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更新于：2026-01-03
Edaravone/Dexborneol
依达拉奉右莰醇
更新于：2026-01-03
概要
基本信息
原研机构 |
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 中国 (2020-07-29), |
最高研发阶段(中国)批准上市 |
特殊审评突破性疗法 (美国)、突破性疗法 (中国)、特殊审批 (中国) |
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结构/序列
分子式C10H18O |
InChIKeyDTGKSKDOIYIVQL-QXFUBDJGSA-N |
CAS号464-45-9 |
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关联
50
项与 依达拉奉右莰醇 相关的临床试验NCT07091994
A Prospective, Multicentre, Randomized Controlled Trial of Edaravone Dexborneol in Acute Ischemic Stroke With Active Malignancy
NCT06674460
Treatment of Acute Ischemic Stroke With Edaravone Dexborneol Sublingual Tablets in Small Vessel Disease: A Randomized, Double-Blind, Placebo-Controlled Study
ChiCTR2500109257
Exploratory Study on Sublingual Edaravone Dexborneol in Improving the Effective Reperfusion Rate of Large Vessel Occlusion in Acute Ischemic Stroke
100 项与 依达拉奉右莰醇 相关的临床结果
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100 项与 依达拉奉右莰醇 相关的转化医学
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100 项与 依达拉奉右莰醇 相关的专利（医药）
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57
项与 依达拉奉右莰醇 相关的文献（医药）2025-12-01NEUROCHEMICAL RESEARCH
A Novel Mutation in Exon 10 of the NOTCH3 Gene in Human Cerebral Microvascular Endothelial Cells Induces CADASIL-Like Pathology and the Therapeutic Effect of Edaravone Dexborneol on Hereditary and Non-hereditary Cerebral Small Vessel Disease
Article
作者: Fang, Qi ; Ma, Yu-Qi ; Xu, Yuan ; Du, Huaping ; Zhang, Hui-Ling ; Zhang, Jia-Ying ; Sun, Li ; Liu, Yuan
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations in the NOTCH3 gene. We reported a novel mutation in the exon 10 of the NOTCH3 gene (NOTCH3 p.C533S) in a Chinese family with CADASIL. This study aimed to identify NOTCH3 p.C533S-induced CADASIL-like pathogenic mechanisms and to observe the therapeutic effects of edaravone dexborneol (EDB) on CADASIL, which is clinically used for acute ischemic stroke in China. We generated human cerebral microvascular endothelial cells (hCMEC) carrying NOTCH3 p.C533S mutation (NOTCH3 p.C533S hCMECs) using CRISPR/Cas9-mediated NOTCH3 knock-in with a donor plasmid. The NOTCH3 p.C533S hCMECs exhibited CADASIL-like pathology, characterized by a loss of tight junctions, diminished proliferative and migratory capacities, and an upregulation in pro-inflammatory cytokines. The NOTCH3 p.C533S hCMECs induced neuronal ferroptosis, pro-inflammatory activation of astrocytes and microglia with accumulated lipid droplets and oligodendrocytes damage. Mechanistically, utilizing metabolomics and multiple biochemical approaches, we identified that downregulated vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) pathway contribute to the reduced activities of glutathione reductase (GR) and argininosuccinate synthase 1 (ASS1), resulting in reduced glutathione and arginine levels, as well as NOTCH3 p.C533S hCMECs degeneration. EDB treatment could partially reverse CADASIL- and non-hereditary cerebral small vessel disease-like pathology by restoring the VEGF/VEGFR-regulated ASS1 and GR. The NOTCH3 p.C533S mutation causes hCMEC degeneration associated with VEGF/VEGFR pathway impairment-mediated cellular metabolic reprogramming and inflammation. The progression of CADASIL is intensified by a cascade of interactions between compromised hCMEC and surrounding neurons and glial cells. EDB may offer a promising therapeutic approach for cerebral small vessel disease including CADASIL and non-hereditary one.
2025-12-01Journal of Stroke & Cerebrovascular Diseases
Efficacy and safety of edaravone dexborneol in acute large vessel occlusion patients with successful recanalization after endovascular treatment
Article
作者: Wang, Liyuan ; Xu, Tianyi ; Yun, Chunhua ; Duan, Zhenhui ; Zhao, Zhenqiang ; Chen, Xiangliang ; Liu, Wenhua ; Li, Wei ; Yang, Meipin ; Xiong, Yunyun ; Wang, Kangmeng ; Huang, Kailai
BACKGROUND AND PURPOSE:
Edaravone dexborneol (ED) is a novel cytoprotective drug for treating acute ischemic stroke (AIS) with synergistic antioxidant and anti-inflammatory effects. This study aimed to assess the efficacy and safety of ED in acute large vessel occlusion (LVO) patients with successful recanalization after endovascular treatment (EVT).
