and behavior. Although two large early-PD trials (SPARK/cinpanemab and PASADENA/prasinezumab) missed primary endpoints, PASADENA showed a trend toward slower motor progression. Based on phase 2b PADOVA and its OLE plus long-term PASADENA follow-up, Roche has advanced prasinezumab into phase III. LRRK2 inhibition/degradation. LRRK2 is a validated target. On October 8, 2025, Arvinas reported positive phase I data for the LRRK2 degrader ARV102, showing good CSF exposure and robust target knock-down (>90% peripherally, >50% in CSF) with reductions in downstream biomarkers (pRab10 and urinary BMP). Gene therapy. AAV2-GAD delivery to the subthalamic nucleus showed safety and improvement on the treated side in advanced PD; AAV2-AADC overexpression in the putamen enhances levodopa conversion, producing ~30% improvement in UPDRS (on/off medication) at 6 months and reduced medication needs, though 4-year follow-up suggests benefits trend back toward baseline—highlighting the need to optimize delivery and combinations. ▲ Fig. 5 Drug targets under development for Parkinson’s disease 04 Stroke Stroke comprises ischemic and hemorrhagic types, with ischemic stroke predominating. The ischemic cascade involves multiple CNS cell types: in the core, neurons undergo morphological changes with loss of soma and axons; microglia and astrocytes also react. Post-ischemia, BBB permeability increases; leukocytes, monocytes, and macrophages infiltrate the lesion, releasing either neurotoxic or neurotrophic factors with potentially protective or harmful effects on injured brain tissue. ▲ Fig. 6 Pathology of stroke5 • Current strategies Management emphasizes both acute reperfusion and secondary prevention. For the acute phase, IV thrombolysis within 4.5 hours remains foundational. Beyond alteplase, guidelines and reviews support tenecteplase (TNK) 0.25 mg/kg as an alternative in selected scenarios. For large-vessel occlusion, perfusion-imaging–guided selection enables mechanical thrombectomy in the 6–24 hour window. For secondary prevention, short-term dual antiplatelet therapy (aspirin + clopidogrel) in minor stroke/high-risk TIA confers most of its benefit within 21 days of initiation. In patients with atrial fibrillation, oral anticoagulation (preferably DOACs) is first-line; when long-term anticoagulation is unsuitable, left atrial appendage occlusion (LAAO) can be considered as an alternative or adjunct. • Frontline R&D themes Targeted agents： 1. glenzocimab (anti-GPVI): aims to curb thrombosis while controlling bleeding risk. 2. 3K3A-APC: offers neuro- and vasculo-protection; early studies suggest good safety and favorable bleeding-related signals. 3. nerinetide (PSD-95 inhibitor peptide): neutral overall, but potential benefit in subgroups not receiving tPA or under specific workflow conditions—suggesting population/process dependence. Cell and gene therapies：1. SB623 (gene-modified mesenchymal stromal cells) for chronic-phase functional recovery improved upper-limb scales with good safety. 2. MultiStem (allogeneic MAPC) appears safe/feasible with dosing at 18–36 hours; pivotal phase III confirmation is ongoing. 3. AAV delivery (e.g., VEGF/neurotrophic/anti-inflammatory factors) shows encouraging preclinical evidence, but safe and efficient BBB crossing remains a translational bottleneck. ▲ Fig. 7 Drug targets under development for stroke 05 Other Neurological Diseases and Therapeutic Frontiers Beyond AD, PD, and stroke, neurological disorders include multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), amyotrophic lateral sclerosis (ALS), generalized myasthenia gravis (gMG), migraine, and more. With the evolution of targeted drugs and platform technologies, an expanding array of innovative therapies is delivering new hope:NMOSD: Three approved mechanisms—complement C5 inhibitors (eculizumab/ravulizumab), anti-CD19 (inebilizumab), and anti-IL-6R (satralizumab). Migraine: Central sensitization and the CGRP pathway are key. The American Headache Society now lists CGRP-pathway therapies (erenumab, fremanezumab, galcanezumab, eptinezumab) as first-line options for prevention. gMG: