2,6-Dimethoxy-1,4-benzoquinone
(Synonyms: 2,6-二甲氧基-1,4-苯醌) 目录号 : GC64627
2,6-Dimethoxy-1,4-benzoquinone 是一种天然植物化学物质，是一种已知的吸脂诱导因子。2,6-Dimethoxy-1,4-benzoquinone 具有抗癌、抗炎、抗脂肪、抗菌和抗疟疾的作用。
Cas No.:530-55-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2,6-Dimethoxy-1,4-benzoquinone, a natural phytochemical, is a known haustorial inducing factor. 2,6-Dimethoxy-1,4-benzoquinone exerts anti-cancer, anti-inflammatory, anti-adipogenic, antibacterial, and antimalaria effects[1].子
[1]. Tomonori Kamiya , et al. 2,6-Dimethoxy-1,4-benzoquinone, isolation and identification of anti-carcinogenic, anti-mutagenic and anti-inflammatory component from the juice of Vitis coignetiae. Food Chem Toxicol. 2018 Dec;122:172-180.
[2]. Jennifer Mach. A shot in the dark: how parasitic plants find host roots Plant Cell. 2010 Apr;22(4):995.
| Cas No. | 530-55-2 | SDF | Download SDF |
| 别名 | 2,6-二甲氧基-1,4-苯醌 | ||
| 分子式 | C8H8O4 | 分子量 | 168.15 |
| 溶解度 | DMSO : 5.56 mg/mL (33.07 mM; ultrasonic and warming and heat to 60°C) | 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 | 5.9471 mL | 29.7354 mL | 59.4707 mL |
| 5 mM | 1.1894 mL | 5.9471 mL | 11.8941 mL |
| 10 mM | 0.5947 mL | 2.9735 mL | 5.9471 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。
2,6-Dimethoxy-1,4-benzoquinone Inhibits 3T3-L1 Adipocyte Differentiation via Regulation of AMPK and mTORC1
Planta Med 2019 Feb;85(3):210-216.PMID:30199902DOI:10.1055/a-0725-8334.
2,6-Dimethoxy-1,4-benzoquinone is a natural phytochemical present in fermented wheat germ. It has been reported to exhibit anti-inflammatory, antitumor, and antibacterial activities. However, the anti-adipogenic effects of 2,6-Dimethoxy-1,4-benzoquinone and the mechanisms responsible have not previously been elucidated. Such findings may have ramifications for the treatment of obesity. 2,6-Dimethoxy-1,4-benzoquinone (5 and 7.5 µM) significantly reduced the expression of various adipogenic transcription factors, including peroxisome proliferator-activated receptor-γ and CCAAT/enhancer binding protein α as well as adipocyte protein 2 and fatty acid synthase. 2,6-Dimethoxy-1,4-benzoquinone upregulated AMP-dependent protein kinase phosphorylation and inhibited the mature form of sterol regulatory element-binding protein 1c. Notably, 2,6-Dimethoxy-1,4-benzoquinone attenuated mammalian target of rapamycin complex 1 activity in 3T3-L1 and mouse embryonic fibroblast cells. These findings highlight a potential role for 2,6-Dimethoxy-1,4-benzoquinone in the suppression of adipogenesis. Further studies to determine the anti-obesity effects of 2,6-Dimethoxy-1,4-benzoquinone in animal models appear warranted.
2,6-Dimethoxy-1,4-benzoquinone increases skeletal muscle mass and performance by regulating AKT/mTOR signaling and mitochondrial function
Phytomedicine 2021 Oct;91:153658.PMID:34332284DOI:10.1016/j.phymed.2021.153658.
