Edaravone (MCI-186)

别名: MCI-186; NCI-C03952; MCI 186; NSC 12; MCI186; Radicut; trade name: Radicava; Methylphenylpyrazolone; Norantipyrine; Norphenazone; Phenylmethylpyrazolone; Arone 依达拉奉; 吡唑啉酮; 1-苯基-3-甲基-5-吡唑啉酮; 3-甲基-1-苯基-2-吡唑啉-5-酮; 1-苯基-3-甲基-5-吡唑酮; 3-甲基-1-苯基-5-吡唑啉酮; Adaravone 艾达拉丰
目录号: V2065 纯度: ≥98%
Edaravone(原名Radicut;MCI-186;NCI-C03952;NSC 12;Norantipyrine;Norphenazone;商品名:Radicava)是一种新型有效的自由基清除剂,已在临床上用于减少缺血性中风后的神经元损伤。
Edaravone (MCI-186) CAS号: 89-25-8
产品类别: MMP
产品仅用于科学研究,不针对患者销售
规格 价格 库存 数量
10 mM * 1 mL in DMSO
1g
5g
10g
25g
100g
Other Sizes

Other Forms of Edaravone (MCI-186):

  • 依达拉奉 d5
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InvivoChem产品被CNS等顶刊论文引用
纯度/质量控制文件