FcRn antagonists (efgartigimod, rozanolixizumab) and complement C5 inhibitors (eculizumab, ravulizumab) have established a molecularly targeted paradigm, improving symptoms and accelerating remission. • Gene and cell therapies accelerating into the clinicHuntington’s disease (HD): Allele-selective ASO WVE-003 lowers mutant HTT with acceptable safety; AMT-130 (AAV-miHTT) phase I/II long-term follow-up suggests signals of slowed disease progression. Refractory epilepsy: ASO zorevunersen/STK-001 upregulates SCN1A with early signals of seizure reduction and behavioral/cognitive improvement; gene-regulation therapy ETX101 (AAV9) has entered phase I/II for SCN1A-positive Dravet syndrome; an inhibitory interneuron cell therapy NRTX1001 in adult MTLE phase I shows marked seizure reduction with good tolerability. Spinal muscular atrophy (SMA): A tri-pillar framework is established—ASO (nusinersen), gene therapy (onasemnogene abeparvovec, AAV9-SMN1), and oral small-molecule splicing modulation (risdiplam). 06 Summary of Therapeutic Directions Neurological disorders feature low mortality but high disability , now the top contributor to global disease burden. Treatment is shifting from symptomatic control to disease modification with precise stratification.AD: Anti-Aβ antibodies (lecanemab, donanemab) slow progression in early populations; blood biomarkers and BBB-shuttling technologies (e.g., Brainshuttle) are moving into practice. Anti-tau and anti-inflammatory approaches (e.g., selective neutralization of soluble TNF) are important complements. PD: Dopamine replacement remains foundational, while α-synuclein immunotherapy, LRRK2 inhibition/degradation, and gene therapy approach key validation milestones. Stroke: Dual-pronged care—acute reperfusion (TNK and extended-window thrombectomy) and individualized secondary prevention (short-term DAPT, DOACs, LAAO). Others: NMOSD, gMG, and migraine already have clear targeted paradigms; gene/cell therapies are rapidly advancing in HD, epilepsy, SMA, and beyond. • Future priorities will focus on1. Cross-BBB delivery and durability—TfR-mediated shuttles, quantitative CNS exposure, and long-acting subcutaneous formulations. 2. Gene therapy—AAV/ASO precision control with immune evasion, enhancing persistence and safety margins. 3. AOC (antibody–oligonucleotide conjugates)—cell/region-specific delivery enabling gene silencing, up-regulation, or splice correction, offering new solutions for refractory epilepsy, inherited movement disorders, and more. ▶ Ref 1. Global status report on neurology 2. GBD 2021 Nervous System Disorders Collaborators. Global, regional, and national burden of disorders affecting the nervous system, 1990-2021: a systematic analysis for the Global Burden of Disease Study 2021. Lancet Neurol. 2024;23(4):344-381. doi:10.1016/S1474-4422(24)00038-3 3. Kamatham PT, Shukla R, Khatri DK, Vora LK. Pathogenesis, diagnostics, and therapeutics for Alzheimer's disease: Breaking the memory barrier. Ageing Res Rev. 2024;101:102481. doi:10.1016/j.arr.2024.102481 4. Morris HR, Spillantini MG, Sue CM, Williams-Gray CH. The pathogenesis of Parkinson's disease. Lancet. 2024;403(10423):293-304. doi:10.1016/S0140-6736(23)01478-2 5. Qin C, Yang S, Chu YH, et al. Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions. Signal Transduct Target Ther. 2022;7(1):215. Published 2022 Jul 6. doi:10.1038/s41392-022-01064-1 1 推荐阅读三优十周年｜AI-STAL 智能超万亿分子库发展历程三优十周年｜打造全球顶尖的原创新药创新工场三优十周年｜抗体治疗50年风雨江湖三优十周年｜针对宠物疾病的单克隆抗体药物三优十周年｜CAR-T细胞治疗现状挑战与未来三优十周年｜服务篇-体外药效筛选解决方案三优十周年｜AI-STAL篇-Anticalin靶向蛋白库三优十周年｜靶点篇-自身免疫疾病靶点介绍创新前沿｜三优生物类器官产学研联盟启航中和抗体“硬核出击”，斩断CHIKV病毒感染链三优十周年｜服务篇-靶点至PCC药物研发三优十周年｜靶点篇-六大恶性肿瘤靶点介绍创新前沿｜2025ADC热门靶点与技术创新启示三优十周年｜AI-STAL篇-高等电点单域抗体库 6类分子形式之环状多肽分子产生系统解决方案关于三优生物三优生物是一家以“让天下没有难做的创新生物药”为使命，以超万亿分子库和智能科技驱动的生物医药高科技企业。公司致力于打造全球顶尖的原创新药创新工场。公司以智能超万亿分子库（AI-STAL）为核心；以干湿结合、国际领先的创新生物药智能化及一体化研发平台为依托；以多样化的业务模式推动全球创新药物的研发及产业化。公司总部位于中国上海，在亚洲、北美洲、欧洲等多地建立了业务中心，形成了全球化的业务网络，现有投产及布局的研发及GMP场地20000多平方米。公司已与全球2000多家药企、生技公司等建立了良好的合作关系，已赋能1200多个新药研发项目；已完成50多个合作研发项目，其中10多个协同研发项目已推至IND及临床研发阶段。公司已申请130多项发明专利，其中30多项发明专利已获得授权，并获得了国家级高新技术企业、上海市专精特新、ISO9001、ISO27001等10余项资质及体系认证。 11

