Butylphthalide (3-n-Butylphthalide)
(Synonyms: 丁基苯酞; 3-n-Butylphthalide; 3-Butylphthalide) 目录号 : GN10524
Butylphthalide (3-n-Butylphthalide) 具有广泛的药理活性的天然化合物，主要被用于治疗急性缺血性中风。
Cas No.:6066-49-5
Sample solution is provided at 25 µL, 10mM.
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Butylphthalide (3-n-Butylphthalide) is a natural compound with a wide range of pharmacological activities, primarily used for the treatment of acute ischemic stroke[1]. The mechanisms of action of Butylphthalide include antioxidant effects and mitochondrial protection[2]. Butylphthalide can also improve symptoms of myocardial infarction[3]. In addition, Butylphthalide has the potential to treat tissue damage induced by ischemia-reperfusion[4].
In vitro, pretreatment of SV40-transformed rat aortic endothelial cells with Butylphthalide (1μM) for 6 hours, followed by oxygen-glucose deprivation (OGD) for 6 hours, significantly enhances PGC-1α expression and protects cells from OGD-induced damage, increasing cell viability[5]. Pretreatment of SH-SY5Y cells with Butylphthalide (5μM) for 6 hours, followed by stimulation with 6-OHDA (100μM) for 24 hours, significantly increases cell viability, reduces cell apoptosis and ROS production, inhibits NLRP3 inflammasome activation and related inflammatory factor expression, alleviates mitochondrial damage, and decreases abnormal aggregation of α-synuclein (α-Syn)[6].
In vivo, Butylphthalide (200mg/kg) is administered intraperitoneally once daily to C57BL/6 mice starting at 8 weeks of age until the 10th week. Butylphthalide significantly alleviates behavioral deficits induced by Rotenone, reduces the loss of dopaminergic neurons, and inhibits microglial activation[7]. Butylphthalide (4mg/kg) is administered intraperitoneally as a single dose to rats with middle cerebral artery occlusion/reperfusion (MCAO/R) model. Butylphthalide significantly alleviates behavioral deficits induced by MCAO/R, reduces brain infarct volume, inhibits microglial activation, suppresses ferroptosis by activating the Nrf2/HO-1 signaling pathway, and alleviates lipid peroxidation, iron accumulation, and mitochondrial damage induced by ischemia-reperfusion[8].
References:
[1] Chen XQ, Qiu K, Liu H, et al. Application and prospects of butylphthalide for the treatment of neurologic diseases. Chin Med J (Engl). 2019 Jun 20;132(12):1467-1477.
[2] Zhu T, Wang L, Feng Y, et al. Classical Active Ingredients and Extracts of Chinese Herbal Medicines: Pharmacokinetics, Pharmacodynamics, and Molecular Mechanisms for Ischemic Stroke. Oxid Med Cell Longev. 2021 Mar 13;2021:8868941.
[3] Bai M, Pan CL, Jiang GX, et al. Effects of butylphthalide on oxidative stress and inflammatory response in rats with myocardial infarction through Akt/Nrf2 signaling pathway. Eur Rev Med Pharmacol Sci. 2019 Nov;23(21):9642-9650.
[4] Lu P, Li WP, Zhou BJ, et al. N-butylphthalide (NBP) ameliorated ischemia/reperfusion-induced skeletal muscle injury in male mice via activating Sirt1/Nrf2 signaling pathway. Physiol Rep. 2024 Dec;12(23):e70149.
[5] Wei H, Zhan LP, Zhang B, et al. dl-3n-butylphthalide reduces oxygen-glucose deprivation-induced endothelial cell damage by increasing PGC-1α. Eur Rev Med Pharmacol Sci. 2019 May;23(10):4481-4490.
[6] Que R, Zheng J, Chang Z, et al. Dl-3-n-Butylphthalide Rescues Dopaminergic Neurons in Parkinson's Disease Models by Inhibiting the NLRP3 Inflammasome and Ameliorating Mitochondrial Impairment. Front Immunol. 2021 Dec 1;12:794770.
[7] Liu Y, Duan R, Li P, et al. 3-N-butylphthalide attenuates neuroinflammation in rotenone-induced Parkinson's disease models via the cGAS-STING pathway. Int J Immunopathol Pharmacol. 2024 Jan-Dec;38:3946320241229041.