纯度: ≥98%

产品描述
Edaravone(以前称为Radicut;MCI-186;NCI-C03952;NSC 12;Norantipyrine;Norphenazone;商品名:Radicava)是一种新型有效的自由基清除剂,已在临床上用于减少缺血性中风后的神经元损伤。 2017年5月,依达拉奉被FDA批准用于治疗肌萎缩侧索硬化症(ALS)患者。在用组织纤溶酶原激活剂治疗的大鼠中,依达拉奉可抑制 MMP-9 相关的脑出血。它于2017年5月5日获得FDA批准用于治疗肌萎缩侧索硬化症(ALS)。依达拉奉 (Edaravone) 减少谷氨酸引起的细胞凋亡和坏死。依达拉奉 (500 μM) 预处理可将这些变化逆转至大约正常水平。
生物活性&实验参考方法
靶点
MMP-9-related brain hemorrhage
体外研究 (In Vitro)
依达拉奉对谷氨酸毒性具有治疗和预防作用。依达拉奉预处理降低了谷氨酸对 SGN 的毒性。依达拉奉可减少谷氨酸引起的坏死和细胞凋亡。通过 500 μM 依达拉奉预处理,这些改变恢复到接近正常水平。 Edaravone 对谷氨酸诱导的 SGN 细胞凋亡的保护作用与 Bcl-2 蛋白家族和 PI3K/Akt 通路相关 [4]。
体内研究 (In Vivo)
在脑缺血时,依达拉奉可减少神经元损伤并防止内皮损伤,从而发挥神经保护作用。当 eNOS 存在时,可以挽救缺血性中风的有用 NOS 会增加,但当依达拉奉存在时,nNOS 和 iNOS(有毒的 NOS)会减少。依达拉奉预处理可减少溶栓治疗引起的出血事件和再灌注后脑水肿[1]。依达拉奉大大减少了梗死面积;依达拉奉组大鼠的平均梗死面积为227.6 mm3,明显小于对照组大鼠(264.0 mm3)。此外,依达拉奉治疗可减少缺血后出血量(依达拉奉治疗组大鼠为 53.4 mm3,对照组为 53.4 mm3)。 176.4 毫米)。此外,与未治疗的大鼠 (63.2%) 相比,接受依达拉奉治疗的大鼠出血量与梗死体积的比率 (23.5%) 降低 [2]。给予依达拉奉(20 mg/kg)的大鼠的胼胝体、生发基质和大脑皮层显示星形胶质细胞活性(胶质纤维酸性蛋白)和凋亡细胞(caspase-3)降低[3]。
酶活实验
Ho.33342和碘化丙啶(PI)双染色法检测细胞凋亡和坏死[4]
SGNs与谷氨酸和依达拉奉(500 μM)。对照细胞未经任何处理。用PBS洗涤细胞两次,用95%乙醇固定10 分钟,然后用Ho.33342染色(10 mg/mL)和PI(50 mg/mL)在37°C下保持30 min。在绿光(515–560)下通过荧光显微镜检查形态学变化 nm)和紫外线(340–380 nm)。每组在5个随机选择的场中计数至少500个细胞。所有治疗重复三次
分光光度计检测GSH含量、SOD活性和MDA水平[4]
SGN与2 mM谷氨酸10 min,预处理或不预处理500 μM依达拉奉2 h在前面。对照细胞未经任何处理。然后用冰冷的PBS洗涤细胞两次,超声处理,并收获用于以下测定。根据制造商的说明,通过商业检测试剂盒测量所有组的细胞内GSH含量、SOD活性和MDA水平。使用分光光度计测量最佳波长下的OD值,并计算与对照细胞相比的相对水平。所有实验重复三次。
细胞实验
药物治疗[4]
在96孔或24孔板中传代培养的SGNs(1.0×105/mL)用2 mM谷氨酸盐10分钟。然后用正常DMEM代替培养基。将不同浓度的依达拉奉添加到培养基中20 分钟之前或2 h、 6 h、 和12 谷氨酸处理后h。所有的剂量和时间点都是通过初步实验确定的(数据未显示)
MTT和台盼蓝染色法评估细胞活力[4]
细胞活力通过MTT法和台盼蓝染色进行定量。MTT(5 mg/mL,20 μL)加入每个孔中并孵育4 如上所述药物处理后,在37°C下放置h。除去培养基并将细胞沉淀溶解在DMSO中。然后,在570测量光密度(OD)值 nm,使用ELISA读取器。所有实验重复三次。根据以下公式计算细胞相对活力:
单间牢房  相对的  生存能力  (%)=ODexperimentODcontrol×100%
ODblank被用作零
在台盼蓝染色中,用0.4%台盼蓝将SGNs染色5 分钟。显微镜下拍照,然后计数台盼蓝阳性和阴性细胞。细胞存活率定义为阴性细胞的百分比。
动物实验
20 mg/kg
Mice and rats
药代性质 (ADME/PK)
Absorption, Distribution and Excretion
One study investigated the absorption of edaravone in healthy adults, who either received a single oral (105 mg/mL) or intravenous (60 mg/60 min) dose. The mean Cmax (CV%) and Tmax were 1656 (44.3) ng/mL and 0.5 hours, respectively, following oral administration. The absolute oral bioavailability is about 57% because of first-pass metabolism. The mean Cmax (CV%) and Tmax were 1253 (18.3) ng/mL and one hour, respectively, following intravenous administration. When intravenously administered, the maximum plasma concentration (Cmax) of edaravone was reached by the end of infusion. The Cmax and area under the concentration-time curve (AUC) of edaravone increases more than dose-proportional over the dose range of 30 to 300 mg. Edaravone does not accumulate in plasma with once-daily or multiple-dose administration. The Cmax and AUC decreased when the oral suspension formulation of edaravone was administered with a high-fat meal.