临床研究临床结果

2025-10-22

·卫医荟

科普 | 帕友为啥白天爱打盹？警惕“日间过度嗜睡”

看到这个标题你也许会问，打个盹而已，有必要警惕吗？对于帕友来说，有必要！日间过度嗜睡是啥？日间过度嗜睡指的是白天应该保持清醒的时候却无法抑制睡意，轻则可能非常困倦，重则随时倒头就睡，不论场景。调查显示，日间嗜睡导致的交通事故和工伤事件是偶然发生的两倍以上[1,2]。更不用说突然睡着导致的跌倒、骨折等危害。这就是为什么要警惕日间过度嗜睡。日间过度嗜睡在帕友中非常常见，九成以上的帕友都有这个问题，只是可能被忽略掉了。约70%的日间过度嗜睡主要表现为非常困倦，而有近30%则是每天至少一次突然睡着，甚至是在走路、开车或与人交谈中[3]。如何自查日间过度嗜睡？日间过度嗜睡主要通过问卷调查来评估，最常用的问卷叫艾普沃斯（Epworth）嗜睡量表，帕友可以对照下面的问题来自查一下有没有日间过度嗜睡（也可以请家人或看护者帮忙回答）：在下面8个场景中，你有多大可能打瞌睡？0分代表从不打瞌睡，1分是轻微可能，2分是中度可能，3分代表有很大可能会打瞌睡。坐着看书或看手机时坐着看电视时在公共场所（比如电影院、办公室开会、餐厅等）坐着不动时乘坐交通工具超过1小时环境允许时，下午躺下休息时坐着与人交谈时在没有饮酒的情况下，午餐后安静坐着时遇到堵车，需要停车数分钟时我们把分数全部加起来，如果总分超过10分就提示有过度嗜睡了，要是超过16分那就属于非常严重的嗜睡，可能会带来危险。出现日间过度嗜睡我该怎么办？那帕友该如何警惕呢？首先，抗帕药的使用会影响到嗜睡。例如服用多巴胺受体激动剂，比如普拉克索和吡贝地尔，尤其用药量较大的帕友，会更容易发生日间嗜睡[4]。而有研究发现，嗜睡的帕友长期使用左旋多巴或司来吉兰（早上、上午服药，不应睡前服用），1年后嗜睡得到了显著改善[5]。如果有日间嗜睡表现的患者，就诊时需要将这种症状提前告知医生，以选择合适的药物。此外，如果有夜间翻身困难、四肢频繁抽搐也要告知医生，在睡前增加相对长效的抗帕药（比如恩他卡朋双多巴等），减少夜间运动症状波动对睡眠的干扰。第二，生活方式调整对睡眠有很大影响，帕友需要尽量营造安静（或有助眠白噪音）、黑暗的睡眠环境，睡前不要饮酒、咖啡或浓茶。白天不要睡太多，避免晚上睡不着，坚持有规律的作息时间（早睡早起）。坚持做到以上几点，一定会对帕友的觉醒和睡眠健康颇有助益。专家点评日间嗜睡确实非常容易被帕友忽略，有时觉得只是打盹而已，也许是晚上没睡好，或者平时每天都要打盹，觉得很正常。但日间过度嗜睡会随帕金森病进展逐渐加重，以及部分药物治疗还可能诱发嗜睡，严重的嗜睡会增加事故风险，还会危害心血管健康，不容忽视。临床建议，帕友要养成良好的睡眠习惯，配合医生达成合适的治疗方案（例如司来吉兰等对日间过度嗜睡症状有潜在获益的治疗药物），遵医嘱正确服药，争取减缓日间过度嗜睡及解决其他睡眠障碍问题。专家简介费国强教授复旦大学附属中山医院神经内科副主任医师复旦大学附属中山医院（厦门）神经内科执行副主任上海市医学会神经病学分会痴呆与认知障碍学组委员厦门市医学会神经内科分会副主任委员厦门市中西医结合学会神经内科分会副主任委员厦门市医学行为科学学会副会长福建省医学会罕见病分会委员厦门市医学会精神病学分会委员厦门市神经内科质控中心、脑卒中质控中心委员获评2023年度厦门市“最美医师” 擅长神经内科疾病，尤其神经退行病如痴呆、帕金森病等疾病的诊治主持上海市科委基金、福建省卫健委、厦门市科技局等科研项目，发表各类论文近20篇参考文献 Bonsignore MR, Randerath W, Schiza S, et al. European Respiratory Society statement on sleep apnoea, sleepiness and driving risk[J]. Eur Respir J, 2021, 57(2):2001272. Melamed S, Oksenberg A. Excessive daytime sleepiness and risk of occupational injuries in non‑shift daytime workers[J]. Sleep, 2002, 25(3): 315‑322. Liu H, Li J, Wang X, Huang J, Wang T, Lin Z, Xiong N. Excessive Daytime Sleepiness in Parkinson's Disease. Nat Sci Sleep. 2022 Sep 7;14:1589-1609. 黄珅,胡世玉,马建军,等.帕金森病患者日间过度嗜睡影响因素[J].中国老年学杂志,2022,42(16):3971-3974. 耿海威,王坚,孙一忞,等.帕金森病患者日间嗜睡的影响因素分析[J].中国临床神经科学,2020,28(06):625-632. 仅供医疗专业人士参考

