Post-stroke cognitive impairment (PSCI) refers to a clinical syndrome characterized by cognitive impairment that occurs after a stroke event and persists for at least 24 weeks. Due to the early recovery of conditions such as delirium and transient cognitive impairment after stroke, the diagnosis of PSCI often requires cognitive assessment at 12 to 24 weeks post-stroke to determine the severity of cognitive impairment. It can be classified according to the severity of cognitive impairment as post-stroke cognitive impairment no dementia (PSCIND) and post-stroke dementia (PSD). Recent large international cohort studies have reported an incidence rate of PSCI ranging from 24% to 53.4%, and patients with PSCI have a significantly higher mortality rate compared to those without cognitive impairment. Guidelines such as American Heart Association/American Society of Anesthesiologists (AHA/ASA) and the Chinese "Expert Consensus on the Management of Post-Stroke Cognitive Impairment" propose integrating cognitive impairment and stroke intervention strategies. Early comprehensive intervention and treatment for high-risk individuals after stroke, aiming to delay or prevent the progression from PSCIND to PSD, are the primary goals in the current treatment of PSCI. However, there is currently a lack of large randomized controlled trials (RCTs) for PSCI, and research is still needed to determine whether cognitive-enhancing drugs can reduce the risk of PSCI occurrence and improve outcomes and prognosis for PSCI patients. A randomized, double-blind, multicenter clinical study involving 281 non-dementia vascular cognitive impairment (VCI) patients showed that the overall cognitive scores of patients treated with donepezil for 24 weeks significantly improved compared to the placebo group.
The aim of this study is to evaluate the effectiveness of donepezil in the treatment of post-stroke cognitive impairment. It will be a multicenter, randomized, double-blind, placebo-controlled trial with a 48-week treatment duration. The study will observe the difference in PSCI incidence rate between the donepezil treatment group and the conventional stroke treatment group at 24 weeks and evaluate the improvement in post-stroke cognitive impairment after 6 months of donepezil treatment compared to conventional treatment.
This study will be conducted in two stages: the first stage (0-24 weeks) aims to assess whether donepezil can reduce the risk of PSCI occurrence and will be a multicenter, randomized, double-blind, placebo-controlled study. The second stage (24-48 weeks) aims to evaluate whether donepezil can improve the prognosis of PSCI patients and will also be a multicenter, randomized, double-blind, placebo-controlled study.

开始日期2024-04-01

申办/合作机构

复旦大学

NCT04675450

/ Withdrawn临床2期

A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Multiple Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Efficacy of n-Butylphthalide (NBP) Softgel Capsules Administered to Patients With Metastatic Breast Cancer to Prevent Nab-paclitaxel Induced Toxic Neuropathy

Phase 2, randomized, double-blind, Placebo-Controlled, Multiple Dose Study for the treatment of Patients with Metastatic Breast Cancer.

开始日期2023-06-30

申办/合作机构

Conjupro Biotherapeutics, Inc.

[+1]

ChiCTR2100053112

/ Recruiting临床4期IIT

DL-3-n-butylphthalide Therapy for Cerebral Hypoperfusion in Unilateral Internal Carotid System Stenosis (BUTCH): A Clinical Multiple-center Study

开始日期2021-12-01

申办/合作机构-

100 项与左旋丁苯酞相关的临床结果

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100 项与左旋丁苯酞相关的转化医学

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100 项与左旋丁苯酞相关的专利（医药）

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项与左旋丁苯酞相关的文献（医药）

2025-05-01·Phytochemistry

Five racemic phthalides from the aerial parts of Lycopodiastrum casuarinoides and their neuroprotective activities

Article

作者: Liu, Lin ; Chen, Xi ; Liu, Xue-Jin ; Liu, Ren ; Huang, Chao-Hui ; Tan, Gui-Shan ; Liu, Yang ; Min, Shan-Xue ; Hu, Hui-Ling

Five racemic phthalides (1-5), including four undescribed phthalides monomers [(+)-1, (+)-2, (-)-2 and (-)-3], four undescribed phthalide dimers [(+)-4, (-)-4, (+)-5 and (-)-5], together with two known compounds [(-)-1 and (+)-3], were isolated from the aerial parts of Lycopodistrum casuarinoides. Their chemical structures were delineated by extensive spectroscopic data (UV, 1D/2D NMR, HRESIMS), in combination with the comparison of the experimental and calculated electronic circular dichroism spectra, calculated spin-spin coupling constants, and calculated NMR. All compounds were reported from Lycopodiaceae family for the first time. In addition, all isolates were tested for their neuroprotective effects on HT-22 cell injury induced by glutamate. Interestingly, among the five racemic phthalides, only the homologous dimers [(±)-5] displayed significant differences in neuroprotective effects, and (-)-5 exhibited the best neuroprotective activity against glutamate-induced HT-22 cells damage, with 29.3% increase rate in cell survival at 5 μM concentration. The neuroprotective effect of (-)-5 at different concentrations is equivalent to that of the positive control drug D/L-3-n-butylphthalide (racemic NBP). Furthermore, the biological evaluation revealed that (-)-5 could ameliorate glutamate-induced neuronal cell death via the Bax/Bcl-2 anti-apoptotic pathway.