In Japanese and Caucasian healthy volunteer studies, edaravone was excreted mainly in the urine as its glucuronide conjugate (60-80% of the dose up to 48 hours). Approximately 6-8% of the dose was recovered in the urine as the sulfate conjugate, and <1% of the dose was recovered in the urine as the unchanged drug. _In vitro_ studies suggest that the sulfate conjugate of edaravone is hydrolyzed back to edaravone, which is then converted to the glucuronide conjugate in the kidney before excretion into the urine.
After intravenous administration, edaravone has a mean volume of distribution of 63.1 L, suggesting substantial tissue distribution. Edaravone has an apparent volume of distribution of 164 L following oral administration. Edaravone readily crosses the blood-brain barrier.
Following intravenous administration, the total clearance of edaravone is estimated to be 35.9 L/h. The apparent total clearance of edaravone is estimated to be 67.9L/h following oral administration.
Metabolism / Metabolites
The metabolites of edaravone have not been fully characterized. Edaravone is metabolized to a sulfate conjugate and a glucuronide conjugate, which are not pharmacologically active. The glucuronide conjugation of edaravone involves multiple uridine diphosphate glucuronosyltransferase (UGT) isoforms (UGT1A1, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, UGT2B7, and UGT2B17). In human plasma, edaravone is mainly detected as the sulfate conjugate, which is presumed to be formed by sulfotransferases. Oral edaravone results in 1.3- and 1.7-fold higher exposures for both sulfate and glucuronide metabolites, respectively, when compared to intravenously-administered edaravone because of first-pass metabolism.
Biological Half-Life
The mean terminal elimination half-life of edaravone is approximately 4.5 to nine hours. The half-lives of its metabolites range from three to six hours.
毒性/毒理 (Toxicokinetics/TK)
Hepatotoxicity
Serum aminotransferase elevations occur in a small proportion of patients on edaravone therapy, but the frequency, timing of onset, duration and severity of these elevations has not been defined. The rates of abnormal liver tests during edaravone therapy were said to be similar to those during placebo treatment. Most elevations resolved spontaneously, and there were no reports of drug discontinuation for serum enzyme elevations. Clinically apparent liver injury due to edaravone was not reported in the prelicensure trials and has not been reported with subsequent clinical use of edaravone, but the numbers of patients treated have been few. Thus, clinically apparent liver injury from edaravone must be rare if it occurs at all.
Likelihood score: E (unlikely cause of clinically apparent liver injury).
Protein Binding
Edaravone is 92% bound to human serum proteins, mainly to albumin, with no concentration dependence in the range of 0.1 to 50 micromol/L.
参考文献