2025-10-20

·Business Wire

Alto Neuroscience Announces $50 Million Private Placement Financing

MOUNTAIN VIEW, Calif.--(BUSINESS WIRE)--Alto Neuroscience, Inc. (“Alto”) (NYSE: ANRO), a clinical-stage biopharmaceutical company focused on the development of novel precision medicines for neuropsychiatric disorders, announced today that it has entered into a securities purchase agreement with institutional and accredited investors to sell securities in a private placement financing (the “PIPE”) for gross proceeds of approximately $50 million, before deducting offering expenses. The financing was led by Perceptive Advisors, with participation by new and existing institutional investors, including Commodore Capital, Vestal Point Capital, Vivo Capital, and a large biotech dedicated investor. Alto intends to use the proceeds from the PIPE to accelerate the development of ALTO-207, a fixed-dose combination of pramipexole (a dopamine D3-preferring D3/D2 agonist) and ondansetron, following a successful FDA meeting regarding the development path of the program, as well as for working capital and general corporate purposes. Alto expects to initiate a Phase 2b study of ALTO-207 in treatment resistant depression (TRD) by mid-2026, which has the potential to be a pivotal study. With the funding from the PIPE, the Company now also expects to initiate a Phase 3 study of ALTO-207 in TRD patients by early 2027. “We appreciate the support of this esteemed group of investors, which reflects strong confidence in Alto’s precision psychiatry platform and clinical pipeline,” said Amit Etkin, M.D., Ph.D., founder and chief executive officer of Alto Neuroscience. “Following the successful outcome of our FDA meeting for ALTO-207, this financing positions us to advance the program more rapidly toward pivotal studies and patients in need.” In the PIPE, Alto is selling an aggregate of 3,832,263 shares of its common stock at a price of $5.914 per share and, in lieu of common stock to certain investors, pre-funded warrants to purchase up to an aggregate of 4,622,251 shares of common stock at a purchase price of $5.9139 per pre-funded warrant. Each pre-funded warrant has an exercise price of $0.0001 per share of common stock, will be immediately exercisable, subject to certain conditions set forth in each pre-funded warrant, and will not expire. The PIPE is expected to close on October 21, 2025, subject to customary closing conditions. The financing was priced at-the-market under NYSE rules. Cooley LLP served as counsel to Alto for this transaction. The securities to be sold in the PIPE, including the shares of common stock underlying the pre-funded warrants, have not been registered under the Securities Act of 1933, as amended, or applicable state securities laws. Accordingly, these securities may not be offered or sold in the United States except pursuant to an effective registration statement or an applicable exemption from the registration requirements of the Securities Act. Alto has agreed to file a registration statement with the Securities and Exchange Commission (SEC) registering the resale of the shares of common stock and shares of common stock issuable upon the exercise of the pre-funded warrants issued in the PIPE. This press release shall not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or other jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such jurisdiction. About ALTO-207 ALTO-207 is a fixed-dose combination of pramipexole, a dopamine D3-preferring D3/D2 agonist, approved for the treatment of Parkinson’s disease with demonstrated antidepressant effect, and ondansetron, an antiemetic, selective 5-HT3 receptor antagonist. As a fixed-dose combination, ALTO-207 is designed to enable rapid titration and higher dosing by mitigating the dose-limiting adverse events typically experienced with pramipexole. ALTO-207 is being developed to address the significant unmet need for patients with treatment resistant depression. In a randomized, placebo-controlled Phase 2a clinical trial evaluating ALTO-207 in 32 patients with depression ALTO-207 met primary and secondary endpoints demonstrating significantly greater improvements on MADRS compared to placebo. Patients randomized to receive ALTO-207 reached a mean dose of 4.1mg per day. ALTO-207 was well tolerated in the maintenance period of the study with an adverse event rate similar to placebo. About Alto Neuroscience Alto Neuroscience is a clinical-stage biopharmaceutical company with a mission to redefine psychiatry by leveraging neurobiology to develop personalized and highly effective treatment options. Alto’s Precision Psychiatry Platform™ measures brain biomarkers by analyzing EEG activity, neurocognitive assessments, wearable data, and other factors to better identify which patients are more likely to respond to Alto product candidates. Alto’s clinical-stage pipeline includes novel drug candidates in bipolar depression, major depressive disorder, treatment resistant depression (TRD), and schizophrenia, and other mental health conditions. Forward-Looking Statements This press release may contain forward-looking statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements may be identified by words such as “aims,” “anticipates,” “believes,” “could,” “estimates,” “expects,” “forecasts,” “goal,” “intends,” “look forward,” “may,” “plans,” “possible,” “potential,” “seeks,” “will” and variations of these words or similar expressions that are intended to identify forward-looking statements, although not all forward-looking statements contain these words. Forward-looking statements in this press release include, but are not limited to, the timing, size and closing of the proposed PIPE; expectations regarding market conditions, the satisfaction of customary closing conditions related to the PIPE and the anticipated use of proceeds therefrom; statements regarding Alto’s expectations about the potential benefits, activity, effectiveness, tolerability, and safety of its product candidates and Precision Psychiatry Platform (“Platform”); statements regarding Alto’s expectations for the design, timing, and results of its planned Phase 2b and Phase 3 trials of ALTO-207 in TRD; Alto’s expectations with regard to the general design and results of its research and development programs and clinical trials, including the timing of enrollment and the timing and availability of data from such trials; Alto’s business strategy and financial position, as well as Alto’s expectations regarding funding, operating and working capital expenditures; and other statements that are not historical fact. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various factors, including the risks and uncertainties associated with market conditions and the satisfaction of customary closing conditions related to the proposed financing, uncertainties inherent in the initiation, progress and completion of clinical trials, and other important factors, any of which could cause Alto’s actual results to differ from those contained in the forward-looking statements, which are described in greater detail in the section titled “Risk Factors” in each of Alto’s Annual Report on Form 10-K for the fiscal year ended December 31, 2024 and Alto’s Quarterly Report on Form 10-Q for the fiscal quarter ended June 30, 2025 filed with the SEC as well as in other filings Alto may make with the SEC in the future. Any forward-looking statements contained in this press release speak only as of the date hereof, and Alto expressly disclaims any obligation to update any forward-looking statements contained herein, whether because of any new information, future events, changed circumstances or otherwise, except as required by law.

