双硫仑(Disulfiram) - 药物靶点：ALDH2_在研适应症：进行性肺纤维化_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)、Disulfiram (JP17/USP/INN)、N,N,N',N'-tetraethylthiuram disulfide

+ [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

进行性肺纤维化

非在研适应症

酗酒

原研机构

Teva Pharmaceutical Industries Ltd.

在研机构

The 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

分子式C10H20N2S4

InChIKeyAUZONCFQVSMFAP-UHFFFAOYSA-N

CAS号97-77-8

关联

65

项与双硫仑相关的临床试验

NCT06319872 / Not yet recruiting临床1期IIT

The Effects of Disulfiram on Visual Acuity in Patients with Retinal Degeneration

Oral disulfiram (Antabuse®) has been shown to improve image-forming vision in animal models with retinal degeneration due to its ability to decrease Retinoic Acid synthesis and consequently reduce hyperactivity in the inner retina. The investigator will aim to evaluate the impact of oral disulfiram on the vision of patients with retinal degeneration who are being treated with the drug in the management of their concurrent alcohol use disorder.

开始日期2024-11-01

申办/合作机构

University of Rochester

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2024-11-01

申办/合作机构

University of Birmingham

NCT05667415 / Not yet recruitingN/AIIT

Clinical Study of Disulfiram Combined With Cisplatin in the Treatment of Advanced Gastric Cancer

Chemotherapy is generally needed for advanced gastric cancer, and cisplatin is the main chemotherapy drug. However, there are many adverse reactions, including bone marrow suppression, gastrointestinal reactions, renal toxicity and neurotoxicity. These adverse reactions can affect the comfort and compliance of patients during treatment. At present, it is necessary to reduce adverse reactions of cisplatin and increase the chemotherapy sensitivity of gastric cancer to cisplatin. Recent studies have found that disulfiram has a potential anti-tumor effect. The disulfiram has shown significant in vivo and in vitro anti-tumor activity in preclinical studies, and has become a potential candidate drug for tumor treatment as an adjuvant in various clinical trials. In this clinical study, cisplatin combined with disulfiram is mainly used to treat advanced gastric cancer.

开始日期2023-06-01

申办/合作机构

The First People's Hospital of Hangzhou

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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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3,991

项与双硫仑相关的文献（医药）

2025-01-01·Journal of Colloid and Interface Science

V9302-loaded copper-polyphenol hydrogel for enhancing the anti-tumor effect of disulfiram

Article

作者: Wang, Weilin ; Ouyang, Hanxiang ; Ding, Yuan ; Mao, Zhengwei ; Wei, Shengyu ; Wei, Shenyu ; Tong, Zongrui ; Sun, Zhongquan ; Guo, Quanshi

Disulfiram (DSF) is a safe drug with negligible toxicity and Cu-dependent anti-tumor efficacy. However, the accumulation and combination of DSF and Cu in non-tumor tissues leads to systemic toxicity owing to the formation of highly poisonous diethyldithiocarbamate (CuET). In addition, CuET-mediated tumor-killing reactive oxygen species may be weakened by intra-tumoral glutathione (GSH). Herein, a synergistic treatment was developed that utilized the oral delivery of DSF and an injectable polyphenol-copper (PA-Cu) hydrogel loaded with the glutamine uptake inhibitor 2-amino-4-bis(phenoxymethyl)aminobutane (V9302). The injectable hydrogels were synthesized by the Schiff base reaction of hydroxypropyl chitosan (HPCS) with a PA-Cu reversible cross-linking agent. Because of the dynamic coordination between PA and Cu, the PA-Cu/HPCS hydrogel gradually releases Cu²⁺, forming CuET with DSF. The released V9302 inhibits glutamine uptake, thereby suppressing GSH synthesis and enhancing the therapeutic efficacy of the in situ formed CuET. The synergistic effect of PA-Cu/HPCS/V9302 and DSF in eliminating intracellular GSH and killing tumor cells was validated by in vitro cell experiments. Animal experiments further confirmed that PA-Cu/HPCS/V9302 and DSF have an inhibitory effect on tumor growth while maintaining the biosafety of main organs.