[1]. Neuroprotective effects of edaravone: a novel free radical scavenger in cerebrovascular injury. CNS Drug Rev, 2006. 12(1): p. 9-20.

[2]. Edaravone, a free radical scavenger, attenuates cerebral infarction and hemorrhagic infarction in rats with hyperglycemia. Neurol Res, 2013.

[3]. Edaravone reduces astrogliosis and apoptosis in young rats with kaolin-induced hydrocephalus. Childs Nerv Syst. 2016 Dec 17. [Epub ahead of print].

[4]. Protective Effect of Edaravone on Glutamate-Induced Neurotoxicity in Spiral Ganglion Neurons. Neural Plast. 2016;2016:4034218. Epub 2016 Nov 10.

其他信息
1-phenyl-3-methyl-5-pyrazolone appears as white to off-white powder or crystals. (NTP, 1992)
Edaravone is a pyrazolone that is 2,4-dihydro-3H-pyrazol-3-one which is substituted at positions 2 and 5 by phenyl and methyl groups, respectively. It has a role as a radical scavenger and an antioxidant.
Edaravone is a free radical scavenger and neuroprotective agent with antioxidant properties. It has three tautomers. Edaravone works to scavenge reactive oxygen species, which have been implicated in neurological disorders, such as amyotrophic lateral sclerosis (ALS) and cerebral ischemia. The intravenous formulation of edaravone was first approved in Japan in 2001 for the treatment of acute ischemic stroke. It was later approved for the treatment of amyotrophic lateral sclerosis (ALS) in Japan and South Korea in 2015, followed by the FDA approval in May 2017 and Health Canada approval in October 2018. The oral suspension formulation of edaravone was approved by the FDA in May 2022 and by Health Canada in November 2022. Edaravone was initially granted orphan designation by the European Medicines Agency on June 19, 2015 and was under regulatory review in Europe. However, the drug manufacturer, Mitsubishi Tanabe Pharma, withdrew the Marketing Authorization Application (MAA) for edaravone from the European market on May 24, 2019, in response to the request made by the Committee for Medicinal Products for Human Use (CHMP) for a long-term study demonstrating the long-term efficacy and safety of edaravone. Edaravone was also investigated in other disorders, such as Alzheimer's disease, neuropathic pain, and ischemia-induced nerve injury.
Edaravone is a free radical scavenger and neuroprotective agent used for therapy of amyotrophic lateral sclerosis. Edaravone is associated with a low rate of serum aminotransferase elevations during therapy but has not been linked to instances of clinically apparent, acute liver injury.
Edaravone has been reported in Homo sapiens with data available.
An antipyrine derivative that functions as a free radical scavenger and neuroprotective agent. It is used in the treatment of AMYOTROPHIC LATERAL SCLEROSIS and STROKE.
Drug Indication
Edaravone is indicated for the treatment of amyotrophic lateral sclerosis (ALS) in the US and Canada. It is also indicated to treat acute ischemic stroke in Japan.
Treatment of amyotrophic lateral sclerosis
Treatment of amyotrophic lateral sclerosis
Mechanism of Action
Oxidative stress and reactive oxygen species (ROS) production have been implicated in various neurological disorders, such as amyotrophic lateral sclerosis (ALS) and cerebral ischemia. Oxidative stress caused by excess ROS damages endothelial cells in the cerebral vasculature as well as neuronal cell membranes, leading to neuronal cell death. Edaravone is a free radical scavenger that scavenges and suppresses the generation of hydroxyl radicals and peroxynitrite radicals. The exact mechanism of action of edaravone in ALS has not been fully elucidated; however, edaravone is thought to mediate therapeutic effects via its antioxidant properties. Since oxidative stress has been implicated in the pathophysiology of ALS and cerebral ischemia, inhibiting lipid peroxidation, suppressing endothelial cell damage induced by lipid peroxides, and scavenging free radicals may lead to neuroprotective effects. Edaravone has no effect on superoxide production. It is suggested that edaravone may also possess anti-inflammatory properties, as it inhibited neutrophil activation and suppressed inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) expression in animal models. It was also shown to ameliorate ROS-induced inflammatory oxidative stress after ischemic brain reperfusion.
Pharmacodynamics
Edaravone works to delay the disease progression of neurological disorders such as ischemic stroke and ALS by limiting the extent of neuronal damage or death.
*注: 文献方法仅供参考, InvivoChem并未独立验证这些方法的准确性
化学信息 & 存储运输条件
分子式
C10H10N2O
分子量
174.2
精确质量
174.079
元素分析
C, 68.95; H, 5.79; N, 16.08; O, 9.18
CAS号
89-25-8
相关CAS号
Edaravone-d5;1228765-67-0
PubChem CID
4021
外观&性状
Light yellow to yellow solid
密度
1.2±0.1 g/cm3
沸点
333.0±11.0 °C at 760 mmHg
熔点
126-128 °C(lit.)
闪点
155.2±19.3 °C
蒸汽压
0.0±0.7 mmHg at 25°C
折射率
1.606
LogP
0.44
tPSA
32.67
氢键供体(HBD)数目
0
氢键受体(HBA)数目
2
可旋转键数目(RBC)
1
重原子数目
13
分子复杂度/Complexity
241
定义原子立体中心数目
0
SMILES
O=C1CC(C)=NN1C1C=CC=CC=1
InChi Key
QELUYTUMUWHWMC-UHFFFAOYSA-N
InChi Code
InChI=1S/C10H10N2O/c1-8-7-10(13)12(11-8)9-5-3-2-4-6-9/h2-6H,7H2,1H3
化学名
5-methyl-2-phenyl-2,4-dihydro-3H-pyrazol-3-one
别名
MCI-186; NCI-C03952; MCI 186; NSC 12; MCI186; Radicut; trade name: Radicava; Methylphenylpyrazolone; Norantipyrine; Norphenazone; Phenylmethylpyrazolone; Arone
HS Tariff Code
2934.99.9001
存储方式

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

运输条件
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
溶解度数据
溶解度 (体外实验)
DMSO: 35 mg/mL (200.9 mM)
Water:<1 mg/mL
Ethanol:35 mg/mL (200.9 mM)
溶解度 (体内实验)
配方 1 中的溶解度: ≥ 2.5 mg/mL (14.35 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中,混匀;然后向上述溶液中加入50 μL Tween-80,混匀;加入450 μL生理盐水定容至1 mL。
*生理盐水的制备:将 0.9 g 氯化钠溶解在 100 mL ddH₂O中,得到澄清溶液。

