盐酸地美波林(Dimebolin hydrochloride) - 药物靶点：H1 receptor_在研适应症：超敏反应，过敏性鼻炎_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Dimebolin、Dimebon、Latrepirdine

+ [4]

靶点

H1 receptor

作用机制

H1 receptor拮抗剂(组胺H1受体拮抗剂)

治疗领域

免疫系统疾病感染耳鼻咽喉疾病+ [1]

在研适应症

超敏反应过敏性鼻炎

非在研适应症

阿尔茨海默症亨廷顿舞蹈病肝功能衰竭

原研机构-

在研机构-

非在研机构

Pfizer Inc.MediVation, Inc.

最高研发阶段批准上市

首次获批日期

俄罗斯 (1983-01-01),

超敏反应过敏性鼻炎

最高研发阶段(中国)-

特殊审评孤儿药 (美国)

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结构/序列

分子式C21H27Cl2N3

InChIKeyGTWLIQOLGOZTLF-UHFFFAOYSA-N

CAS号97657-92-6

关联

34

项与盐酸地美波林相关的临床试验

NCT06292351

/ Active, not recruiting临床2期

Multicenter Randomized Double-blind Placebo-controlled Three-arm Parallel-group Clinical Study to Evaluate the Efficacy and Safety of DMB-I in the Treatment of Dementia Associated With Alzheimer's Disease

The purpose of this study is to assess the efficacy and safety of DMB-I for the treatment of patients with Alzheimer type dementia.

开始日期2023-12-27

申办/合作机构

Bigespas LTD

EUCTR2009-018123-32-DE

/ Not yet recruitingN/A

HORIZON-Plus: An Open-Label Extension of the HORIZON Protocol (DIM20) Evaluating the Safety of Dimebon (Latrepirdine) in Subjects with Huntington Disease - HORIZON-Plus

开始日期2010-06-07

申办/合作机构-

NCT01066546

/ Terminated临床3期

An Open-Label Extension To The B1451006 Protocol To Evaluate The Safety And Efficacy Of Dimebon (Latrepirdine, PF-01913539) In Subjects With Moderate-To-Severe Alzheimer's Disease

The purpose of this study is to evaluate the long-term safety and tolerability of dimebon in subjects with moderate-to-severe Alzheimer's Disease.

开始日期2010-04-01

申办/合作机构

Pfizer Inc.

[+1]

100 项与盐酸地美波林相关的临床结果

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100 项与盐酸地美波林相关的转化医学

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100 项与盐酸地美波林相关的专利（医药）

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222

项与盐酸地美波林相关的文献（医药）

2024-01-09·Current computer-aided drug design

In-silico Design, ADMET Screening, Prime MM-GBSA Binding Free Energy Calculation and MD Simulation of Some Novel Phenothiazines as 5HT6R Antagonists Targeting Alzheimer’s Disease

Article

作者: N, Ramalakshmi ; V, Prema ; A, Meena

Background::

Alzheimer's disease is a type of dementia that affects neuronal function, leading to a decline in cognitive functions. Serotonin-6 (5HT6) receptors are implicated in the etiology of neurological diseases. 5HT6 receptor antagonists act as anti-dementia agents. PDB ID: 7YS6 represents a membrane protein, and amplification and overexpression of this protein are associated with Alzheimer's disease. Coumarin-fused phenothiazines are significant anti-Alzheimer's agents due to their inhibitory activity on the Serotonin- 6 receptor.

background::

Alzheimer’s disease is a type of dementia, affecting neuronal function and leading to decline in cognitive functions. Serotonin-6 (5HT6) receptors are responsible for the etiology of neurological diseases. The 5HT6 receptor antagonists are acting as anti-dementia agents. PDB id: 7YS6 is a membrane protein. Amplification and over expression of this protein is connected to Alzheimer’s disease. Coumarin fused phenothiazines are consequential anti-Alzheimer’s agents because of their Serotonin-6 receptor inhibitory activity.

Objectives::

Numerous previously unreported Coumarin-substituted Phenothiazines [A2 to A50] were designed using in-silico methods to evaluate their 5HT6 receptor antagonistic activity. Molecular modeling techniques were employed to study the ligands [A2 to A50] in interaction with the Serotonin-6 receptor (PDB ID: 7YS6) using Schrödinger Suite 2019-4.

