Neoechinulin A
目录号 : GC64126
Neoechinulin A 是一种异戊烯基吲哚生物碱，具有清除、神经营养因子样和抗凋亡活性。Neoechinulin A 诱导小鼠记忆改善和抗抑郁样作用。
Cas No.:51551-29-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Neoechinulin A is an isoprenyl indole alkaloid that exhibits scavenging, neurotrophic factor-like, and anti-apoptotic activities. Neoechinulin A induces memory improvements and antidepressant-like effects in mice[1][2].
Neoechinulin A (RAW264.7 macrophages; 3 hours; cells then stimulated with LPS (1 μg/mL) for 18 hours) suppresses PGE2, TNF-α, and IL-1β production in a dose-dependent manner[2].Neoechinulin A can suppress the production of pro-inflammatory mediators and cytokines including NO, PGE2, TNF-α, and IL-1β. Further, it reduced the expression of iNOS and COX-2 in LPS-stimulated RAW264.7 macrophages by inhibiting the NF-κB and p38 MAPK signaling pathways[2]. Neoechinulin A suppresses amyloid-β oligomer-induced microglia activation and thereby protects PC-12 cells from inflammation-mediated toxicity[3].
In the Y-maze test, the intracerebroventicular (i.c.v.) administration of LPS (10 μg/mouse) significantly decreased spontaneous alternation behavior, which was prevented by the prior administration of neoechinulin A (300ng/mouse, i.c.v.)[1].
[1]. Humbert M, et al. Masitinib combined with standard gemcitabine chemotherapy: in vitro and in vivo studies in human pancreatic tumour cell lines and ectopic mouse model. PLoS One. 2010;5(3):e9430. Published 2010 Mar 4.
[2]. Kim KS, et al. Anti-inflammatory effect of neoechinulin a from the marine fungus Eurotium sp. SF-5989 through the suppression of NF-кB and p38 MAPK Pathways in lipopolysaccharide-stimulated RAW264.7 macrophages. Molecules. 2013;18(11):13245-13259. Published 2013 Oct 25.
[3]. Dewapriya P, et al. Neoechinulin A suppresses amyloid-β oligomer-induced microglia activation and thereby protects PC-12 cells from inflammation-mediated toxicity. Neurotoxicology. 2013;35:30-40.
| Cas No. | 51551-29-2 | SDF | Download SDF |
| 分子式 | C19H21N3O2 | 分子量 | 323.39 |
| 溶解度 | 储存条件 | 4°C, away from moisture and light | |
| 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 | 3.0922 mL | 15.4612 mL | 30.9224 mL |
| 5 mM | 0.6184 mL | 3.0922 mL | 6.1845 mL |
| 10 mM | 0.3092 mL | 1.5461 mL | 3.0922 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。
Neoechinulin A as a Promising SARS-CoV-2 Mpro Inhibitor: In Vitro and In Silico Study Showing the Ability of Simulations in Discerning Active from Inactive Enzyme Inhibitors
Mar Drugs 2022 Feb 24;20(3):163.PMID:35323462DOI:10.3390/md20030163.
The COVID-19 pandemic and its continuing emerging variants emphasize the need to discover appropriate treatment, where vaccines alone have failed to show complete protection against the new variants of the virus. Therefore, treatment of the infected cases is critical. This paper discusses the bio-guided isolation of three indole diketopiperazine alkaloids, Neoechinulin A (1), echinulin (2), and eurocristatine (3), from the Red Sea-derived Aspergillus fumigatus MR2012. Neoechinulin A (1) exhibited a potent inhibitory effect against SARS-CoV-2 Mpro with IC50 value of 0.47 μM, which is comparable to the reference standard GC376. Despite the structural similarity between the three compounds, only 1 showed a promising effect. The mechanism of inhibition is discussed in light of a series of extensive molecular docking, classical and steered molecular dynamics simulation experiments. This paper sheds light on indole diketopiperazine alkaloids as a potential structural motif against SARS-CoV-2 Mpro. Additionally, it highlights the potential of different molecular docking and molecular dynamics simulation approaches in the discrimination between active and inactive structurally related Mpro inhibitors.
Neoechinulin A induced memory improvements and antidepressant-like effects in mice
Prog Neuropsychopharmacol Biol Psychiatry 2016 Nov 3;71:155-61.PMID:27495355DOI:10.1016/j.pnpbp.2016.08.002.