临床2期临床结果上市批准

100 项与盐酸普拉克索相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
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适应症	国家/地区	公司	日期
不宁腿综合征	欧盟	Boehringer Ingelheim International GmbH	1997-10-13
不宁腿综合征	冰岛	Boehringer Ingelheim International GmbH	1997-10-13
不宁腿综合征	列支敦士登	Boehringer Ingelheim International GmbH	1997-10-13
不宁腿综合征	挪威	Boehringer Ingelheim International GmbH	1997-10-13
帕金森病	美国	Boehringer Ingelheim GmbH	1997-07-01

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适应症	最高研发状态	国家/地区	公司	日期
Tourette 综合征	临床3期	美国	Boehringer Ingelheim GmbH	2008-05-01
Tourette 综合征	临床3期	德国	Boehringer Ingelheim GmbH	2008-05-01
舞蹈手足徐动症	临床3期	中国	Boehringer Ingelheim GmbH	2008-04-01
帕金森病（青年型、早发型）	临床3期	美国	Boehringer Ingelheim GmbH	2007-05-01
帕金森病（青年型、早发型）	临床3期	日本	Boehringer Ingelheim GmbH	2007-05-01
帕金森病（青年型、早发型）	临床3期	阿根廷	Boehringer Ingelheim GmbH	2007-05-01
帕金森病（青年型、早发型）	临床3期	奥地利	Boehringer Ingelheim GmbH	2007-05-01
帕金森病（青年型、早发型）	临床3期	捷克	Boehringer Ingelheim GmbH	2007-05-01
帕金森病（青年型、早发型）	临床3期	芬兰	Boehringer Ingelheim GmbH	2007-05-01
帕金森病（青年型、早发型）	临床3期	德国	Boehringer Ingelheim GmbH	2007-05-01

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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