Methods::

Molecular modeling studies of the designed ligands [A2 to A50] were conducted using the Glide module. In-silico ADMET screening was performed using the QikProp module, and binding free energy calculations were carried out using the Prime MM-GBSA module within the Schrödinger Suite. The binding affinity of the designed ligands [A2 to A50] towards 5HT6 receptors was determined based on Glide scores. Subsequently, ligand A31 underwent a 100 ns molecular dynamics simulation using the Desmond module of Schrödinger Suite 2020-1, which is based in New York, NY.

Results::

The majority of the designed ligands exhibited strong hydrogen bonding interactions and hydrophobic associations with the serotonin-6 receptor, which hinder its activity. These ligands achieved remarkable Glide scores within the range of -4.2859 to -7.7128, in comparison to reference standards such as Idalopirdine (-7.78149), Intepirdine (-5.20103), Latrepirdine (-5.54853), and the co-crystallized ligand (-7.02889). In-silico ADMET properties for these ligands fell within the recommended values for drug-likeness. It is worth noting that the MM-GBSA binding free energy of the most potent inhibitor was positive, indicating a strong binding interaction. Additionally, the dynamic behavior of the protein (7YS6)-ligand (A31) complex was studied by subjecting ligand A31 to a 100 ns molecular dynamics simulation.

result::

Majority of the designed ligands had proclaimed good hydrogen bonding interconnection and hydrophobic associations to hamper serotonin-6. The ligands got remarkable glide scores in the range of -4.2859 to -7.7128 by comparing with the standards Idalopirdine (-7.78149), Intepirdine (-5.20103), Latrepirdine (-5.54853) and Co-crystallized ligand (-7.02889). The in-silico ADMET properties were within the recommended values for drug-likeness. MM-GBSA binding free energy of the most intense inhibitor is positive. The dynamic behaviour of the protein (7YS6)-ligand (A31) complex was studied by subjecting the ligand A31 to molecular dynamics simulation at 100 ns.

Conclusion::

The results of this study reveal strong evidence supporting the potential of coumarin- substituted phenothiazine derivatives as effective Serotonin-6 receptor antagonists. Ligands [A2 to A50], which exhibited noteworthy Glide scores, hold promise for significant anti- Alzheimer activity. Further in-vitro and in-vivo investigations are warranted to explore and confirm their therapeutic potential.

2023-05-01·Current neuropharmacology

Mitochondrial Medicine: A Promising Therapeutic Option Against Various Neurodegenerative Disorders

Review

作者: Almikhlafi, Mohannad A. ; Karami, Mohammed M. ; Alqurashi, Thamer M. ; Alghamdi, Badrah S. ; Majrashi, Mohammed ; Jana, Ankit ; Ashraf, Ghulam Md.

Abstract::

Abnormal mitochondrial morphology and metabolic dysfunction have been observed in many neurodegenerative disorders (NDDs). Mitochondrial dysfunction can be caused by aberrant mitochondrial DNA, mutant nuclear proteins that interact with mitochondria directly or indirectly, or for unknown reasons. Since mitochondria play a significant role in neurodegeneration, mitochondriatargeted therapies represent a prosperous direction for the development of novel drug compounds that can be used to treat NDDs. This review gives a brief description of how mitochondrial abnormalities lead to various NDDs such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. We further explore the promising therapeutic effectiveness of mitochondria- directed antioxidants, MitoQ, MitoVitE, MitoPBN, and dimebon. We have also discussed the possibility of mitochondrial gene therapy as a therapeutic option for these NDDs.

