双硫仑(Disulfiram) - 药物靶点：ALDH2_在研适应症：进行性纤维化间质性肺病，酒精使用障碍_专利_临床

概要

基本信息

药物类型

小分子化药

别名

1,1'-dithiobis(N,N-diethylthioformamide)、bis(diethylthiocarbamoyl) disulfide、Disulfiram (JP17/USP/INN)

+ [8]

靶点

ALDH2

作用机制

ALDH2抑制剂(乙醛脱氢酶抑制剂)

治疗领域

呼吸系统疾病其他疾病

在研适应症

进行性纤维化间质性肺病酒精使用障碍

非在研适应症

酗酒

原研机构

Teva Pharmaceutical Industries Ltd.

在研机构

The Trustees of Columbia University in The City of New YorkThe University of Tokyo Hospital

非在研机构

Teva Women's Health, Inc.

最高研发阶段临床2期

首次获批日期

美国 (1951-08-28),

酗酒

最高研发阶段(中国)-

特殊审评-

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结构/序列

分子式C10H20N2S4

InChIKeyAUZONCFQVSMFAP-UHFFFAOYSA-N

CAS号97-77-8

关联

66

项与双硫仑相关的临床试验

NCT06793488

/ Not yet recruiting早期临床1期IIT

Neural Mechanisms of Anxiety During Early and Protracted Abstinence in Alcohol Use Disorder

The goal of this study is to better understand the underlying neurobiological basis of anxiety that emerges during abstinence in patients with alcohol use disorder (AUD). The main questions it aims to answer are:
1. To characterize anxiety itself as well as anxiety related-neurobiological circuitry in early abstinence in AUD
2. To examine how anxiety and anxiety related-neurobiological circuitry change over the course of abstinence in AUD
Researchers will recruit both participants with AUD and healthy volunteers.
The participants with AUD will be prescribed disulfiram, a medication that helps participants with AUD stay abstinent. Healthy volunteers will not receive antabuse. Patients with AUD will undergo fMRI scanning both after 1 week and 3 months of disulfiram treatment. Healthy volunteers will undergo fMRI once.

开始日期2025-03-01

申办/合作机构

The Trustees of Columbia University in The City of New York

[+1]

NCT05626920

/ Recruiting临床1/2期IIT

A Cross-over Randomized Control Trial to Evaluate the Retinaldehyde Dehydrogenase Inhibitor, Disulfiram, in Improving Retinal Sensitivity in Eyes Affected by Inherited Retinal Degeneration

Aberrant retinoic acid signaling driven by the degenerating outer retina leads to pathological changes to the inner retina. The resulting hyperactivity of retinal ganglion cells leads to further diminution of the remaining vision in those afflicted with inherited retinal diseases. Inhibition of this pathway has led to improved visual function in murine models of retinal degeneration. This can be accomplished in humans with the FDA-approved irreversible inhibitor of aldehyde dehydrogenases, disulfiram.

开始日期2025-01-03

申办/合作机构

University of Washington

ISRCTN99747720

/ Recruiting早期临床1期IIT

Impact of Oral Disulfiram on Aldehyde Dehydrogenase (ALDH) Mediated Ocular Fibrosis in Mucous Membrane Pemphigoid (OcMMP). An experimental medicine study evaluating oral disulfiram repurposed to probe the ALDH mediated profibrotic mechanism in ocular disease (MMP-Oral-DSF)

开始日期2024-12-04

申办/合作机构

University of Birmingham

100 项与双硫仑相关的临床结果

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100 项与双硫仑相关的转化医学

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100 项与双硫仑相关的专利（医药）

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6,883

项与双硫仑相关的文献（医药）

2025-04-01·International Journal for Parasitology-Drugs and Drug Resistance

Investigation of the threonine metabolism of Echinococcus multilocularis: The threonine dehydrogenase as a potential drug target in alveolar echinococcosis

Article

作者: Lundström-Stadelmann, Britta ; Regnault, Clement ; Kaethner, Marc ; Vetter, Laura ; Schürch, Stefan ; Lochner, Martin ; Preza, Matías ; Grossenbacher, Philipp ; Ramírez, Daniel Villalobos ; Müller, Joachim ; Zumstein, Pascal ; Bartetzko, Anissa