NCT04759703 (CTgov)	临床2/3期	阿片相关性障碍 \| 舞蹈手足徐动症 \| 阿片滥用 ... 更多	75	Pramipexole (Pramipexole)	築醖遞襯窪蓋選夢醖夢(顧觸遞糧積膚製夢鏇壓) = 獵膚襯憲網鏇鬱獵衊築鏇夢艱醖製獵糧積鏇獵 (廠積鹹醖窪鹽鏇蓋顧製, 3.44) 更多	-	2025-09-22
				Placebo (Placebo)	築醖遞襯窪蓋選夢醖夢(顧觸遞糧積膚製夢鏇壓) = 鹹構簾構鑰構鑰襯觸顧鏇夢艱醖製獵糧積鏇獵 (廠積鹹醖窪鹽鏇蓋顧製, 6.56) 更多
NCT06457204 (CTgov)	临床1期	-	28	Pramipexole (Reference - Sifrol® (Pramipexole) Manufactured in Ingelheim)	憲鹽齋願鬱鑰積選膚觸(夢齋選夢艱憲糧築鬱醖) = 簾餘齋遞鏇醖艱鹽簾齋壓鏇築積鏇壓構構觸繭 (餘糧繭鑰簾淵選鹹淵醖, NA) 更多	-	2025-08-28
				Ennigerloh+Pramipexole (Test - Sifrol® (Pramipexole) Manufactured in Ennigerloh)	憲鹽齋願鬱鑰積選膚觸(夢齋選夢艱憲糧築鬱醖) = 製餘膚廠糧窪襯夢構製壓鏇築積鏇壓構構觸繭 (餘糧繭鑰簾淵選鹹淵醖, NA) 更多
ISRCTN84666271 (Literature) 人工标引	N/A	难治性抑郁症	150	pramipexole	繭觸築壓齋簾廠積鬱獵(齋網襯鬱齋鑰構積夢衊) = 餘衊鬱壓簾鬱餘範願鹹網鹹蓋積蓋鹽積蓋糧餘 (簾遞製淵遞築觸顧夢醖, 4.9) 更多	积极	2025-06-29
				Placebo	繭觸築壓齋簾廠積鬱獵(齋網襯鬱齋鑰構積夢衊) = 鑰鏇觸選淵醖廠鬱襯衊網鹹蓋積蓋鹽積蓋糧餘 (簾遞製淵遞築觸顧夢醖, 4.0) 更多
NCT03842709 (CTgov)	早期临床1期	慢性疼痛	13	Placebo (Standard Treatment + Placebo)	糧夢選膚鹽繭艱壓遞淵(製簾淵鏇簾鏇簾鬱範醖) = 獵鹹鹹鏇簾鏇鏇糧膚壓鬱鹹構齋膚選築憲衊鬱 (製餘築齋顧鏇醖壓簾選, 1) 更多	-	2024-10-23
				Pramipexole Oral Tablet (Standard Treatment + Pramipexole)	糧夢選膚鹽繭艱壓遞淵(製簾淵鏇簾鏇簾鬱範醖) = 觸膚觸艱夢顧獵積膚鹹鬱鹹構齋膚選築憲衊鬱 (製餘築齋顧鏇醖壓簾選, 3.2) 更多
NCT04160520 (Pubmed \| Front Pain Res (Lausanne))	临床1/2期	急性疼痛	19	Control group (morphine and oral placebo pill)	憲衊蓋衊鑰廠襯鏇顧淵(鹽醖積願願鑰鹽選簾鹹) = 積糧鹽顧襯襯鏇衊齋餘鹽觸襯齋獵壓艱願窪簾 (餘齋壓築醖繭積壓鹹艱 )	积极	2024-09-24
