L-3-n-Butylphthalide
(Synonyms: (–)-3-Butylphthalide, levo-3-n-Butylphthalide, (S)-(–)-3-Butylphthalide, L-NBP) 目录号 : GC49436
A phthalide with antiplatelet and neuroprotective activities
Cas No.:3413-15-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
L-3-n-Butylphthalide is a phthalide that has been found in A. graveolens and has antiplatelet and neuroprotective activities.1 It inhibits ADP-, collagen-, and arachidonic acid-induced platelet aggregation ex vivo when administered at doses ranging from 3 to 100 mg/kg and inhibits thrombus formation in a collagen and epinephrine-induced rat model of experimental thrombosis. L-3-n-Butylphthalide (10 and 30 mg/kg per day) reduces amyloid-β-induced decreases in glutathione peroxidase (GPX) activity and decreases malondialdehyde (MDA) levels in the cortex and hippocampus and improves spatial learning and memory in the Morris water maze in a rat model of Alzheimer’s disease induced by intracerebroventricular infusion of amyloid-β (1-40) .2
1.Peng, Y., Zeng, X., Feng, Y., et al.Antiplatelet and antithrombotic activity of L-3-n-butylphthalide in ratsJ. Cardiovasc. Pharmacol.43(6)876-881(2004) 2.Peng, Y., Xing, C., Xu, S., et al.L-3-n-butylphthalide improves cognitive impairment induced by intracerebroventricular infusion of amyloid-beta peptide in ratsEur. J. Pharmacol.621(1-3)38-45(2009)
| Cas No. | 3413-15-8 | SDF | |
| 别名 | (–)-3-Butylphthalide, levo-3-n-Butylphthalide, (S)-(–)-3-Butylphthalide, L-NBP | ||
| Canonical SMILES | CCCC[C@H]1C2=CC=CC=C2C(O1)=O | ||
| 分子式 | C12H14O2 | 分子量 | 190.2 |
| 溶解度 | DMSO: 10 mg/ml,Ethanol: 10 mg/ml | 储存条件 | -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 | 5.2576 mL | 26.2881 mL | 52.5762 mL |
| 5 mM | 1.0515 mL | 5.2576 mL | 10.5152 mL |
| 10 mM | 0.5258 mL | 2.6288 mL | 5.2576 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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
L-3-n-Butylphthalide attenuates cognitive deficits in db/db diabetic mice
Metab Brain Dis 2019 Feb;34(1):309-318.PMID:30506335DOI:10.1007/s11011-018-0356-6.
Numerous epidemiological studies have shown that diabetes mellitus (DM) is associated with dementia and cognition decline. However, there is currently no effective treatment for diabetes-induced cognitive dysfunction. The neuroprotective effect of L-3-n-Butylphthalide (L-NBP) has been demonstrated in vascular dementia animal models. The purpose of this study was to determine whether L-NBP can ameliorate cognitive deficits in db/db mice, a model of obesity and type 2 diabetes. The mice were administered with vehicle or L-NBP (120 mg/kg) by gavage daily for 6 weeks. Then, Morris water maze tasks were performed, and hippocampal LTP was recorded in vivo. Next, the synaptic structure of the CA1 hippocampus region was investigated via electron microscopy. Finally, the expression levels of MDA, SOD, 8-OHdG, and NADPH oxidase subunits gp91 and p67, as well as the expression of NF-κB p65, TNF-α, IL-1β and caspase-3 were measured by Western blot, RT-PCR and ELISA. Treatment with L-NBP significantly attenuated the learning and memory deficits in db/db mice. Concomitantly, L-NBP also increased hippocampus synaptic plasticity, characterized by an enhanced in vivo LTP, and suppressed oxidative stress, as indicated by increased SOD activity and decreased MDA, 8-OHdG, and NADPH oxidase subunits p67 and gp91. L-NBP also significantly decreased NF-κB p65, TNF-α, IL-1βand caspase-3 levels in the hippocampus. L-NBP significantly ameliorated cognitive decline in type 2 diabetic mice, and this effect was accompanied by an improvement in hippocampal plasticity and an amelioration of oxidative stress, inflammation and apoptosis cascades. Thus, L-NBP may be a promising therapeutic agent against DM-mediated cognitive dysfunction.
L-3-n-Butylphthalide promotes restoration after an experimental animal model of intracerebral hemorrhage
Int J Med Sci 2021 Apr 29;18(12):2607-2614.PMID:34104092DOI:10.7150/ijms.60342.
Intracerebral hemorrhage (ICH) is a devastating type of stroke with high morbidity and mortality, and the effective therapies for ICH remain to be explored. L-3-n-Butylphthalide (NBP) is widely used in the treatment of ischemic stroke. However, few studies evaluated the therapeutic effects of NBP on ICH. Therefore, the present study aims to evaluate the effects of NBP on ICH and its potential mechanism. The rats were randomly divided into sham-operated group, saline-treated (ICH + saline) group, and NBP-treated (ICH + NBP) group. The ICH model of SD rats induced by IV collagenase was established. The modified Garcia JH score was used to detect the neurological deficit in rats. Western Blot and immunohistochemistry analysis was applied to test the levels of UBIAD1 and caspase-3 expressions in the perihematomal region. The rates of apoptotic cells were detected by TUNEL staining. The results showed that NBP up-regulated the expression of UBIAD1, reduced the apoptotic cells in the perihematomal region, and improved the neurological deficit. Taken together, our study added some new evidence to the application of NBP in ICH treatment.