Alveolar echinococcosis (AE) is a severe zoonotic disease caused by the metacestode stage of the fox tapeworm Echinococcus multilocularis. We recently showed that E. multilocularis metacestode vesicles scavenge large amounts of L-threonine from the culture medium. This motivated us to study the effect of L-threonine on the parasite and how it is metabolized. We established a novel metacestode vesicle growth assay with an automated readout, which showed that L-threonine treatment led to significantly increased parasite growth. In addition, L-threonine increased the formation of novel metacestode vesicles from primary parasite cell cultures in contrast to the non-proteinogenic threonine analog 3-hydroxynorvaline. Tracing of [U-¹³C]-L-threonine and metabolites in metacestode vesicles and culture medium resulted in the detection of [U-¹³C]-labeling in aminoacetone and glycine, indicating that L-threonine was metabolized by threonine dehydrogenase (TDH). EmTDH-mediated threonine metabolism in the E. multilocularis metacestode stage was further confirmed by quantitative real-time PCR, which demonstrated high expression of emtdh in in vitro cultured metacestode vesicles and also in metacestode samples obtained from infected animals. EmTDH was enzymatically active in metacestode vesicle extracts. The compounds disulfiram, myricetin, quercetin, sanguinarine, and seven quinazoline carboxamides were evaluated for their ability to inhibit recombinantly expressed EmTDH. The most potent inhibitors, albeit not very strong or highly specific, were disulfiram, myricetin and sanguinarine. These compounds were subsequently tested for activity against E. multilocularis metacestode vesicles and primary parasite cells and only sanguinarine demonstrated significant in vitro activity. However, TDH is not its only cellular target, and it is also known to be highly toxic. Our findings suggest that additional targets of sanguinarine should be explored, and that it may serve as a foundation for developing more specific compounds against the parasite. Moreover, the EmTDH assay could be a valuable high-throughput, target-based platform for discovering novel anti-echinococcal compounds.

2025-04-01·INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES

Targeting tubulin protein to combat fungal disease: Design, synthesis, and its new mechanistic insights of benzimidazole hydrazone derivatives

Article

作者: Zhou, Xiang ; Liu, Liwei ; Yang, Song ; Li, Mei ; Meng, Jiao ; Wu, Yuanyuan ; Long, Yu ; Wu, Zhibing ; Zheng, Zhicheng ; Shao, Lihui ; Li, Zhenhua

As the vital the biomacromolecule in eukaryotic cells, tubulin protein is essential for preserving cell shape, facilitating cell division, and cell viability. Tubulin has been approved as promising target for anticancer, and antifungal therapy. However, there are still many gaps in tubulin-targeted fungicidal discovery. To expand the structural diversity of benzimidazoles and achieve the distinct interaction model, a series of novel benzimidazole hydrazone derivatives were therefore synthesized. Antifungal results showed that compound A₉ was the most effective, achieving an EC₅₀ value of 2.88 μg/mL in vitro against Colletotrichum sublineola. In vivo assay, compound A₉ displayed encouraging efficacy, outperforming the reference agents ferimzone and tetramethylthiuram disulfide. Interestingly, mechanistic studies indicated that, compared with carbendazim, compound A₉ might form stronger interactions with tubulin, exemplified by the presence of multiple hydrogen bonds and π-π interactions, leading to intracellular microtubule aggregation in compound A₉-treated cells. The significantly different interactions models between A₉-tubulin and carbendazim-tubulin complexes may endow to produce the low resistance risk. Additionally, compound A₉ possessed low phytotoxicity and satisfactory ADME properties. This study not only provides a structural basis for the development of benzimidazole-based fungicides targeting tubulin but also offers new insights into the use of immunofluorescence assays in tubulin-targeting studies.