METHODS:
Data from three comprehensive stroke centers of consecutive AIS-LVO patients treated with EVT were retrospectively included in this study. Patients were divided into ED and non-ED groups. The primary efficacy outcome was the shift of the modified Rankin Scale (mRS) score at 90 days. The secondary efficacy outcomes included functional independence (mRS score 0-2) and excellent outcome (mRS 0-1) at 90 days. Safety outcomes included mortality within 90 days and symptomatic intracranial hemorrhage (sICH) within 48 h.
RESULTS:
A total of 231 patients with successful recanalization after EVT were included in the analysis, of whom 84 (36.4 %) were in the ED group and 147 (63.6 %) were in the non-ED group. After adjustment for potential confounders, ED was associated with a favorable shift in the 90-day mRS score (common adjusted odds ratio [aOR], 2.09; 95 % confidence interval [CI], 1.05-4.14; P = 0.035). The proportions of sICH (4.76 % vs. 7.41 %; aOR, 0.44; 95 % CI, 0.10-2.02; P = 0.290) and 90-day mortality (6.41 % vs. 8.8 %; aOR, 0.37; 95 %CI, 0.06-2.31; P = 0.280) were numerically lower in the ED group than in the non-ED group, but these differences were not statistically significant.
CONCLUSIONS:
Among AIS-LVO patients with successful recanalization after EVT, ED may be associated with an improved functional outcome without an increased risk of sICH and mortality.
2025-12-01EUROPEAN JOURNAL OF PHARMACOLOGY
Edaravone dexborneol attenuates cerebral Ischemia–Reperfusion injury via cGAS–STING inhibition, STX17-Mediated autophagic flux restoration, and NLRP3 inflammasome suppression
Article
作者: Pang, Meng ; Hou, Shuai ; Wang, Weihua ; Wang, Yanqiang ; Yang, Hang ; Zhang, Yifeng ; Wang, Xiaolu
Acute ischemic stroke (AIS) is a leading cause of death and disability worldwide. Although intravenous thrombolysis and mechanical thrombectomy improve vascular recanalization, reperfusion often induces secondary cerebral ischemia-reperfusion injury (CI/RI), which limits therapeutic efficacy. Edaravone dexborneol (EDB) has been validated in large phase II and III clinical trials to be safe and effective in improving 90-day functional outcomes in AIS patients. However, the precise mechanisms by which EDB confers neuroprotection during reperfusion remain unclear. In this study, we employed a rat middle cerebral artery occlusion/reperfusion (MCAO/R) model and oxygen-glucose deprivation/reoxygenation (OGD/R) microglial model to investigate the mechanistic effects of EDB. We found that EDB treatment markedly reduced infarct volume, cerebral edema, and neurological deficits, while preserving mitochondrial membrane potential and alleviating neuronal apoptosis. Mechanistically, EDB inhibited the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway, which acted as an upstream regulatory hub. This inhibition promoted Syntaxin 17 (STX17)-mediated autophagosome-lysosome fusion and restored autophagic flux, while simultaneously suppressing NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and pyroptosis-related gene expression. Rescue experiments with the STING agonist 2'3'-cyclic GMP-AMP (2'3'-cGAMP) reversed these protective effects, confirming the central role of the cGAS-STING axis. In conclusion, this study identifies a novel mechanism whereby EDB alleviates CI/RI through dual regulation of autophagy and inflammation via inhibition of cGAS-STING signaling. These findings not only provide new mechanistic insights but also support the clinical potential of EDB as an adjunctive therapy for AIS reperfusion injury.