				Experimental group (half-dosed morphine and oral pramipexole pill)	憲衊蓋衊鑰廠襯鏇顧淵(鹽醖積願願鑰鹽選簾鹹) = 鹹艱築艱遞範壓醖鬱壓鹽觸襯齋獵壓艱願窪簾 (餘齋壓築醖繭積壓鹹艱 )
AAN2023	临床3期	帕金森病	519	P2B001	製餘鬱積願廠鹽膚構襯(齋餘顧鑰遞襯選艱選鑰) = 構餘衊積餘蓋鑰襯糧簾齋壓築鹽範鑰願壓簾蓋 (繭願夢餘鏇齋選夢鏇襯 ) 更多	积极	2023-04-25
				Pramipexole-ER-0.6mg (PPX)	製餘鬱積願廠鹽膚構襯(齋餘顧鑰遞襯選艱選鑰) = 淵憲醖廠憲醖範製網廠齋壓築鹽範鑰願壓簾蓋 (繭願夢餘鏇齋選夢鏇襯 ) 更多
AAN2023	N/A	帕金森病	-	P2B001 (low dose combination of extended-release pramipexole and rasagiline)	艱夢獵壓膚遞齋糧顧壓(窪製遞餘艱衊遞顧壓壓) = 膚夢膚衊鹹願製廠願積遞選鏇鹽鹽鹽顧範膚醖 (網糧艱鹽憲鹹網膚廠選 ) 更多	-	2023-04-25
				Extended-Release pramipexole (Prami-ER)	艱夢獵壓膚遞齋糧顧壓(窪製遞餘艱衊遞顧壓壓) = 醖膚願糧鏇簾壓獵築網遞選鏇鹽鹽鹽顧範膚醖 (網糧艱鹽憲鹹網膚廠選 ) 更多
NCT03521635 (CTgov)	临床4期	帕金森病	98	Pramipexole (Pramipexole Sustained Release)	獵構範鬱廠範憲艱鑰憲(構鏇艱顧窪觸餘夢淵窪) = 鬱願鬱構鹽顧衊顧鏇顧構窪觸鹹窪壓簾艱夢醖 (淵範範餘鏇遞顧鹹範鑰, 1.16) 更多	-	2021-02-16
				Pramipexole (Pramipexole Immediate Release)	獵構範鬱廠範憲艱鑰憲(構鏇艱顧窪觸餘夢淵窪) = 網窪顧積蓋壓艱網齋網構窪觸鹹窪壓簾艱夢醖 (淵範範餘鏇遞顧鹹範鑰, 1.20) 更多
NCT02397837 (PRAM-BD, CTgov)	临床4期	躁郁症	103	Pramipexole (Pramipexole)	鹹繭鹹醖壓鬱鬱網範夢(壓築觸鏇顧網選鹹壓築) = 憲艱鹽築壓醖獵壓觸網簾蓋艱鬱夢築廠顧艱廠 (網蓋積齋壓製鹹鬱鹹範, 12.33) 更多	-	2020-02-28
				Placebo (Placebo)	鹹繭鹹醖壓鬱鬱網範夢(壓築觸鏇顧網選鹹壓築) = 願醖膚繭夢鬱製膚簾鏇簾蓋艱鬱夢築廠顧艱廠 (網蓋積齋壓製鹹鬱鹹範, 10.45) 更多
NCT03765138 (CTgov)	临床3期	重度抑郁症 \| 创伤后应激障碍	1	Pramipexole+PE	遞觸觸範選鑰構蓋鏇製(鹽願襯構獵獵鬱艱窪範) = 廠獵壓鏇糧積簾艱齋顧窪襯鏇糧廠蓋鑰齋鏇壓 (鬱壓鏇願積夢範觸襯膚, 醖繭窪繭鏇蓋壓餘壓夢 ~ 廠壓艱夢壓構淵遞窪簾) 更多	-	2019-11-26