2023-02-01·European journal of medicinal chemistry

Wiskostatin and other carbazole scaffolds as off target inhibitors of dynamin I GTPase activity and endocytosis

Article

作者: Cardoso, David ; Cossar, Peter J ; Chiew, Beatrice ; Young, Kelly A ; Robinson, Phillip J ; Hamilton, Michael P ; Russell, Cecilia C ; Baker, Jennifer R ; Chau, Ngoc ; Mathwin, Daniel ; McCluskey, Adam

Wiskostatin (1-(3,6-dibromo-9H-carbazol-9-yl)-3-(dimethylamino)propan-2-ol) (1) is a carbazole-based compound reported as a specific and relatively potent inhibitor of the N-WASP actin remodelling complex (S-isomer EC₅₀ = 4.35 μM; R-isomer EC₅₀ = 3.44 μM). An NMR solution structure showed that wiskostatin interacts with a cleft in the regulatory GTPase binding domain of N-WASP. However, numerous studies have reported wiskostatin's actions on membrane transport and cytokinesis that are independent of the N-WASP-Arp2/3 complex pathway, but offer limited alternative explanation. The large GTPase, dynamin has established functional roles in these pathways. This study reveals that wiskostatin and its analogues, as well as other carbazole-based compounds, are inhibitors of helical dynamin GTPase activity and endocytosis. We characterise the effects of wiskostatin on in vitro dynamin GTPase activity, in-cell endocytosis, and determine the importance of wiskostatin functional groups on these activities through design and synthesis of libraries of wiskostatin analogues. We also examine whether other carbazole-based scaffolds frequently used in research or the clinic also modulate dynamin and endocytosis. Understanding off-targets for compounds used as research tools is important to be able to confidently interpret their action on biological systems, particularly when the target and off-targets affect overlapping mechanisms (e.g. cytokinesis and endocytosis). Herein we demonstrate that wiskostatin is a dynamin inhibitor (IC₅₀ 20.7 ± 1.2 μM) and a potent inhibitor of clathrin mediated endocytosis (IC₅₀ = 6.9 ± 0.3 μM). Synthesis of wiskostatin analogues gave rise to 1-(9H-carbazol-9-yl)-3-((4-methylbenzyl)amino)propan-2-ol (35) and 1-(9H-carbazol-9-yl)-3-((4-chlorobenzyl)amino)propan-2-ol (43) as potent dynamin inhibitors (IC₅₀ = 1.0 ± 0.2 μM), and (S)-1-(3,6-dibromo-9H-carbazol-9-yl)-3-(dimethylamino)propan-2-ol (8a) and (R)-1-(3,6-dibromo-9H-carbazol-9-yl)-3-(dimethylamino)propan-2-ol (8b) that are amongst the most potent inhibitors of clathrin mediated endocytosis yet reported (IC₅₀ = 2.3 ± 3.3 and 2.1 ± 1.7 μM, respectively).