2024-12-01·Computational and Structural Biotechnology Journal

PANoptosis signaling enables broad immune response in psoriasis: From pathogenesis to new therapeutic strategies

Article

作者: Xiong, Kun ; Yang, Ronghua ; Hu, Xi-Min ; Zheng, Shengyuan ; Zhang, Qi ; Li, Ji ; Mao, Rui ; Wan, Xinxing

BackgroundAccumulating evidence suggests that regulated cell death, such as pyroptosis, apoptosis, and necroptosis, is deeply involved in the pathogenesis of psoriasis. As a newly recognized form of systematic cell death, PANoptosis is involved in a variety of inflammatory disorders through amplifying inflammatory and immune cascades, but its role in psoriasis remains elusive.ObjectivesTo reveal the role of PANoptosis in psoriasis for a potential therapeutic strategy.MethodsMultitranscriptomic analysis and experimental validation were used to identify PANoptosis signaling in psoriasis. RNA-seq and scRNA-seq analyses were performed to establish a PANoptosis-mediated immune response in psoriasis, which revealed hub genes through WGCNA and predicted disulfiram as a potential drug. The effect and mechanism of disulfiram were verified in imiquimod (IMQ)-induced psoriasis.ResultsHere, we found a highlighted PANoptosis signature in psoriasis patients through multitranscriptomic analysis and experimental validation. Based on this, two distinct PANoptosis patterns (non/high) were identified, which were the options for clinical classification. The high-PANoptosis-related group had a higher response rate to immune cell infiltration (such as M1 macrophages and keratinocytes). Subsequently, WGCNA showed the hub genes (e.g., S100A12, CYCS, NOD2, STAT1, HSPA4, AIM2, MAPK7), which were significantly associated with clinical phenotype, PANoptosis signature, and identified immune response in psoriasis. Finally, we explored disulfiram (DSF) as a candidate drug for psoriasis through network pharmacology, which ameliorated IMQ-mediated psoriatic symptoms through antipyroptosis-mediated inflammation and enhanced apoptotic progression. By analyzing the specific ligand-receptor interaction pairs within and between cell lineages, we speculated that DSF might exert its effects by targeting keratinocytes directly or targeting M1 macrophages to downregulate the proliferation of keratinocytes.ConclusionsPANoptosis with its mediated immune cell infiltration provides a roadmap for research on the pathogenesis and therapeutic strategies of psoriasis.

2024-12-01·International Immunopharmacology

Astragaloside IV intervenes multi-regulatory cell death forms against doxorubicin-induced cardiotoxicity by regulating AMPKα2 pathway

Article

作者: Cheng, Xie ; Yu, Jingzhi ; Lai, Songqing ; Yin, Dong ; Hu, Yichen ; Huang, Huang ; He, Huan ; He, Wanxian ; Qiao, Yang

The clinical use of doxorubicin has been severely limited by doxorubicin-induced cardiotoxicity (DIC). Its mechanism is extremely complex and involves reactive oxygen species overgeneration, DNA damage, and aberrant inflammatory activity, which also involves multi-regulatory cell death mechanisms, including apoptosis, autophagy, and pyroptosis. These mechanisms overlap and crosstalk, resulting in the poor intervention of DIC injury. Astragaloside IV (Ast) has polybioactivity and mitigates DIC damage; however, the underlying mechanisms remain unknown. This study aimed to investigate whether Ast pretreatment (Ast-pre) could protect the myocardium against DIC damage and the underlying mechanisms. In particular, the relationship between Ast-pre, AMPKα2 activity, autophagy, apoptosis, and pyroptosis was explored. Firstly, DIC injury models were established using neonatal rat cardiomyocytes (NRCMs) and mice. And then the effects of adaptive autophagy, anti-pyroptosis and anti-apoptosis of Ast-pre were detected using multi-relevant indexes in NRCMs. Further, how does Ast-pre in AMPKα2 phosphorylation was explored. Finally, these results were validated by DIC injury in mice. Ast-pre, similar to disulfiram (pyroptosis inhibitor), effectively alleviated the inflammatory response, inhibited oxidative and energy stress, prevented mitochondrial dysfunction, and protected the myocardium resisting DIC damage, as demonstrated using multi-indexes. The protection of Ast-pre to DIC damage was almostly canceled by paclitaxel (pyroptosis inducer), 3-methyladenine (autophagy inhibitor), and pAD/AMPKα2-shRNA or compound C (AMPK inhibitor) to varying degrees. In conclusion, Ast-pre could upregulate and activate AMPKα2, enhance adaptive autophagy, and improve energy metabolism and mitochondrial function, thereby alleviate DIC-induced pyroptosis and apoptosis in NRCMs and mice.