2025-03-01·BIOMATERIALS

Anti-pyroptosis biomimetic nanoplatform loading puerarin for myocardial infarction repair: From drug discovery to drug delivery

Article

作者: Zhu, Ziyang ; Wang, Kun ; Li, Yongyong ; Zhu, Ke ; Huang, Qi ; Dong, Haiqing ; Man, Fulong ; Zhao, Jun ; Huang, Li ; Li, Yan ; Liu, Yiqiong ; Yang, Zichen ; Sun, Yu ; Jun Zhao ; Zheng, Xiao

Pyroptosis is a critical pathological mechanism implicated in myocardial damage following myocardial infarction (MI), and the crosstalk between macrophages and pyroptotic cardiomyocytes presents a formidable challenge for anti-pyroptosis therapies of MI. However, as single-target pyroptosis inhibitors frequently fail to address this crosstalk, the efficacy of anti-pyroptosis treatment post-MI remains inadequate. Therefore, the exploration of more potent anti-pyroptosis approaches is imperative for improving outcomes in MI treatment, particularly in addressing the crosstalk between macrophages and pyroptotic cardiomyocytes. Here, in response to this crosstalk, we engineered an anti-pyroptosis biomimetic nanoplatform (NM@PDA@PU), employing polydopamine (PDA) nanoparticles enveloped with neutrophil membrane (NM) for targeted delivery of puerarin (PU). Notably, network pharmacology is deployed to discern the most efficacious anti-pyroptosis drug (puerarin) among the 7 primary active monomers of TCM formulations widely applied in clinical practice and reveal the effect of puerarin on the crosstalk. Additionally, targeted delivery of puerarin could disrupt the malignant crosstalk between macrophages and pyroptotic cardiomyocytes, and enhance the effect of anti-pyroptosis by not only directly inhibiting cardiomyocytes pyroptosis through NLRP3-CASP1-IL-1β/IL-18 signal pathway, but reshaping the inflammatory microenvironment by reprogramming macrophages to anti-inflammatory M2 subtype. Overall, NM@PDA@PU could enhance anti-pyroptosis effect by disrupting the crosstalk between M1 macrophages and pyroptotic cardiomyocytes to protect cardiomyocytes, ameliorate cardiac function and improve ventricular remodeling, which providing new insights for the efficient treatment of MI.

19

项与双硫仑相关的新闻（医药）

2024-11-15

·医学新视点

常用降糖、减肥药，还能用于戒酒？JAMA子刊：这两种药作用更佳

▎药明康德内容团队编辑喝酒伤身，这可不是一句空话。长期大量饮酒可导致酒精使用障碍的发生，患者对酒精使用的控制力削弱，导致生理依赖，耐受性增加以及心理、社会功能和身体的损害。相关研究显示，酒精使用障碍的终生患病率为9%，男性患病率是女性的48倍之多。心理社会支持治疗是酒精使用障碍治疗的基石，药物治疗数据比较有限，但整体也是有效的。既往动物实验发现，胰高血糖素样肽-1受体激动剂（GLP-1 RA）可减少酒精的使用，这提示GLP-1 RA或有潜力作为降低酒精危害的治疗方式。近日，JAMA Psychiatry发表一项研究，结果以简短报告的形式发布，表明GLP-1 RA中的司美格鲁肽和利拉鲁肽有助于减少酒精使用障碍患者的饮酒量，降低住院风险。截图来源：JAMA Psychiatry 这是一项观察性研究，纳入年龄16~64岁确诊为酒精使用障碍的患者22万多例，其中63.5%为男性，36.5%为女性，平均年龄40岁。中位随访8.8年间，其中6276例患者使用GLP-1 RA（主要为利拉鲁肽、艾塞那肽、度拉糖肽和司美格鲁肽），7.5万例患者接受酒精使用障碍药物（主要为disulfiram、acamprosate和纳曲酮）治疗。共有13万多（58.5%）的酒精使用障碍患者住院接受治疗。研究结果显示，接受GLP-1RA治疗的患者中，使用司美格鲁肽的患者风险最低，其中因酒精使用障碍住院风险降低了36%（aHR=0.64，95%CI：0.50~0.83），因任何物质使用障碍（指使用精神活性物质导致的任何精神障碍）住院风险降低了32%（aHR=0.68，95%CI：0.54~0.85）。其次是利拉鲁肽，其因酒精使用障碍住院风险降低了28%（aHR=0.72，95%CI：0.57~0.92），因任何物质使用障碍住院风险降低了22%（aHR=0.78，95%CI：0.64~0.97）。使用任何治疗酒精使用障碍的药物均可适当降低因酒精使用障碍住院风险和因任何物质使用障碍住院风险。 ▲使用不同药物的患者，因酒精使用障碍住院风险（A）和因任何物质使用障碍住院风险（B）差异（图片来源：参考文献[1]）此外，研究人员还发现，司美格鲁肽和利拉鲁肽可分别使因躯体症状住院风险降低22%（aHR=0.78，95%CI：0.68~0.90）和21%（aHR=0.79，95%CI：0.69~0.91），但并不能降低患者企图自杀的风险。研究第一作者兼通讯作者，来自东芬兰大学的Markku Lähteenvuo教授表示：“我们的研究结果表明，GLP-1RA不仅能够治疗糖尿病和肥胖，还可能有助于治疗酒精使用障碍和物质使用障碍，当然，这一发现仍需在随机对照试验中进一步验证”。点击文末“阅读原文/Read more”，即可访问JAMA Psychiatry官网阅读完整论文。推荐阅读欢迎投稿：学术成果、前沿进展、临床干货等主题均可，点此了解投稿详情。参考资料 [1]Lähteenvuo M, Tiihonen J, Solismaa A, Tanskanen A, Mittendorfer-Rutz E, Taipale H. Repurposing Semaglutide and Liraglutide for Alcohol Use Disorder. JAMA Psychiatry. Published online November 13, 2024. doi:10.1001/jamapsychiatry.2024.3599 [2] 王岚,王冉,王学义.酒精使用障碍的危害及风险[J].神经疾病与精神卫生，2024，22（4）：229-233. [3]University of Eastern Finland. Obesity-fighting drugs may reduce alcohol consumption in individuals with alcohol use disorder.13-Nov-2024.https://www.eurekalert.org/news-releases/1064676 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「医学新视点」微信公众号留言联系。如有其他合作需求，请联系wuxi_media@wuxiapptec.com 分享，点赞，在看，传递医学新知