1

项与盐酸地美波林相关的新闻（医药）

2024-10-04

·同写意

曙光初现，提前布局下一个“重磅药物摇篮”？

本届大会以“共建创新生态共赢产业未来”为主题，聚焦生物医药出海与国际化创新、创新药投融资、医疗器械等产业发展风向标，打造“高端化、国际化、专业化、立体化”的年度盛会。近日，礼来Kisunla（通用名：Donanemab，多奈单抗）在日本获批用于治疗早期症状性阿尔茨海默病，礼来的阿尔兹海默症药物版图全球化进程加速。暨2023年7月6日，卫材的Leqembi（通用名：Lecanemab，仑卡奈单抗）成为20年来首款获得FDA完全批准的阿尔茨海默病新疗法以来，阿尔茨海默病药物利好频传。除了仑卡奈单抗的全球化进展外，2024年7月FDA更是双批了礼来的多奈单抗Kisunla以及Alpha Cognition公司的Zunveyl（Benzgalantamine，苯加兰他敏）上市。这说明阿尔兹海默症市场近20年的沉寂终被打破。那么，在频频利好之下，投资者们不禁发问阿尔兹海默症市场会成为下一个“重磅炸弹药物”摇篮吗？ 1 潜力无限：足够大的摇篮深度众所周知，年销售额超过10亿美元的上市药物，被称为“重磅炸弹”。自第一个重磅炸弹药物“泰胃美”面世以来，洛赛克、耐信、阿司匹林一直到现今的K药、O药、司美格鲁肽，整个药物史，也可以说是这些“重磅炸弹”药物的江湖史。药物经济价值通常与其对应疾病的治疗价值挂钩。如果把药物看作武林高手，那么对症领域就是他们的门派根基。根据2024年柳叶刀杂志发表的全球疾病负担研究数据GBD 2021相关研究结果，阿尔兹海默症位于2021年全球DALY的前25个3级原因，排名第25位。（注：伤残调整生命年（Disability-Adjusted Life Year，DALY）‌是一种用于量化疾病负担的指标，它表示从发病到死亡所损失的全部健康寿命年，包括因早死所致的寿命损失年和疾病所致伤残引起的健康寿命损失年。）简单做个比较，前25大三级原因中肺癌排名第17位，糖尿病排名第7位。根据药智网文章数据显示，2024上半年全球销售额top100药物中，肿瘤药物占比约46%、而肺癌是其中的第一大癌种。此外，糖尿病药物占比约12%。经过十年的发展，同样跃迁至前25大致命因素的阿尔兹海默症其重要性与治疗价值不言而明。除了极高的治疗价值外，从市场的拓展性来讲，根据WHO的数据，随着社会老龄化，全球痴呆症患者人数预计将从2019年的5500万增加到2050年的1.39亿。预计到2030年，痴呆症相关的诊治费用也将增加一倍以上，从2019年的每年1.3万亿美元增加到2.8万亿美元，而阿尔兹海默症是痴呆症的主要类型。不仅如此，阿尔茨海默病（AD）是一种与年龄正相关的疾病。据文献统计，其在65-74岁人群中发病率约为5%，在75-84岁人群中发病率约为13.1%，在85岁以上人群中发病率约为33.3%。全球人口老龄化预示着目前患有这种疾病的人数将显著增加，并预测未来受影响的人数将激增。2015年至2050年间，世界60岁以上人口的比例将几乎翻一番，从12%增至22%，达到21亿人。结合阿尔兹海默症的治疗价值与市场拓展性来看，这个领域成为重磅药物炸弹摇篮的可能性可谓十拿九稳。但事实上从1906年发现该病至今，仍然未有重磅药物的诞生，原因究竟几何？ 2 药企们的“死亡之谷” 从1906年阿尔兹海默症被发现至今，涌现出了许多关于其发病机制的理论学说，如β淀粉样蛋白假说、Tau蛋白异常修饰学说、线粒体级联假说、遗传因素等。如此多的假说意味着阿尔兹海默症的研发之路并非坦途。根据美国药物生产与研发协会发布的研究报告，2000年到2017年，药企针对AD累计投入的研发费用已超过6000亿美元，但这一时期内仅有4款AD药物获得批准。