Neoechinulin A is an isoprenyl indole alkaloid that exhibits scavenging, neurotrophic factor-like, and anti-apoptotic activities. However, the effectiveness of Neoechinulin A in animal models of disease has not yet been explored. In the present study, we investigated the effects of Neoechinulin A on memory impairment in lipopolysaccharide (LPS)-treated mice and its antidepressant-like effects in mice. In the Y-maze test, the intracerebroventicular (i.c.v.) administration of LPS (10μg/mouse) significantly decreased spontaneous alternation behavior, which was prevented by the prior administration of Neoechinulin A (300ng/mouse, i.c.v.). None of the treatments altered the locomotor activity of mice. Moreover, the administration of Neoechinulin A decreased the immobility time in the forced-swim test or tail suspension test, which was prevented by the prior administration of WAY100635 (an antagonist of 5-HT1A receptors) and parachlorophenylalanine (an inhibitor of tryptophan hydroxylase). These results suggest that Neoechinulin A improves memory functions in LPS-treated mice, and also exerts antidepressant-like effects through changes in the 5-HT system.
Neoechinulin A impedes the progression of rotenone-induced cytotoxicity in PC12 cells
Biol Pharm Bull 2011;34(2):243-8.PMID:21415535DOI:10.1248/bpb.34.243.
Neoechinulin A, an indole alkaloid from marine fungi, can protect PC12 cells from the cytotoxicity of 1-methyl-4-phenylpyridinium (MPP(+)), a Parkinson disease-inducing neurotoxin, by ameliorating downstream events resulting from mitochondrial complex I inactivation. However, the cytoprotective mechanisms remained unclear. In this study, by using rotenone, another parkinsonian-inducing neurotoxin targeting mitochondrial complex I, we investigated the cytoprotective mechanism of Neoechinulin A. Rotenone-induced cell death was associated with accelerated glucose consumption, and excess glucose supplementation in the culture medium almost completely suppressed cell death, suggesting that glucose deficiency in the medium is critical for triggering cell death in this model. Co-treatment with Neoechinulin A, but not Neoechinulin A pre-treatment before rotenone exposure, significantly impeded cell death by rotenone. Although the presence of Neoechinulin A did not affect the accelerated glycolytic turnover in rotenone-treated cells, it paradoxically decreased ATP levels in the cells, suggesting increased ATP consumption. Although the link between the decreased ATP levels and cytoprotection is not clear at present, it suggests that Neoechinulin A may ameliorate rotenone toxicity by activating a cytoprotective machinery that requires ATP.
Neoechinulin A suppresses amyloid-β oligomer-induced microglia activation and thereby protects PC-12 cells from inflammation-mediated toxicity
Neurotoxicology 2013 Mar;35:30-40.PMID:23261590DOI:10.1016/j.neuro.2012.12.004.
A pathological hallmark of Alzheimer's disease (AD), aggregation and deposition of amyloid-β peptides, has been recognized as a potent activator of microglia-mediated neuroinflammation and neuronal dysfunction. Therefore, downregulation of microglial activation has a significant therapeutic demand. In this study, focus was given to evaluate the ability of Neoechinulin A, an indole alkaloid isolated from marine-derived Microsporum sp., to attenuate microglial activation by oligomeric amyloid-β 1-42 (Aβ42). Neoechinulin A treatment significantly inhibited the generation of reactive oxygen and nitrogen species in Aβ42-activated BV-2 microglia cells. In addition, we found that Neoechinulin A significantly suppressed the production of neurotoxic inflammatory mediator tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and prostaglandin E2 (PGE2) in activated BV-2 cells. Moreover, the treatment downregulated the protein and gene expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β and IL-6. Further, activated microglia-mediated apoptosis of PC-12 pheochromocytoma cells was significantly repressed by Neoechinulin A. The molecular mechanism studies suggested that Neoechinulin A may block the phosphorylation of mitogen-activated protein kinase (MAPK) molecule p38, apoptosis signal-regulating kinase 1 (ASK-1) and nuclear translocation of nuclear factor-κB (NF-κB) p65 and p50 subunits. Regulation of these signalling pathways have most probably contributed to the anti-inflammatory activity of Neoechinulin A. Collectively, these results suggest that with further studies Neoechinulin A have a potential to be developed as a modulator of neuroinflammatory process in AD.
Neoechinulin A protects PC12 cells against MPP+-induced cytotoxicity
J Antibiot (Tokyo) 2008 May;61(5):330-3.PMID:18654001DOI:10.1038/ja.2008.48.
Neoechinulin A, an alkaloid from Eurotium rubrum, can protect neuronal PC12 cells against cytotoxicity of a potent oxidant, peroxynitrite. Because involvement of peroxynitrite has been suggested in the pathogenesis of Parkinson's disease, we assessed whether this alkaloid could also protect PC12 cells from the cytocidal action of 1-methyl-4-phenylpyridine (MPP+), a neurotoxin capable of provoking acute Parkinson's-like neurodegeneration in humans. Neoechinulin A could protect PC12 cells from MPP+ cytotoxicity without protecting against mitochondrial complex I dysfunction, suggesting the alkaloid can ameliorate downstream events of mitochondrial failure. Thus, Neoechinulin A has the potential to intervene in this progressive neurodegeneration.