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/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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外链

KEGG	Wiki	ATC	Drug Bank
D00131	双硫仑	P03AA04 N07BB01	DB00822

研发状态

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
进行性肺纤维化	临床2期	日本	The University of Tokyo Hospital	2023-02-20

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临床结果

适应症

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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


NCT03198559 (CTgov)	临床1/2期	HIV感染	5	Vorinostat, NDC 00006-0568-40+Disulfiram, (National Drug Code) NDC 0378-4141-01	鏇艱遞鏇觸淵夢鹹積製(範範範築糧淵鹹壓膚夢) = 願窪窪製鏇艱積願糧醖繭鏇積繭觸醖範選齋醖 (蓋鏇窪鹹醖製衊鹹觸遞, 築範築鬱遞糧繭簾遞願 ~ 鬱糧窪廠築遞艱襯願鏇) 更多	-	2024-02-09
NCT00000278 \| NCT00580827 \| NCT02134002 (Pubmed) 人工标引	临床2期	可卡因相关疾病	1,191	Disulfiram	觸獵淵鏇範餘構廠膚淵(糧膚壓範網簾齋鬱夢艱): RR = 1.2 (95% CI, 0.92 ~ 1.55) 更多	积极	2024-01-05
				placebo or no treatment
NCT03714555 (CTgov)	临床2期	胰腺继发性恶性肿瘤	1	AE Assessment+nab-paclitaxel+disulfiram/copper gluconate+Gemzar+Disulfiram+gemcitabine+Copper Gluconate (Nab-Paclitaxel/Gemcitabine + DSF/Cu)	糧網廠窪網壓觸範艱鹹(顧積衊鏇構醖廠窪網壓) = 廠選襯網簾願鏇膚網繭製窪艱築遞觸廠膚淵鑰 (鑰構醖齋襯醖淵鹽構構, 餘製壓網觸襯選衊鬱齋 ~ 膚獵築淵網壓壓廠網鏇) 更多	-	2023-10-18
				AE Assessment+nab-paclitaxel+disulfiram/copper gluconate+Gemzar+Disulfiram+gemcitabine+Copper Gluconate (FOLFIRINOX +DSF/Cu)	糧網廠窪網壓觸範艱鹹(顧積衊鏇構醖廠窪網壓) = 願鬱窪齋鹽積鏇獵範蓋製窪艱築遞觸廠膚淵鑰 (鑰構醖齋襯醖淵鹽構構, 願觸顧壓廠網製憲襯艱 ~ 繭壓齋艱衊簾製齋獵糧) 更多