L-3-n-Butylphthalide improves synaptic and dendritic spine plasticity and ameliorates neurite pathology in Alzheimer's disease mouse model and cultured hippocampal neurons
Mol Neurobiol 2021 Mar;58(3):1260-1274.PMID:33146400DOI:10.1007/s12035-020-02183-y.
Alzheimer's disease (AD) is the most common cause of dementia among elderly people. Despite enormous efforts, the pathogenesis of AD still remains unclear and no drug has yet been proved to be disease-modifying. As the basis of learning and memory, the plasticity of synapse and dendritic spine has been impaired during AD progression. Previous studies have showed a protective effect of L-3-n-Butylphthalide (L-NBP) on cognitive deficits in AD, we wonder whether this protective effect is associated with positive alterations on synapse and dendritic spines. In this study, we first of all confirmed the anti-dementia effect of L-NBP in 13-month-old APP/PS1 mice, and then investigated the alterations in synaptic and dendritic spine plasticity due to L-NBP treatment both in vivo and in vitro. We also conducted preliminary studies and found the possible mechanisms related to the inhibition of over-activated complement cascade and the remodeling of actin cytoskeleton. Besides, we also found extra benefits of L-NBP on presynaptic dystrophic neurites and attempted to give explanations from the view of autophagy regulation. Taken together, our study added some new evidence to the application of L-NBP in AD treatment and provided deeper insight into the relevant mechanisms for future study.
L-3-n-Butylphthalide Promotes Neurogenesis and Neuroplasticity in Cerebral Ischemic Rats
CNS Neurosci Ther 2015 Sep;21(9):733-41.PMID:26215907DOI:10.1111/cns.12438.
Aims: This study investigated whether anticerebral ischemia new drug, L-3-n-Butylphthalide (l-NBP), improved behavioral recovery and enhanced hippocampal neurogenesis after cerebral ischemia in rats. Methods and results: The middle cerebral artery of rats was blocked for 2 h. The daily oral administrations of 30 mg/kg l-NBP or vehicle were begun from the second day until the rats were sacrificed. L-NBP treatment markedly increased 5-bromo-2'-deoxyuridine (BrdU)-positive cells in the hippocampal dentate gyrus (DG) of injured hemisphere on day 28 after ischemia. The amount of newborn cells and newly mature neurons was also increased. The expressions of growth-associated protein-43 and synaptophysin were significantly elevated in l-NBP-treated rats. However, l-NBP markedly reduced the percentage of BrdU(+) /GFAP(+) cells. Additionally, the levels of catalytical subunit of protein kinase A (PKA), protein kinase B (Akt), and cAMP response element-binding protein (CREB) were significantly increased, and the activation of the signal transducer and activation of transcription 3 (STAT3) and the expressions of cleaved caspase-3 and Bax were obviously inhibited by l-NBP. Consequently, l-NBP attenuated the behavioral dysfunction. Conclusions: It first demonstrates that l-NBP may improve the behavioral outcome of cerebral ischemia by promoting neurogenesis and neuroplasticity. Activation of CREB and Akt and inhibition of STAT3 signaling might be involved in.
L-3-n-Butylphthalide Effectively Improves the Glymphatic Clearance and Reduce Amyloid-β Deposition in Alzheimer's Transgenic Mice
J Mol Neurosci 2021 Jun;71(6):1266-1274.PMID:33188502DOI:10.1007/s12031-020-01752-z.
Amyloid-β (Aβ) deposit in the parenchyma is a major characteristic in Alzheimer's disease (AD), and the impaired glymphatic clearance contributes to the Aβ accumulation. It was reported that L-3-n-Butylphthalide (NBP) showed the potential neuroprotective effect in the rodent models of AD. The effects of NBP on the glymphatic system were explored in this study. In the wild-type mice, both CSF tracer influx and perivascular drainage increased after NBP treatment compared with vehicle treatment. Moreover, NBP promoted the perivascular drainage of Aβ via increased cerebral pulsation, which could be inhibited by propranolol. Then, we studied the potential of 3-month NBP treatment on Aβ deposits in 8-month-old APP/PS1 transgenic mice. NBP daily treatments remarkably improved cognitive behavior in Morris water maze. Furthermore, NBP could reduce Aβ deposition and decrease parenchymal Aβ levels. In addition, NBP markedly improved the perivascular AQP4 localization. Our results indicated that NBP could enhance the glymphatic clearance and reduce parenchymal Aβ deposit in the APP/PS1 mice, suggesting that it may have potential in the treatment of AD.