临床结果AHA会议

2024-11-13

·drugs

Ozempic Could Help Curb Alcoholism

WEDNESDAY, Nov. 13, 2024 -- The blockbuster GLP-1 drug semaglutide ( Ozempic , Wegovy ) could curb drinking for people battling alcohol use disorder , helping them to avoid crises that require hospitalization, new research shows. Numerous studies had already hinted that semaglutide might act on appetite centers in the brain to suppress the urge to drink, just as it does the urge to overeat. Now, researchers in Finland say their nearly nine-year study of almost 228,000 Swedish people with alcohol use disorder who were taking semaglutide had a 36% lower odds of requiring hospitalization. Use of a second drug in the same class of GLP-1 medications, liraglutide ( Victoza ), was linked to a 28% reduction in hospitalizations, the team reported Nov. 13 in the journal JAMA Psychiatry . The study couldn't prove cause and effect, only associations. However, based on these and prior findings, the researchers say that "clinical trials are urgently needed to confirm these findings." The research was led by Dr. Markku Lähteenvuo , of the University of Eastern Finland. Besides the finding that both semaglutide and liraglutide appeared to help keep people with alcohol use disorder out of the hospital, the study also found that semaglutide, in particular, was linked to a decreased risk for suicide. The researchers also noted that the two GLP-1 drugs appeared to outperform standard anti- alcoholism medications, such as naltrexone, disulfiram and acamprostate, in lowering hospitalizations among people with alcohol use disorder, although better studies are needed to confirm that. The Finnish group noted that better treatments for alcohol use disorder are desperately needed, "because existing treatments may not be suitable for all patients." Whatever your topic of interest, subscribe to our newsletters to get the best of Drugs.com in your inbox.