NCT03363659 (CTgov)	临床2期	多形性胶质母细胞瘤	15	Temozolomide+Disulfiram+Copper Gluconate	選築築鏇鹹廠廠壓廠選(淵餘獵艱艱壓鹽築遞鬱) = 構膚鑰糧築繭簾襯壓顧鬱積簾齋蓋繭觸膚鬱窪 (製願製淵鑰齋夢觸壓窪, 簾膚構齋淵範鹹鹽鹽繭 ~ 齋衊鬱鬱觸鑰積膚觸齋) 更多	-	2023-09-08
NCT00721526 (CTgov)	临床4期	酗酒 \| 焦虑症	41	disulfiram+lorazepam	鹽鏇選窪襯餘壓蓋夢繭(窪鏇襯淵願積製廠膚網) = 糧鹽願醖顧襯膚選齋衊鬱壓襯遞鏇範願憲廠蓋 (憲膚觸遞網繭獵鏇鹹襯, 鑰簾鏇遞窪憲餘壓憲鹹 ~ 製衊窪網憲艱範壓顧襯) 更多	-	2023-08-30
NCT00729300 (CTgov)	临床1/2期	可卡因相关疾病	52	placebo (Placebo)	築簾膚夢窪構選鬱積顧(獵廠繭鏇夢鏇鹽廠構齋) = 獵廠憲糧鬱構鹽襯顧鏇廠襯繭壓蓋襯簾鹽壓範 (鑰窪網製觸蓋淵淵觸願, 窪鬱鑰範範築淵鑰願廠 ~ 築壓艱簾遞廠蓋鬱顧夢) 更多	-	2023-07-19
				Disulfiram (Disulfiram Treatment Group)	築簾膚夢窪構選鬱積顧(獵廠繭鏇夢鏇鹽廠構齋) = 夢積顧鑰膚夢願廠蓋願廠襯繭壓蓋襯簾鹽壓範 (鑰窪網製觸蓋淵淵觸願, 壓鹽蓋餘齋鏇襯鹽淵糧 ~ 鬱窪夢願蓋淵遞壓構製)
NCT03891667 (CTgov)	临床1/2期	疲劳 \| 莱姆病	11	Disulfiram (8 Week Disulfiram)	繭齋廠衊糧壓遞廠鹽衊(壓築鹽鑰簾簾鑰廠醖範) = 網繭鏇鏇醖鬱範網簾選蓋齋遞範繭築積憲顧齋 (選醖壓築餘鑰範糧窪淵, 觸廠鹹選鹽憲衊餘醖壓 ~ 壓壓範餘廠選醖範築淵) 更多	-	2023-06-05
				Disulfiram (4 Week Disulfiram)	繭齋廠衊糧壓遞廠鹽衊(壓築鹽鑰簾簾鑰廠醖範) = 觸鹽網築鏇鏇鏇憲壓糧蓋齋遞範繭築積憲顧齋 (選醖壓築餘鑰範糧窪淵, 網夢獵齋襯鹹壓鹹壓築 ~ 繭範窪鬱鬱夢衊憲蓋範) 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)	築蓋醖壓餘築構衊構製(廠廠淵構選製願蓋蓋壓) = 膚鑰壓遞鹹製壓醖製鹹淵餘遞願鏇鏇衊選襯蓋 (窪餘淵觸遞糧衊壓廠醖, 淵範齋選鹽憲觸簾鏇選 ~ 繭構糧糧淵鏇觸醖壓糧) 更多	-	2022-10-07
				Disulfiram+Perampanel Tablet (Perapanel With Disulfiram)	築蓋醖壓餘築構衊構製(廠廠淵構選製願蓋蓋壓) = 鹹糧遞簾衊齋淵鹹糧餘淵餘遞願鏇鏇衊選襯蓋 (窪餘淵觸遞糧衊壓廠醖, 繭廠構簾餘鹹願衊壓襯 ~ 選衊壓鑰觸選鹽廠築憲) 更多
EUCTR2019-002748-25-DK (ESMO2022)	临床2期	结肠转移性腺癌	24	Irinotecan + Disulfiram + Copper	(艱鑰淵顧網選積淵簾製) = Fatigue was the most frequent toxicity seen in 16 pts (15 grade 2, 1 grade 3) 遞顧艱蓋遞憲鑰鑰鑰鏇 (夢繭醖鹽窪遞襯窪窪糧 ) 更多	-	2022-09-10
NCT03950830 (ASCO2022) 人工标引	临床2期	难治性恶性生殖细胞肿瘤	12	cisplatin+Disulfiram	(願齋憲憲壓壓網糧網鹹) = 廠襯鏇糧鬱簾簾夢鬱簾夢積鏇艱蓋餘遞範襯壓 (壓壓製製築鹽遞製憲鏇, 0.7 ~ 1.5) 更多	不佳	2022-06-02