即使对那些强大的MNC巨头们来说，阿尔兹海默症也是百年难以攻破的魔障。 2010年3月，辉瑞宣布同Medivation联合研制的阿兹海默症候选药物Dimebon（该项目是2008年辉瑞以7亿多美金的高价，从Medivation公司手中获得的），第三期临床试验失败。 2012年8月，强生与辉瑞宣布终止联合研发的Bapineuzumab静脉注射液III期临床研究，原因是该药在III期临床试验中对未携带ApoE4基因的轻度至中度阿尔茨海默病患者在功能恢复上未能达到预期目标。 2016年8月，礼来就已宣布FDA授予了口服BACE抑制剂AZD3293治疗阿尔茨海默氏症临床开发项目的快速通道地位。然而到2016年年底，其III期临床药物Solanezumab却没有达到主要临床终点，宣告失败。 2022年8月2日，罗氏Aβ单抗Crenezumab一项II期临床宣告失败，这项临床在2013年11月登记，研究历时超过8年。同年11月14日其在研的阿尔兹海默症（AD，老年痴呆）药物（ganteneruma）三期临床研究失败。尚未阐明的发病机制、难以测量的治疗效果，都让无数药企对这一块儿可望而不可及的香饽饽长吁短叹。有文献显示在2024年所统计的阿尔茨海默病药物开发管线中，目前有164项试验和127种药物，而2023年有187项试验评估141种AD药物。管线中的NCE数量不成比例地减少（从101个减少到88个，减少了13%）。 2024 年阿尔茨海默病药物开发管线；来源：Alzheimer's disease drug development pipeline: 2024 这也许意味着，很多企业在死亡之谷面前丧失了勇气。并且在过去一年的临床试验里，有10项终止，4项撤回，1项暂停，7项变为“未知”状态，如此高的异常率，也许更是说明了阿尔兹海默症的研发难度。曾有数据显示，阿尔茨海默症的药物研发失败率99.6%，为各领域新药研发失败率之首，与之相比,癌症的药物研究失败率也仅为81%。在如此高的研发失败率面前，阿尔兹海默症药物市场沉寂如此之久似乎也能理解。困境还不止如此，尽管前面我们提到今年阿尔兹海默症药物市场利好频频，但其中的潜在风险仍然值得关注。比如，欧洲药品管理局（EMA）于7月26日表示，应拒绝卫材和渤健阿尔茨海默药Leqembi的上市许可，这与美国FDA对这一药的态度相反。原因是在关键临床试验中，Leqembi仅略减缓了早期阿尔茨海默病患者的认知和功能衰退速度，与安慰剂相比降低了约27%，且可能导致ARIA包括脑肿胀或出血，在极少数情况下可能致命。药效的难以界定与副作用是阿尔兹海默症药物们在上市后同样会面临的问题，可以预见的是在未来很长一段时间里，药企们都在陷在死亡之谷里挣扎。 3 前奏已响：一小步即是一大步绝对潜力的市场与难度值点满的研发困境，摇篮曲还将奏响吗？答案是肯定的。引用批准Leqembi的FDA顾问小组成员西北大学范伯格医学院神经学教授Simuni博士的话，“每个人都在纠结的问题是其临床意义是什么，这绝对是一个很小的改变，但必须放在疾病早期这一背景下考虑。” 从当前FDA最新获批的几种阿尔兹海默症药物来看，其有效性与安全性仍然存疑。但是，在“稀缺法则”的加持下，任何的进步相较于此前的无能为力，其效用都是指数级增加的。以Leqembi为例，根据卫材2024年Q1财报显示，Leqembi在过去三个月内实现增长，三个月销售额约0.41亿美元，同比增长+8785%。其中美国市场收入约0.28亿美元，中国市场销售额约1000万元。并且，卫材预测Leqembi在 2024财年的全球收入将达到约3.7亿美元，在2030年Leqembi全球销售额或将达到70亿美元。在这样强劲的增长预期下，Leqembi作为先行者已经揭开了千亿市场的一角。不仅如此，从研发端口来说，除了近期上市药物所基于的Aβ抗体疗法外，新疗法也是迎来了新曙光。 