2025-03-01·Neurotherapeutics

Spatial metabolic analysis of the regulatory effects of DL-3-n-butylphthalide in a cerebral ischemia-reperfusion mouse model

Article

作者: Sun, Weiping ; Deng, Jianwen ; Wang, Zhaoxia ; Huang, Yining ; Jin, Haiqiang ; Liu, Ran ; Jia, Jingjing ; Shen, Zhiyuan ; Peng, Qing ; Lu, Yuxuan

DL-3-n-butylphthalide (NBP) exhibits promising pharmacological efficacy against ischemia-reperfusion injury, but its protective effects may involve many mechanisms that are yet to be fully understood. This study aimed to profile the metabolic alterations induced by NBP during the process of ischemia-reperfusion using spatial metabolomics. Our study found that NBP could significantly reduce the ischemic area and restore physical function by potentially modulating pathways of the citrate cycle, pyruvate metabolism, autophagy, and unsaturated fatty acid biosynthesis. During the process of ischemia-reperfusion, NBP played a therapeutic role in improving energy supply, decreasing autophagy, and improving unsaturated fatty acid biosynthesis. Subsequent studies confirmed improvements in relevant indices of mitochondrial morphology, autophagy, and ferroptosis after treatment with NBP. These findings shed light on novel mechanisms underlying the efficacy of NBP in treating cerebral ischemia/reperfusion injury associated with ischemic stroke.

2025-03-01·Epilepsy & Behavior

Butylphthalide may inhibit blood–brain barrier disruption through complement-related pathways to alleviate cognitive impairment in epileptic mice

Article

作者: Xiao, Yuqing ; Jin, Xing ; Zhuang, Weihao ; Zhao, Linqian ; Liu, Qichang ; Chen, Shihao ; Xu, Huiqin

BACKGROUNDTemporal lobe epilepsy is often accompanied by comorbid symptoms such as anxiety, depression, and cognitive dysfunction. Research indicates a close relationship between blood-brain barrier (BBB) impairment and these symptoms. DL-3n-butylphthalide (NBP) has been reported to protect the BBB, but the molecular mechanisms by which NBP protects the BBB in epilepsy models remain unclear. This study investigated the protective effects of NBP on the BBB in epileptic mice to alleviate the comorbid symptoms associated with epilepsy.METHODSWe utilized Mendelian randomization to explore the association between VEGFA and epilepsy. In the animal experiments, adult male C57BL/6 mice were used to establish a KA-induced epilepsy model, receiving daily intraperitoneal injections of NBP for 30 days. After this period, behavioral experiments and Western blot analyses were conducted to assess whether the comorbid symptoms of epilepsy and BBB disruption were alleviated. Subsequently, RNA sequencing was performed to analyze potential signaling pathways involved in the pharmacological effects of NBP.RESULTSElevated circulating levels of VEGFA may be a risk factor for the onset of epilepsy. Animal experiments demonstrated that NBP treatment improved BBB disruption in KA-induced epileptic mice and alleviated depressive and anxious behaviors, as well as cognitive impairments. RNA sequencing results suggest that the pharmacological effects of NBP may be mediated through the inhibition of complement and coagulation cascades.CONCLUSIONNBP can protect the integrity of the BBB in KA-induced epileptic mice, inhibiting depression, anxiety behaviors, and cognitive dysfunction. This pharmacological effect may be associated with pathways involving complement and coagulation cascades.