配方 2 中的溶解度: ≥ 2.5 mg/mL (14.35 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中,混匀。
*20% SBE-β-CD 生理盐水溶液的制备(4°C,1 周):将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中,得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (14.35 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加,逐一添加), 澄清溶液。
例如,若需制备1 mL的工作液,可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。


请根据您的实验动物和给药方式选择适当的溶解配方/方案:
1、请先配制澄清的储备液(如:用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液,按从左到右的顺序依次添加助溶剂,澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明,并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中,混合均匀/澄清;向上述体系中加入50 μL Tween-80,混合均匀/澄清;然后继续加入450 μL ddH2O (或 saline)定容至 1 mL;

3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出,可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果,工作液请现配现用!
6、如不确定怎么将母液配置成体内动物实验的工作液,请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。
制备储备液 1 mg 5 mg 10 mg
1 mM 5.7405 mL 28.7026 mL 57.4053 mL
5 mM 1.1481 mL 5.7405 mL 11.4811 mL
10 mM 0.5741 mL 2.8703 mL 5.7405 mL

1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;

2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;

3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);

4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。

计算器

摩尔浓度计算器可计算特定溶液所需的质量、体积/浓度,具体如下:

  • 计算制备已知体积和浓度的溶液所需的化合物的质量
  • 计算将已知质量的化合物溶解到所需浓度所需的溶液体积
  • 计算特定体积中已知质量的化合物产生的溶液的浓度
使用摩尔浓度计算器计算摩尔浓度的示例如下所示:
假如化合物的分子量为350.26 g/mol,在5mL DMSO中制备10mM储备液所需的化合物的质量是多少?
  • 在分子量(MW)框中输入350.26
  • 在“浓度”框中输入10,然后选择正确的单位(mM)
  • 在“体积”框中输入5,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案17.513 mg出现在“质量”框中。以类似的方式,您可以计算体积和浓度。

稀释计算器可计算如何稀释已知浓度的储备液。例如,可以输入C1、C2和V2来计算V1,具体如下:

制备25毫升25μM溶液需要多少体积的10 mM储备溶液?
使用方程式C1V1=C2V2,其中C1=10mM,C2=25μM,V2=25 ml,V1未知:
  • 在C1框中输入10,然后选择正确的单位(mM)
  • 在C2框中输入25,然后选择正确的单位(μM)
  • 在V2框中输入25,然后选择正确的单位(mL)
  • 单击“计算”按钮
  • 答案62.5μL(0.1 ml)出现在V1框中
g/mol

分子量计算器可计算化合物的分子量 (摩尔质量)和元素组成,具体如下:

注:化学分子式大小写敏感:C12H18N3O4  c12h18n3o4
计算化合物摩尔质量(分子量)的说明:
  • 要计算化合物的分子量 (摩尔质量),请输入化学/分子式,然后单击“计算”按钮。
分子质量、分子量、摩尔质量和摩尔量的定义:
  • 分子质量(或分子量)是一种物质的一个分子的质量,用统一的原子质量单位(u)表示。(1u等于碳-12中一个原子质量的1/12)
  • 摩尔质量(摩尔重量)是一摩尔物质的质量,以g/mol表示。
/

配液计算器可计算将特定质量的产品配成特定浓度所需的溶剂体积 (配液体积)

  • 输入试剂的质量、所需的配液浓度以及正确的单位
  • 单击“计算”按钮
  • 答案显示在体积框中
动物体内实验配方计算器(澄清溶液)
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)
第二步:请输入动物体内配方组成(配方适用于不溶/难溶于水的化合物),不同的产品和批次配方组成不同,如对配方有疑问,可先联系我们提供正确的体内实验配方。此外,请注意这只是一个配方计算器,而不是特定产品的确切配方。
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计算结果:

工作液浓度 mg/mL;

DMSO母液配制方法 mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。

体内配方配制方法μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL ddH2O,混匀澄清。

(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
            (2) 一定要按顺序加入溶剂 (助溶剂) 。