临床结果

2024-08-07

·生物探索

NI丨周兆才/焦石联合团队发现靶向p97-Npl4复合物组装选择性抑制肿瘤浸润Treg细胞以发展更安全有效的抗肿瘤免疫策略

引言调节性T细胞（Treg）能够抑制针对自身抗原的异常免疫反应，防止免疫系统过度活化，对于维持机体免疫耐受和避免自身免疫性疾病至关重要。在恶性肿瘤微环境中，Treg也是介导免疫逃逸从而促进肿瘤进展，导致肿瘤免疫治疗耐药甚至疾病超进展的关键因素【1】。一系列靶向Treg的药物已处于临床前和临床研究阶段。然而，系统性靶向清除Treg细胞往往导致严重的自身免疫毒副作用，严重阻碍了靶向Treg细胞的肿瘤免疫疗法在临床上的实际应用。因此，如何在不破坏系统免疫稳态的前提下，选择性靶向肿瘤浸润Treg（TI-Treg）细胞以增强抗肿瘤免疫反应，是该领域面临的重大挑战。 p97 (VCP) 属于AAA-ATP酶家族，可与多种辅因子蛋白结合，广泛参与调控细胞内泛素化蛋白降解、DNA修复、核膜重构、细胞周期以及自噬等一系列生命过程。其中，Npl4是p97发挥功能最重要的辅因子之一。p97与Npl4形成的复合物能够识别和抽取泛素化的蛋白底物，并将其运送到蛋白酶体进行降解，对细胞内蛋白稳态维持至关重要【2】。近年来，p97作为一个抗癌药物靶点而颇受关注，其中一些靶向p97直接杀伤肿瘤细胞的候选药物已进入临床研究阶段。然而，这些p97抑制剂（如CB-5083）大多针对其ATP酶活催化中心，从而将阻断或干扰所有p97介导的细胞生物学过程，甚至包括那些在免疫细胞中尚未被阐明的功能。因此，无差别抑制p97酶活性极有可能导致副作用。 2024年8月6日，复旦大学生命科学学院周兆才教授和焦石青年研究员合作在国际学术期刊Nature Immunology在线发表题为Targeting p97-Npl4 interaction inhibits tumor Treg cell development to enhance tumor immunity【3】的研究论文，发现通过靶向p97与Npl4之间的相互作用能够选择性抑制TI-Treg细胞增强抗肿瘤免疫应答，而不破坏机体的系统免疫稳态。该研究团队于2015年报道了p97-Npl4复合物调控RIG-I抗病毒免疫应答的非经典功能【4】；并在此基础上，推断靶向p97-Npl4复合物分子界面（而不是p97酶活催化中心），有望开发特异性更强，毒副作用更小的先导化合物。在此思路指导下，研究团队首先通过AlphaScreen高通量筛选，从8,120种FDA批准的药物中筛选出能够打破p97-Npl4相互作用的化合物Thonzoniumbromide (TB)。之后的体外肿瘤细胞增殖和体内裸鼠成瘤实验均显示TB与CB-5083具有类似的抗癌效果。然而，在一系列免疫健全的小鼠肿瘤模型中，TB均展示出比CB-5083更强的抗癌活性。由此，研究团队猜测TB在体内除了像CB-5083一样直接杀伤肿瘤细胞之外，可能还参与调控了肿瘤免疫。进一步的单细胞测序分析表明TB确实重塑了肿瘤免疫微环境，显著促进了CD8+ T细胞的抗肿瘤活性。同时，T细胞过继转移实验也证实TB抗肿瘤活性很大程度上依赖于T细胞。为了明确TB靶向p97-Npl4互作发挥肿瘤免疫调控功能的具体细胞类型，研究团队根据前期解析的p97-Npl4复合物的三维结构信息【4】，构建了破坏p97与Npl4复合物组装的条件性p973A突变敲入小鼠。研究人员将p973A突变引入CD4+ T细胞之后，却发现其对肿瘤生长并无显著影响。于是，他们又对T细胞的不同亚群进行详细分析，结果发现TB处理显著抑制了肿瘤浸润Treg细胞数量，同时大大促进了Th17细胞数量。进一步，在Treg细胞中特异性敲入p973A突变体之后，肿瘤生长受到显著抑制，伴随TI-Treg数量明显降低而Th17细胞增多。值得注意的是，靶向p97-Npl4复合物组装抑制Treg细胞具有肿瘤特异性，而对外周Treg细胞和机体系统免疫稳态并无显著影响。最后，研究团队深入解析了p97-Npl4复合物通过招募E3泛素连接酶PDLIM2/5促进Stat3泛素化降解，从而调控Treg-Th17分化平衡的分子机制。总而言之，该研究发现了p97-Npl4复合物通过Stat3调控Treg-Th17细胞分化平衡的功能作用；提供了一种选择性抑制肿瘤浸润Treg而不破坏机体系统免疫稳态的肿瘤免疫治疗新策略。图1. 靶向p97-Npl4相互作用选择性抑制肿瘤浸润Treg细胞（Credit: Nature Immunology）参考文献 1. Tay, C., Tanaka, A. & Sakaguchi, S. Tumor-infiltrating regulatory T cells as targets of cancer immunotherapy. Cancer Cell 41, 450-465 (2023). 2. Skrott, Z. et al. Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4. Nature 552, 194-199 (2017). 3. Nie, P. et al. Targeting p97–Npl4 interaction inhibits tumor Treg cell development to enhance tumor immunity. Nature Immunology (2024). 4. Hao, Q. et al. A non-canonical role of the p97 complex in RIG-I antiviral signaling. EMBO J 34, 2903-2920 (2015). https://www-nature-com.libproxy1.nus.edu.sg/articles/s41590-024-01912-y 责编|探索君排版|探索君文章来源|“BioArt” End 往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文 Cell | 是什么决定了细胞的大小？热文 Nature | 2024年值得关注的七项技术热文 Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文 CRISPR技术进化史 | 24年Cell综述