项与左旋丁苯酞相关的新闻（医药）

2024-12-11

·石药集团

一项丁苯酞可改善卒中后失语的研究结果发布

导读 2024年11月22日，河北医科大学第一医院刘晓云教授团队的最新研究结果“Efficacy and safety of DL-3-N-butylphthalide in the treatment of ischemic poststroke aphasia: A randomized clinical trial”在《Annals Of Clinical And Translational Neurology》（IF=4.4）杂志上发表。研究结果表明：丁苯酞软胶囊序贯治疗6个月能够显著提高卒中后失语（PSA）患者的失语商（AQ），回归分析显示丁苯酞软胶囊序贯治疗与AQ的改善独立相关，且安全性良好。这一改善可能与丁苯酞软胶囊提高单胺类神经递质水平相关。研究背景卒中后失语症（PSA）每年影响全球约450万卒中患者，并且导致卒中后抑郁和痴呆患病率升高。目前，PSA的治疗方法是行为干预（以言语语言疗法为主），其有效性已被大量随机对照试验和荟萃分析证实。然而在高卒中患病率的农村地区和低收入人群中康复资源匮乏，因此很难大规模实施行为干预。许多研究表明，药物治疗已经成为治疗PSA的替代或补充疗法。药物治疗PSA主要是利用神经递质活性促进适应性神经可塑性和神经网络。丁苯酞（NBP）是国内目前治疗脑梗死的常用药物。NBP改善了未接受再灌注治疗的脑卒中患者、接受静脉溶栓治疗，以及接受血管内治疗的脑卒中患者90天预后，且不增加不良事件的发生率。NBP还可以通过改善线粒体动力学、抑制神经炎症和氧化应激改善脑血管病患者的认知功能和自理能力。本研究旨在探究NBP序贯治疗是否能够改善急性缺血性卒中后失语患者的语言能力及其潜在机制。研究方法该研究是一项单中心、随机、双盲研究，纳入标准为：年龄≥18岁；因急性脑梗死入院，并伴有任何类型的急性失语，WAB-AQ评分<93.7；病情稳定，保持清醒警觉状态至少30分钟，听力和视力正常或矫正。排除标准如下：既往痴呆；并发进行性神经障碍；头部损伤；神经外科手术；入院时临床诊断为抑郁症；不能用中文（普通话）交流；同时参与其他干预试验。所有患者住院期间均给予NBP注射液（100 mL/瓶，每日2次），疗程为10 ~ 14 d，并记录患者的既往病史、肝肾功能、血脂水平、合并用药和并发症。出院时随机分为NBP组和安慰剂组。NBP组服用NBP软胶囊（0.2g/次，3次/天），安慰剂组服用NBP模拟软胶囊（0.2g/次，3次/天），连续服药6个月。研究结果该研究于2021年7月至2022年8月在河北医科大学第二医院进行，最终118名患者纳入分析，NBP组和安慰剂组分别有61例和57例患者。出院后随访数据（图1）显示，两组之间出院6个月时的AQ改善率差异具有统计学意义（NBP组0.450±0.231 vs.对照组0.310 ±0.271, p=0.003）。并且各组在6个月随访时的mRS评分差异有统计学意义(NBP组[2 (1-3)] vs.安慰剂组[2 (1.5-3)], p=0.037）。图1. NBP组与安慰剂组预后比较对于出院6个月随访时的AQ值，NBP组较安慰剂组表现出升高趋势（图2），mRS评分的变化趋势图如图3所示。NBP组患者的语言评估各项得分的改善程度也高于安慰剂组（图4）。图2. NBP组和安慰剂组AQ随时间变化的折线图图3. NBP组与安慰剂组mRS随时间变化的折线图图4. NBP组和安慰剂组语言评估各项得分的改善以(AQ4-AQ1)/(100-AQ1)为因变量，纳入分组、年龄、教育程度、高血压、糖尿病、既往卒中、mRS1进行回归分析，结果显示NBP治疗与6个月AQ改善独立相关（MD=0.117, 95% CI: 0.031-0.203, p=0.008）（图5）。此外，NBP治疗与6个月时无法独立行走（mRS≥3）呈负相关（OR = 0.279, 95% CI: 0.099-0.786, p=0.016）（图6）。图5. 与6个月AQ恢复程度相关变量的线性回归分析图6. 急性脑梗死后6个月时mRS≥3的相关变量通过收集56例受试者的血浆样本：NBP组27例，安慰剂组29例，比较两组出院时和随访1个月时血浆中神经递质的变化。酪氨酸（Tyr, p=0.043）和5-羟色氨酸（5-HT, p=0.041）的差异有统计学意义（图7）。其中治疗后NBP组3-羟酪胺（DA, p=0.014）和去甲肾上腺素（NE, p=0.042）水平显著升高，安慰剂组在治疗前后无显著变化(DA, p=0.850；NE, p=0.838)。图7. PSA患者外周血神经递质变化的比较研究结论 NBP软胶囊序贯治疗可以改善AIS后失语患者6个月时的AQ和mRS评分，且安全性良好。潜在作用机制可能是NBP胶囊增加了单胺类神经递质水平，促进了神经功能的可塑性。【声明】本新闻旨在旨在为医疗卫生专业人士传递更多医学信息。发布的内容，不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议。

临床结果临床研究

100 项与左旋丁苯酞相关的药物交易

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研发状态

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适应症	最高研发状态	国家/地区	公司	日期
转移性乳腺癌	临床2期	-	Conjupro Biotherapeutics, Inc.	2023-06-30
转移性乳腺癌	临床2期	-	石药集团恩必普药业有限公司	2023-06-30
周围神经系统疾病	临床2期	-	Conjupro Biotherapeutics, Inc.	2023-06-30
周围神经系统疾病	临床2期	-	石药集团恩必普药业有限公司	2023-06-30
阿尔茨海默症	临床前	中国	首都医科大学宣武医院	2023-06-16
急性缺血性卒中	临床前	美国	石药集团恩必普药业有限公司	2018-02-28
脑卒中	临床前	中国	石药集团中奇制药技术（石家庄）有限公司	2005-02-17

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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


Pubmed 人工标引	N/A	失语	118	DL-3-N-butylphthalide (NBP) soft capsules	糧齋製鏇網鬱網鑰選觸(積鏇膚餘襯襯廠獵窪築): Difference (Mean) = 0.106 (95% CI, 0.018 ~ 0.195), P-Value = 0.003 更多	积极	2024-11-22
				Placebo