Background: 2,6-Dimethoxy-1,4-benzoquinone (DMBQ), a natural phytochemical present in fermented wheat germ, has been reported to exert anti-cancer, anti-inflammatory, and anti-adipogenic effects. However, the effect of DMBQ on muscle hypertrophy and myoblast differentiation has not been elucidated. Purpose: We investigated the effect of DMBQ on skeletal muscle mass and muscle function and then determined the possible mechanism of DMBQ. Methods: To examine myogenic differentiation and hypertrophy, confluent C2C12 cells were incubated in differentiation medium with or without various concentrations of DMBQ for 4 days. In animal experiments, C57BL/6 mice were fed DMBQ-containing AIN-93 diet for 7 weeks. Grip strength, treadmill, microscopic evaluation of muscle tissue, western blotting, and quantitative real-time PCR were performed. Results: DMBQ significantly increased fusion index, myotube size, and the protein expression of myosin heavy chain (MHC). DMBQ increased the phosphorylation of protein kinase B (AKT) and p70 ribosomal protein S6 kinase (S6K), whereas the phosphorylation of these proteins was abolished by the phosphoinositide 3-kinase inhibitor LY294002 in C2C12 cells. In addition, DMBQ treatment increased peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), which programs mitochondrial biogenesis, protein levels compared with control C2C12 cells. DMBQ significantly increased maximal respiration and spare respiratory capacity in C2C12 cells. In animal experiments, DMBQ increased skeletal muscle weights and skeletal muscle fiber size compared with the control group values. In addition, the DMBQ group showed increased grip strength and running distance on an accelerating treadmill. The protein expression of total MHC, MHC1, MHC2A, and MHC2B in skeletal muscle was upregulated by DMBQ supplementation. We found that DMBQ increased the phosphorylation of AKT and mammalian target of rapamycin (mTOR), as well as downstream S6K and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) in skeletal muscle. DMBQ also stimulated mRNA expression of PGC1α, accompanied by an increase in mitochondrial DNA content, oxidative phosphorylation (OXPHOS) proteins, and oxidative enzyme activity. Conclusion: Collectively, DMBQ was shown to increase skeletal muscle mass and performance by regulating the AKT/mTOR signaling pathway and enhancing mitochondrial function, which might be useful for the treatment and prevention of skeletal muscle atrophy.
2,6-Dimethoxy-1,4-benzoquinone, isolation and identification of anti-carcinogenic, anti-mutagenic and anti-inflammatory component from the juice of Vitis coignetiae
Food Chem Toxicol 2018 Dec;122:172-180.PMID:30316843DOI:10.1016/j.fct.2018.10.028.
Previously we demonstrated the anti-tumorigenic, anti-mutagenic and anti-inflammatory effects of the juice of Vitis coignetiae (yamabudo), and identified caftaric acid as an anti-mutagenic component from the juice. In the present study, we investigated the isolation of anti-inflammatory components in yamabudo juice supposing that the anti-inflammatory components in yamabudo are also responsible for the anti-tumorigenic activity. The suppressing effect on nitric oxide production in mouse leukemic monocyte with LPS was used as a separation marker. Three components comprising 2,6-Dimethoxy-1,4-benzoquinone (DBQ), fertaric acid and caftaric acid were isolated and identified from the juice of V. coignetiae as anti-inflammatory ingredients. Inhibitory effects were found of DBQ on the mutagenicity of dimethylbenzo[a]anthracene, aflatoxin B1, 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) and amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in the Ames test. Topical application of DBA significantly inhibited TPA-induced edema of mouse ears. The anti-tumorigenic effect of DBQ on the promotion and initiation stages of mouse skin tumorigenesis was investigated, and topical administration of DBQ on the promotion stage significantly decreased tumor development in mice skin. DBQ is a potential candidate for the chemopreventive effect of V. coignetiae.
Chemopreventive effects and anti-tumorigenic mechanisms of 2,6-Dimethoxy-1,4-benzoquinone, a constituent of Vitis coignetiae Pulliat (crimson glory vine, known as yamabudo in Japan), toward 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice
Food Chem Toxicol 2021 Aug;154:112319.PMID:34087405DOI:10.1016/j.fct.2021.112319.