[8] Sun M, Chen J, Liu F, et al. Butylphthalide inhibits ferroptosis and ameliorates cerebral Ischaemia-Reperfusion injury in rats by activating the Nrf2/HO-1 signalling pathway. Neurotherapeutics. 2024 Sep;21(5):e00444.
Butylphthalide (3-n-Butylphthalide) 具有广泛的药理活性的天然化合物，主要被用于治疗急性缺血性中风 [1]。Butylphthalide的作用机制包括抗氧化、保护线粒体机制等[2]。Butylphthalide还可改善心肌梗死的症状[3]。此外，Butylphthalide还具有治疗缺血再灌注诱导组织损伤的潜力[4]。
在体外，Butylphthalide（1μM）预处理SV40转化的大鼠主动脉内皮细胞6h，随后进行氧糖剥夺（OGD）处理6h，可显著增强PGC-1α表达，同时保护细胞免受OGD诱导的损伤，提高细胞存活率[5]。Butylphthalide（5μM）预处理SH-SY5Y细胞6h，随后以6-OHDA（100μM）刺激24h，可显著提高细胞存活率，降低细胞凋亡率和ROS产生，同时抑制NLRP3炎症体激活及相关炎症因子表达，减轻线粒体损伤，减少α-突触核蛋白（α-Syn）异常聚集[6]。
在体内，Butylphthalide（200mg/kg）每天一次腹腔注射，用于处理8周龄开始直至第10周的C57BL/6小鼠。Butylphthalide显著减轻了由Rotenone诱导的行为障碍，减少了多巴胺能神经元的损失，并抑制了小胶质细胞的激活[7]。Butylphthalide（4mg/kg）在通过单次腹腔给药，用于处理脑缺血-再灌注（MCAO/R）大鼠模型。Butylphthalide显著减轻了由MCAO/R诱导大鼠的行为障碍，减少了脑梗死体积，并抑制了小胶质细胞的激活，通过激活Nrf2/HO-1信号通路抑制铁死亡，减轻了缺血再灌注诱导的脂质过氧化、铁积累和线粒体损伤[8]。
| Cell experiment [1]: | |
Cell lines | SV40-transformed aortic rat endothelial cell line (SVAREC) |
Preparation Method | SVAREC cells were cultured in Roswell Park Memorial Institute-1640 (RPMI-1640) medium supplemented with 10% heat-inactivated fetal bovine serum (FBS) at 37°C, 5% CO₂, and 95% air. Cells were subjected to oxygen-glucose deprivation (OGD) for 6 hours in the presence of 1μM Butylphthalide. |
Reaction Conditions | 1μM; 6h |
Applications | Butylphthalide protected eNOS activity during OGD. Butylphthalide treatment significantly alleviated OGD-induced cell injury, improving cell viability and morphology. |
| Animal experiment [2]: | |
Animal models | C57BL/6 mice |
Preparation Method | Mice were intragastrically administered rotenone for 8 consecutive weeks (0.25μmol/L) to induce Parkinson's disease (PD) symptoms. Butylphthalide (200mg/kg/day) was administered intraperitoneally for 6 weeks (from the 5th to the 10th week) to observe its protective effects. |
Dosage form | 200mg/kg; i.p. |
Applications | Butylphthalide alleviated behavioral impairments in rotenone-induced PD mice, protected against dopaminergic neuron loss, inhibited microglial activation, and reduced neuroinflammation by inhibiting the cGAS-STING pathway. |
References: | |
| Cas No. | 6066-49-5 | SDF | |
| 别名 | 丁基苯酞; 3-n-Butylphthalide; 3-Butylphthalide | ||
| 化学名 | 3-butyl-3H-2-benzofuran-1-one | ||
| Canonical SMILES | CCCCC1C2=CC=CC=C2C(=O)O1 | ||
| 分子式 | C12H14O2 | 分子量 | 190.24 |
| 溶解度 | ≥ 19mg/mL in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.2565 mL | 26.2826 mL | 52.5652 mL |
| 5 mM | 1.0513 mL | 5.2565 mL | 10.513 mL |
| 10 mM | 0.5257 mL | 2.6283 mL | 5.2565 mL |
| 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） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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，
体内配方配制方法：取 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 saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Quality Control & SDS
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- Purity: >99.50%
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