2024年7月，在阿尔茨海默病协会国际大会（AAIC）上科学家们提到两种全新的疗法： 1、Lomecel-B治疗：Lomecel-B是从年轻健康成人捐献的骨髓中分离出来的多能干细胞和祖细胞，与安慰剂相比，接受Lomecel-B治疗的患者病情恶化速度总体放缓，目前2a期随机、安慰剂对照试验已经完成； 2、激动性抗TREM2抗体治疗：研究显示TREM2的功能丧失变异与AD的风险增加相关，通过TREM2抗体治疗，其可直接调动小胶质细胞的神经保护能力，以广泛对抗多种病理（Aβ蛋白，Tau磷酸化等），目前已进入早期临床试验阶段。此外，近日Cassava Sciences宣布其正在进行的Simufilam第三期临床试验已顺利通过数据和安全监测委员会（DSMB）的第三次中期阶段安全性审查。（Simufilam可通过靶向调节关键蛋白质——突触膜蛋白受体，有望恢复其正常构象，进而减少Aβ沉积，改善神经元通讯，最终缓解认知衰退症状）经clinicaltrials.gov数据统计，2024年至少有48项3期临床试验正在进行中，包括阿卡迪亚制药ACP-204、AriBio的AR1001、Avanir Pharmaceuticals的AVP-786等，新的强效药物可期。综上，在Leqembi作为先行者强力的增长预期以及新疗法的促动下，阿尔兹海默症市场里重磅炸弹药物们的诞生前奏已被吹响。前奏已响，未来可期。从经济与市场的角度来说，相信阿尔兹海默症一定会是未来重磅炸弹药物们的核心摇篮。而从造福人类的角度，对于阿尔兹海默症病人而言，活着的每一天，都意味着失去。一个领域是否能够出现数量众多的重磅药物炸弹，其显著的经济价值固然令人兴奋。但是，其代表着人类将有富有成效的武器抵御这些强大病魔侵扰的事实才更让人尊重其价值。参考文献：（上下滑动查看更多） 1、国际阿尔茨海默病协会 | 2023 年世界阿尔茨海默病报告 2、Global incidence, prevalence, years lived with disability (YLDs), disability-adjusted life-years (DALYs), and healthy life expectancy (HALE) for 371 diseases and injuries in 204 countries and territories and 811 subnational locations,1990–2021: a systematic analysis for the Global Burden of Disease Study 2021 3、Gill Livingston, Jonathan Huntley, Kathy Y Liu, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. The Lancet. Published:July 31, 2024DOI:https://doi-org.libproxy1.nus.edu.sg/10.1016/S0140-6736(24)01296-0 4、《12款阿尔茨海默病在研新药正在中国开展临床！来自礼来、强生、恒瑞医药等公司》，医药观澜 5、Alzheimer's disease drug development pipeline: 2024， https://doi-org.libproxy1.nus.edu.sg/10.1002/trc2.12465 6、《关注政策出台催化创新药产业景气度提升》，东北证券 7、《“重磅炸弹药物”-医药工业兴衰录》，书籍 8、各公司官网 9、《阿尔茨海默病治疗又有新进展！这两个新疗法你知道吗？》，医学界神经病学频道同写意媒体矩阵，欢迎关注↓↓↓