Previously, we isolated and identified anti-mutagenic and anti-inflammatory components from Vitis coignetiae (crimson glory vine, known as yamabudo in Japan) as 2,6-Dimethoxy-1,4-benzoquinone (DBQ), fertaric acid and caftaric acid. We also reported that the oral intake of a partially purified fraction from yamabudo juice (yamabudo-fr) or DBQ affords significant protection against two-stage skin carcinogenesis in mice. In this study, we found that oral intake of yamabudo-fr or DBQ affords significant protection against a tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced mouse model of lung tumorigenesis. Furthermore, we investigated the anti-tumorigenic mechanisms of yamabudo juice and DBQ. NNK is known to be a DNA-methylating and alkylating agent; thus, we investigated the anti-tumorigenic mechanisms of yamabudo juice and DBQ in relation to DNA methylation. Pretreatment with yamabudo-fr or DBQ dose-dependently decreased formation of O6-methylguanine and N7-methylguanine in DNA of the A549 human lung epithelial-like cell line treated with a methylating agent, 1-methyl-3-nitro-1-nitrosoguanidine. Yamabudo juice and DBQ inhibited the mutagenicity of NNK in the Ames test using Salmonella typhimurium TA1535 but not S. typhimurium YG7108, an alkylguanine DNA alkyltransferase-deficient strain (same as TA1535 but Δadast::Kmr, Δogtst::Cmr). Yamabudo juice and DBQ might accelerate the repair of DNA damage caused by NNK and reduce DNA damage to cells. We also investigated the effects of yamabudo juice and DBQ on signaling pathways in A549 cells. With or without epidermal growth factor stimulation, phosphorylation of Erk1/2, Akt and Stat3 in A549 cells was significantly decreased in the presence of yamabudo juice or DBQ, indicating that yamabudo juice and DBQ suppressed PI3K/AKT, MAPK/ERK and JAK/STAT3 signaling pathways. These results suggest that both initiation and growth/progression steps in carcinogenesis, especially anti-oxidant effects, stimulation of repair of alkyl DNA adducts and suppressed growth signaling pathways are potential anti-tumorigenic targets of yamabudo juice and DBQ in NNK-induced lung tumorigenesis.
Fully reversible redox cycling of 2,6-Dimethoxy-1,4-benzoquinone induced by ascorbate
Biochemistry (Mosc) 1998 Feb;63(2):200-6.PMID:9526115doi
The kinetics of cyclic redox transformation of 2,6-dimethoxy-1, 4-benzoquinone (DMOBQ)--the well-known effective anticancer agent--induced by ascorbate (AscH-) were studied in phosphate buffer, pH 7.40, at 37 degreesC using the Clark electrode and ESR techniques. The process is due to the electron transfer from AscH- to quinone (Q): Q + AscH- --> Q*- + Asc.- + H+ (1), followed by semiquinone (Q.-) oxidation: Q.- + O2 --> Q + O2.- (2). DMOBQ, taken even at submicromolar concentrations, effectively catalyzed AscH- oxidation that manifested itself by intensive oxygen consumption and an increase in the steady-state concentration of the ascorbyl radical (Asc.-). The rate of oxygen consumption, ROX, was kept almost constant for a long time. ROX was found to be proportional to the [Q][AscH-] product and not dependent on the concentrations of the individual reagents. The rate constant for reaction (1) determined from ROX and [Asc.-] was as much as 380 +/- 40 and 280 +/- 30 M-1.sec-1, respectively. When DMOBQ was mixed with the corresponding hydroquinone, QH2, in oxygen-free buffer, the ESR signal of Q.- which formed due to the equilibrium Q + QH2 left and right arrow 2Q.- + 2H+ (3) was observed. The equilibrium constant K3 of (2.6 +/- 0.4).10-5 and the change in the reduction potential, DeltaE3 = E(Q/Q.-) - E(Q.-/QH2), of -280 mV were calculated from the steady-state concentration of Q.- at pH 7.4 and 37 degrees C. From combination of DeltaE3 determined in this study with E7(Q/Q.-) reported in the literature, a value of +190 mV was calculated for the standard second one-electron reduction potential E(Q*-/QH2). The latter is lower by 270-230 mV than that for all the studied 1, 4-hydroquinones. The very beneficial combination of E(Q/Q.-) and E(Q.-/QH2) was suggested to be the basic reason for the perfect work of DMOBQ as a redox cycling agent and its pronounced anticancer activity.