免疫疗法临床研究

100 项与双硫仑相关的药物交易

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D00131	双硫仑	P03AA04 N07BB01	DB00822

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
酗酒	美国	Teva Women's Health, Inc.	1951-08-28

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
进行性纤维化间质性肺病	临床2期	日本	The University of Tokyo Hospital	2023-02-20
酒精使用障碍	临床1期	美国	The Trustees of Columbia University in The City of New York	2025-03-01

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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


DDW2024	N/A	酒精性肝疾病	-	Naltrexone	範醖夢顧獵襯鏇獵憲積(觸襯顧鏇遞觸鬱繭鏇壓) = 觸蓋膚鏇壓積壓蓋範製築襯選選夢顧蓋觸簾築 (顧廠鹹齋顧艱憲襯憲壓 )	-	2024-05-20
				Acamprosate	範醖夢顧獵襯鏇獵憲積(觸襯顧鏇遞觸鬱繭鏇壓) = 構壓餘壓繭鬱繭廠鬱衊築襯選選夢顧蓋觸簾築 (顧廠鹹齋顧艱憲襯憲壓 )
DDW2024	N/A	酒精性肝疾病	-	Naltrexone	選夢築艱鬱繭築憲憲鬱(壓願夢醖鹽壓遞選窪顧) = the rate of AUD medication discontinuation for adverse events was similar in both groups (14% vs 12%) and none were stopped due to suspected DILI 膚糧鬱淵壓構鹹廠製鹹 (鑰醖網窪獵鹽蓋糧簾鹽 ) 更多	-	2024-05-20
				Acamprosate
NCT00000278 \| NCT00580827 \| NCT02134002 (Pubmed \| Cochrane Database Syst Rev) 人工标引	临床2期	可卡因相关疾病	1,191	Disulfiram	餘襯簾餘簾觸網壓壓壓(憲醖壓醖獵構顧範憲壓): RR = 1.2 (95% CI, 0.92 ~ 1.55) 更多	积极	2024-01-05
				Placebo
NCT03363659 (CTgov)	临床2期	多形性胶质母细胞瘤	15	Temozolomide+Disulfiram+Copper Gluconate	範淵積淵憲襯餘獵醖繭(醖齋網網簾衊鏇積醖鹽) = 糧艱網夢夢廠選範鑰選鑰窪築膚膚簾廠網糧願 (製膚願鹽廠選壓淵糧觸, 壓蓋構積淵選積鏇蓋顧 ~ 願鹹選憲襯築襯築膚鏇) 更多	-	2023-09-08
NCT00721526 (CTgov)	临床4期	酗酒 \| 焦虑症	41	disulfiram+lorazepam	願蓋網壓鹽遞淵膚餘齋(夢醖膚網觸獵齋鹹醖糧) = 顧衊醖鹽繭選膚襯顧憲願鑰網襯鹽蓋廠艱簾餘 (壓廠遞顧壓獵範衊醖願, 鹹壓積蓋艱窪願夢簾顧 ~ 窪製繭遞衊餘艱膚選淵) 更多	-	2023-08-30