上市批准加速审批医药出海

100 项与盐酸地美波林相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	盐酸地美波林	R	DB11725

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
超敏反应	俄罗斯	-	1983-01-01
过敏性鼻炎	俄罗斯	-	1983-01-01

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
亨廷顿舞蹈病	临床3期	美国	MediVation, Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	美国	Pfizer Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	澳大利亚	Pfizer Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	澳大利亚	MediVation, Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	加拿大	MediVation, Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	加拿大	Pfizer Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	丹麦	MediVation, Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	丹麦	Pfizer Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	德国	Pfizer Inc.	2009-07-01
亨廷顿舞蹈病	临床3期	德国	MediVation, Inc.	2009-07-01

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临床结果

适应症

分期

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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


NCT00975481 (CTgov)	临床1期	阿尔茨海默症 \| 亨廷顿舞蹈病	36	placebo (Placebo)	鏇願鬱壓鑰壓齋簾顧製(憲鹹壓鏇淵齋簾糧襯觸) = 觸構夢鏇廠選範膚鬱淵築廠膚構壓鹽構艱餘醖 (餘醖蓋簾齋夢獵構餘鬱, 醖選窪蓋憲簾衊夢簾襯 ~ 膚網繭鬱積顧衊選醖繭) 更多	-	2013-04-02
				alprazolam (Alprazolam 1 mg)	鏇願鬱壓鑰壓齋簾顧製(憲鹹壓鏇淵齋簾糧襯觸) = 網遞構顧觸製構觸淵觸築廠膚構壓鹽構艱餘醖 (餘醖蓋簾齋夢獵構餘鬱, 夢廠構鹽襯夢積觸鹹廠 ~ 壓艱觸夢鏇鑰窪廠廠艱) 更多
NCT00838110 (CTgov)	临床3期	阿尔茨海默症	742	dimebon (latrepirdine) (Dimebon (Cohort 1))	範壓積範簾膚製願艱製(膚願衊願夢壓鏇襯壓構) = 選觸壓醖鹹築鬱製願襯餘積範襯窪憲艱築淵鬱 (夢築鹽窪窪窪襯鏇鑰憲, 鹽齋齋願鹽鏇壓網鑰繭 ~ 鏇夢積觸齋艱觸糧淵製) 更多	-	2013-02-08
				Placebo (Placebo (Cohort 1))	範壓積範簾膚製願艱製(膚願衊願夢壓鏇襯壓構) = 鏇積製鹽範顧鏇獵觸顧餘積範襯窪憲艱築淵鬱 (夢築鹽窪窪窪襯鏇鑰憲, 憲衊壓鏇憲製齋鬱醖壓 ~ 遞觸餘廠鏇製願艱遞鑰) 更多
NCT00920946 (Pubmed \| JAMA Neurol)	临床3期	亨廷顿舞蹈病	403	Latrepirdine 20 mg	夢選築壓壓鬱繭艱鹹餘(鑰夢鬱鑰積艱衊鬱醖鏇) = 齋夢鏇醖餘獵鹹築獵顧蓋膚願齋鹹夢蓋網淵築 (觸繭簾繭鹹淵繭範獵襯 )	不佳	2013-01-01
				Placebo	夢選築壓壓鬱繭艱鹹餘(鑰夢鬱鑰積艱衊鬱醖鏇) = 觸願積鑰築壓齋網簾夢蓋膚願齋鹹夢蓋網淵築 (觸繭簾繭鹹淵繭範獵襯 )
NCT00939783 (CTgov)	临床3期	阿尔茨海默症	649	Dimebon (latrepirdine)	憲願顧鬱鬱鹹繭衊選襯(蓋鹽繭夢壓獵顧顧夢鏇) = 糧窪製夢襯壓膚衊憲鬱廠鏇憲鏇廠窪膚衊積顧 (網範範顧蓋範鏇淵壓齋, 齋鑰製遞願窪齋鏇觸廠 ~ 廠齋齋製鏇壓顧願齋艱) 更多	-	2012-11-14
NCT00912288 (CTgov)	临床3期	阿尔茨海默症	86	Dimebon 20 mg po TID (Dimebon)	窪餘衊鹹願繭獵襯夢鹽(遞窪構廠糧築蓋顧餘艱) = 簾築蓋襯製餘艱壓窪鹹願艱鏇襯範網糧簾鏇範 (憲繭廠膚夢鬱糧願鹹鹽, 願襯鏇糧選餘艱鹹鹹夢 ~ 構願鹹壓鏇積淵鬱製齋) 更多	-	2012-10-02
				Placebo po TID (Placebo)	窪餘衊鹹願繭獵襯夢鹽(遞窪構廠糧築蓋顧餘艱) = 糧膚鹽糧鹹願糧範顧糧願艱鏇襯範網糧簾鏇範 (憲繭廠膚夢鬱糧願鹹鹽, 夢築鏇網製鑰網顧糧淵 ~ 齋築積淵廠淵積鑰網鏇) 更多
NCT01066546 (CTgov)	临床3期	阿尔茨海默症	5	Dimebon tablet for oral administration	鹽範顧蓋顧顧鬱衊獵鹽(廠蓋蓋艱選膚鏇網顧簾) = 築糧襯製構製選積夢網窪築廠鬱觸衊獵範壓觸 (憲構艱蓋壓願鹹顧襯選, 襯範窪網顧窪繭鬱齋獵 ~ 簾壓網網鹹簾網憲壓選) 更多	-	2012-10-02
NCT00497159 (Pubmed)	临床2期	亨廷顿舞蹈病	91	Latrepirdine 20 mg	網範網餘醖顧窪艱製膚(選鑰積淵願淵構襯餘積): treatment effect = 0.97 (95% CI, 0.1 ~ 1.85)	-	2010-02-01
				Placebo
AAIC2008	N/A	阿尔茨海默症	183	Dimebon 20 mg	憲遞鬱憲顧窪醖積製遞(鹹築窪淵鑰選衊選簾選) = Dimebon was well-tolerated in both mild and moderate AD patients through one year, with dry mouth as the most common drug-related adverse event (%) reported 齋醖鑰鑰製蓋蓋觸鏇鹹 (襯築願壓憲鏇壓鏇廠鑰 )	积极	2008-07-01
AAIC2007	N/A	阿尔茨海默症	183	Dimebon 20 mg	壓簾鬱鬱衊鹽築網獵獵(觸築夢襯觸獵願膚窪衊) = 糧鹽簾糧蓋遞鹽鬱顧觸憲選廠襯範鏇艱窪繭製 (餘觸醖鑰築鏇鹽衊製築 ) 更多	-	2007-07-01