临床试验信息
A Study to Evaluate the Effect of MCI-186 at Therapeutic and Supra-Therapeutic Doses on the QT Interval(QT)/Corrected QT Interval(QTc) Interval in Healthy Subjects
CTID: NCT04029090
Phase: Phase 1    Status: Completed
Date: 2024-11-21
Bioequivalence of TTYP01 Tablets in Healthy Adult Subjects
CTID: NCT06107205
Phase: Phase 1    Status: Completed
Date: 2024-10-17
Edaravone in the Treatment of Aquaporin-4 Antibody-positive Optic Neuritis
CTID: NCT05540262
Phase: N/A    Status: Recruiting
Date: 2024-02-23
Study of Compound Edaravone Injection for Treatment of Acute Ischemic Stroke
CTID: NCT04984577
Phase: Phase 2    Status: Suspended
Date: 2024-02-20
Bioequivalence Study of Oral Suspension and Intravenous Formulation of Edaravone in Healthy Adult Su
A Phase 3, Multi-center, Open-label, Safety Extension Study of Oral Edaravone Administered over 96 Weeks in Subjects with Amyotrophic Lateral Sclerosis (ALS)
CTID: null
Phase: Phase 3    Status: Completed
Date: 2021-03-22
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A Phase 3, Multi-center, Open-label, Safety Study of Oral Edaravone Administered over 48 Weeks in Subjects with Amyotrophic Lateral Sclerosis (ALS)
CTID: null
Phase: Phase 3    Status: Completed
Date: 2020-05-06


A Phase IIa, multi-centre, randomised, double-blind, placebo controlled, clinical study investigating the safety, tolerability and pharmacokinetics of two different infusion doses over 72 hours of a new regimen and new formulation of MCI-186 in subjects with acute ischemic stroke
CTID: null
Phase: Phase 2    Status: Completed
Date: 2009-01-23
Effect of edaravone against consciousness impairment after encephalitis
CTID: UMIN000010052
Phase: Phase II    Status: Complete: follow-up complete
Date: 2013-02-15
Studies on the effect of free radical scavenger Edaravone against postoperative hyper-perfusion syndrome after STA-MCA bypass surgery for adult moyamoya disease.
CTID: UMIN000008742
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2012-08-21
Intratympanic injection of Edaravone for idiopathic sudden sensorineural hearing loss
CTID: UMIN000008127
Phase:    Status: Complete: follow-up continuing
Date: 2012-06-11
tissue type plasminogen activator(t-PA) and Edaravon combination therapy study
CTID: UMIN000006330
Phase: Phase III    Status: Complete: follow-up complete
Date: 2011-12-10
Efficacy of pretreatment with edaravone on cerebral blood flow in carotid artery stenting.
CTID: UMIN000005303
Phase:    Status: Complete: follow-up complete
Date: 2011-04-01
Safety and efficacy of Edaravone[Nichiiko] in patients with acute noncardiogenic brain embolism
CTID: UMIN000004597
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2010-12-03
Combined therapy with intravenous recombinant tissue plasminogen activator (rt-PA) and edaravone in the acute ischemic stroke patients within 3 hours of onset
CTID: UMIN000002512
Phase:    Status: Complete: follow-up complete
Date: 2009-12-01

生物数据图片
  • Edaravone
    A, Coronal sections from ischemic mice brain stained with TTC. B, Infarct volume was compared between the control and different edaravone groups. C, Neurological deficit scores in the control and different edaravone groups.Stroke.2005 Oct;36(10):2220-5.
  • Edaravone
    A, Lipid peroxidation assessed with HNE immunoreactivity.B, Numbers of HNE-positive cell at the penumbra. C, Western blotting analysis of HNE.D, Densitometric analysis of HNE-modified protein.Stroke.2005 Oct;36(10):2220-5.
  • Edaravone
    A, Oxidative DNA damage assessed by 8-OHdG immunoreactivity. B, Numbers of 8-OHdG-positive cell in the penumbra.Stroke.2005 Oct;36(10):2220-5.
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