100 项与 依达拉奉右莰醇 相关的药物交易
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外链
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研发状态
批准上市
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10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 雄激素不敏感综合征 | 临床3期 | - | 2023-12-28 | |
| 认知功能障碍 | 临床2期 | 中国 | 2024-04-08 | |
| 脑出血 | 临床2期 | - | 2021-03-01 | |
| 高血压脑病 | 临床2期 | - | 2021-03-01 | |
| 颅内出血 | 临床1期 | 美国 | 2018-10-25 | |
| 肌萎缩侧索硬化 | 临床申请 | 美国 | - | |
| 认知障碍 | 临床申请 | 美国 | - | |
| 阿尔茨海默症 | 临床前 | 中国 | 2025-06-21 | |
| 神经炎症 | 临床前 | 中国 | 2024-03-15 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | - | 獵淵鏇繭遞選廠夢鏇襯(衊網鹽觸鏇鹹鏇獵網網): unadjusted odds ratio = 1.37 (95% CI, 0.76 ~ 2.44), P-Value = 0.29 | 不佳 | 2025-03-10 | |||
Placebo | |||||||
N/A | - | 獵餘衊鹽鑰衊鏇簾糧願(餘糧願壓夢餘積鑰觸積) = 醖鏇廠鏇廠繭鏇憲製壓 製製憲獵膚範齋積壓鏇 (簾醖願壓簾製憲壓壓選 ) | 积极 | 2025-01-30 | |||
No Edaravone Dexborneol | 獵餘衊鹽鑰衊鏇簾糧願(餘糧願壓夢餘積鑰觸積) = 艱觸積範壓鑰餘願鏇襯 製製憲獵膚範齋積壓鏇 (簾醖願壓簾製憲壓壓選 ) | ||||||
N/A | 4,684 | 憲夢獵膚艱齋築鹹築蓋(醖壓醖鹹膚鑰鹽顧壓鑰): adjusted common odds ratio = 1.02 (95% CI, 1.02 ~ 1.64), P-Value = 1.30 | 积极 | 2025-01-30 | |||
No Edaravone Dexborneol | |||||||
临床3期 | 914 | 窪夢夢構鹹蓋鹹遞獵網(顧鏇廠願範夢構觸醖糧) = 製積繭醖顧餘醖餘糧遞 構積膚壓範製壓醖廠蓋 (夢窪鑰襯壓獵積製築簾 ) 更多 | 积极 | 2024-02-19 | |||
Placebo | 窪夢夢構鹹蓋鹹遞獵網(顧鏇廠願範夢構觸醖糧) = 蓋鬱選獵顧衊遞鏇構窪 構積膚壓範製壓醖廠蓋 (夢窪鑰襯壓獵積製築簾 ) 更多 | ||||||
临床3期 | - | 憲廠鏇簾餘願淵淵壓網(齋淵範衊願範顧鑰觸鹽) = 初步分析显示，相对于安慰剂， 先必新舌下片显著改善AIS患者治疗后神经功能恢复及独立生活能力，达到预期疗效终点 網網襯構膚築夢繭鹽選 (餘顧廠築願簾衊築鏇醖 ) 达到 | 积极 | 2022-12-01 | |||
Placebo | |||||||
NEWS 人工标引  | N/A | 94 | 積積鏇製憲網餘構製餘(糧膚壓衊襯選選鑰願製) = 範網齋簾糧醖鏇衊願鏇 壓憲壓夢廠醖壓願餘鏇 (鏇憲餘願觸鑰範積網糧, 4.11) 更多 | 积极 | 2022-05-06 | ||
積積鏇製憲網餘構製餘(糧膚壓衊襯選選鑰願製) = 齋積壓齋糧鏇憲衊艱鹹 壓憲壓夢廠醖壓願餘鏇 (鏇憲餘願觸鑰範積網糧, 2.15) 更多 | |||||||
临床3期 | 1,165 | Edaravone+Dexborneol | 製網憲窪鏇蓋遞艱鏇廠(夢範鬱鑰範窪鹹夢襯顧) = 願艱壓齋鏇鏇築膚鬱壓 壓鹹遞繭顧艱鏇艱窪夢 (積窪選壓鏇遞網顧願構 ) 更多 | 优效 | 2021-03-01 | ||
製網憲窪鏇蓋遞艱鏇廠(夢範鬱鑰範窪鹹夢襯顧) = 醖艱夢鏇簾積網鏇壓網 壓鹹遞繭顧艱鏇艱窪夢 (積窪選壓鏇遞網顧願構 ) | |||||||
临床2期 | 385 | 構範積網夢鏇膚遞構遞(襯構夢鹹繭憲鹽鹽夢醖): P-Value = 0.6799 更多 | 积极 | 2019-04-22 | |||
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