NCT00729300 (CTgov)	临床1/2期	可卡因相关疾病	52	placebo (Placebo)	積鏇構顧蓋鹽壓遞衊蓋(鑰簾餘壓壓廠觸製壓網) = 衊構繭製網廠衊蓋願鑰選構艱鏇網簾願簾鏇蓋 (蓋糧齋衊觸鏇網壓簾餘, 齋醖艱廠艱製餘壓積簾 ~ 憲淵鏇膚範範獵獵蓋遞) 更多	-	2023-07-19
				Disulfiram (Disulfiram Treatment Group)	積鏇構顧蓋鹽壓遞衊蓋(鑰簾餘壓壓廠觸製壓網) = 鏇獵壓鑰構襯廠憲襯醖選構艱鏇網簾願簾鏇蓋 (蓋糧齋衊觸鏇網壓簾餘, 鹽積醖構遞網廠憲鏇網 ~ 壓網顧積觸憲繭衊鏇淵)
NCT03891667 (CTgov)	临床1/2期	疲劳 \| 莱姆病	11	Disulfiram (8 Week Disulfiram)	廠鑰範壓繭窪鑰壓製顧(餘選憲餘襯夢範淵窪鹽) = 遞獵餘遞醖積膚膚壓願齋餘鹽鹽衊夢遞淵憲鹹 (遞廠積夢鬱糧製積顧願, 鹹蓋積範鹽鹽齋壓淵膚 ~ 鑰願蓋願醖遞鏇鏇夢觸) 更多	-	2023-06-05
				Disulfiram (4 Week Disulfiram)	廠鑰範壓繭窪鑰壓製顧(餘選憲餘襯夢範淵窪鹽) = 鬱製窪願積獵壓鬱網構齋餘鹽鹽衊夢遞淵憲鹹 (遞廠積夢鬱糧製積顧願, 蓋鹹鏇鑰艱範簾窪繭鑰 ~ 憲窪鏇窪壓範簾淵衊糧) 更多
NCT02678975 (Pubmed)	临床2/3期	复发性胶质母细胞瘤追加	88	Standard-of-care alkylating chemotherapy alone	蓋廠鹽艱鹽網積遞窪鬱(醖繭餘鑰鏇糧鬱顧憲獵) = 鑰憲遞糧觸齋衊鹽窪憲選繭製選製糧醖觸繭淵 (醖襯憲簾願醖襯選願選, 5.4 ~ 10.2) 更多	不佳	2023-03-01
				Standard-of-care alkylating chemotherapy plus disulfiram and copper	蓋廠鹽艱鹽網積遞窪鬱(醖繭餘鑰鏇糧鬱顧憲獵) = 衊艱鏇範顧膚顧艱築醖選繭製選製糧醖觸繭淵 (醖襯憲簾願醖襯選願選, 3.9 ~ 9.3) 更多
NCT04502589 (CTgov)	临床1/2期	酒精使用障碍 \| 酒精相关疾病	4	Perampanel Tablet (Perampanel by Itself)	齋艱獵範窪鬱鑰餘廠築(糧顧遞鏇鑰膚範淵襯製) = 鏇衊構糧觸壓選範選築築壓餘獵鹽網構選願獵 (願齋構範觸壓構壓築繭, 醖憲顧糧齋壓廠獵齋繭 ~ 鹽膚願窪窪鏇顧簾醖鹹) 更多	-	2022-10-07
				Disulfiram+Perampanel Tablet (Perapanel With Disulfiram)	齋艱獵範窪鬱鑰餘廠築(糧顧遞鏇鑰膚範淵襯製) = 窪醖簾憲網襯遞製獵簾築壓餘獵鹽網構選願獵 (願齋構範觸壓構壓築繭, 鏇網夢鏇獵壓襯夢鬱襯 ~ 獵鹽鑰餘醖遞憲糧鑰鑰) 更多
EUCTR2019-002748-25-DK (ESMO2022)	临床2期	结肠转移性腺癌	24	Irinotecan + Disulfiram + Copper	選糧鹽鑰顧餘醖鬱遞顧(廠網膚膚醖夢夢遞積築) = Fatigue was the most frequent toxicity seen in 16 pts (15 grade 2, 1 grade 3) 壓壓鹹積襯選齋餘積醖 (衊範製窪鹽淵製壓網壓 ) 更多	-	2022-09-10