5,7,3',4'-Tetramethoxyflavone
(Synonyms: 木犀草素四甲醚) 目录号 : GC35153
5,7,3',4'-Tetramethoxyflavone 是从 M. exotica 中分离得到的一种多甲氧基黄酮，具有多种生物活性，包括抗真菌、抗疟疾、抗分支杆菌和抗炎活性。5,7,3',4'-Tetramethoxyflavone 可通过靶向 β-catenin 发挥软骨保护作用。
Cas No.:855-97-0
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
5,7,3',4'-Tetramethoxyflavone, one of the major polymethoxyflavones (PMFs) isolated from M. exotica, possesses various bioactivities, including anti-fungal, anti-malarial, anti-mycobacterial, and anti-inflammatory activities. 5,7,3',4'-Tetramethoxyflavone exhibits chondroprotective activity by targeting β-catenin signaling[1].
[1]. Wu L, et al. 5,7,3',4'-Tetramethoxyflavone exhibits chondroprotective activity by targeting β-catenin signaling in vivo and in vitro. Biochem Biophys Res Commun. 2014 Sep 26;452(3):682-8.
| Cas No. | 855-97-0 | SDF | |
| 别名 | 木犀草素四甲醚 | ||
| Canonical SMILES | O=C1C=C(C2=CC=C(OC)C(OC)=C2)OC3=C1C(OC)=CC(OC)=C3 | ||
| 分子式 | C19H18O6 | 分子量 | 342.35 |
| 溶解度 | DMSO: 8.33 mg/mL (24.33 mM) | 储存条件 | Store at 2-8°C,protect from 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 | 2.921 mL | 14.6049 mL | 29.2099 mL |
| 5 mM | 0.5842 mL | 2.921 mL | 5.842 mL |
| 10 mM | 0.2921 mL | 1.4605 mL | 2.921 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。
5,7,3',4'-Tetramethoxyflavone ameliorates cholesterol dysregulation by mediating SIRT1/FOXO3a/ABCA1 signaling in osteoarthritis chondrocytes
Future Med Chem 2021 Dec;13(24):2153-2166.PMID:34608806DOI:10.4155/fmc-2021-0247.
Dyslipidemia has been associated with the development of osteoarthritis. Our previous study found that 5,7,3',4'-Tetramethoxyflavone (TMF) exhibited protective activities against the pathological changes of osteoarthritis. Aim: To investigate the roles of TMF in regulating ABCA1-mediated cholesterol metabolism. Methods: Knockdown and overexpression were employed to study gene functions. Protein-protein interaction was investigated by co-immunoprecipitation, and the subcellular locations of proteins were studied by immunofluorescence. Results: IL-1β decreased ABCA1 expression and induced apoptosis. Therapeutically, TMF ameliorated the effects of IL-1β. FOXO3a knockdown expression abrogated the effects of TMF, and FOXO3a overexpression increased ABCA1 expression by interacting with LXRα. TMF promoted FOXO3a nuclear translocation by activating SIRT1 expression. Conclusions: TMF ameliorates cholesterol dysregulation by increasing the expression of FOXO3a/LXRα/ABCA1 signaling through SIRT1 in C28/I2 cells.
Identification of 5,7,3',4'-Tetramethoxyflavone metabolites in rat urine by the isotope-labeling method and ultrahigh-performance liquid chromatography-electrospray ionization-mass spectrometry
J Agric Food Chem 2012 Aug 22;60(33):8123-8.PMID:22812915DOI:10.1021/jf302043a.
5,7,3',4'-Tetramethoxyflavone (TMF), one of the major polymethoxyflavones (PMFs) isolated from Kaempferia parviflor , has been reported possessing various bioactivities, including antifungal, antimalarial, antimycobacterial, and anti-inflammatory activities. Although several studies on the TMF have been reported, the information about the metabolism of TMF and the structures of TMF metabolites is still not yet clear. In this study, an isotope-labeling method was developed for the identification of TMF metabolites. Three isotope-labeled TMFs (5,7,3',4'-tetramethoxy[3'-D(3)]flavone, 5,7,3',4'-tetramethoxy[4'-D(3)]flavone, and 5,7,3',4'-tetramethoxy[5,4'-D(6)]flavone) were synthesized and administered to rats. The urine samples were collected, and the main metabolites were monitored by ultrahigh-performance liquid chromatography-electrospray ionization-mass spectrometry. Five TMF metabolites were unambiguously identified as 3'-hydroxy-5,7,4'-trimethoxyflavone, 7-hydroxy-5,3',4'-trimethoxyflavone sulfate, 7-hydroxy-5,3',4'-trimethoxyflavone, 4'-hydroxy-5,7,3'-trimethoxyflavone, and 5-hydroxy-7,3',4'-trimethoxyflavone.
5,7,3',4'-Tetramethoxyflavone protects chondrocytes from ER stress-induced apoptosis through regulation of the IRE1α pathway
Connect Tissue Res 2018 Mar;59(2):157-166.PMID:28436754DOI:10.1080/03008207.2017.1321639.
Aim of the study: To investigate the roles of endoplasmic reticulum (ER) transmembrane sensor inositol-requiring enzyme-1 (IRE1)α signaling in ER stress-induced chondrocyte apoptosis, and to determine the molecular mechanisms underlying chondroprotective activity of 5,7,3',4'-Tetramethoxyflavone (TMF) from Murraya exotica. Materials and methods: IRE1α was knocked down by siRNA transfection in chondrocytes, which were harvested from rats' knee cartilages. Chondrocytes with IRE1α deficiency were administrated with tunicamycin (TM) and TMF. Chondrocyte apoptosis was quantified by flow cytometry and DAPI/TUNEL staining. Expression of mRNA and proteins was quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western-blot, respectively. Results: IRE1α deficiency significantly increased the rate of TM-induced chondrocyte apoptosis, down-regulated the expression of pro-survival factors XBP1S and Bcl-2, and up-regulated pro-apoptotic factors CHOP, p-JNK, and caspase-3. TMF suppressed TM-induced chondrocyte apoptosis by activating the expression of IRE1α, which reversed the expression patterns of downstream pro-survival and pro-apoptotic factors due to IRE1α deficiency. Conclusion: The mechanism of TMF in protecting chondrocytes against ER stress-induced apoptosis might be associated with regulating the activity of ER sensor IRE1α and its downstream pathway.
5,7,3',4'-Tetramethoxyflavone exhibits chondroprotective activity by targeting β-catenin signaling in vivo and in vitro
Biochem Biophys Res Commun 2014 Sep 26;452(3):682-8.PMID:25193704DOI:10.1016/j.bbrc.2014.08.129.
Osteoarthritis (OA) is a progressive joint disorder, which remains the leading cause of chronic disability in aged people. This study is the first report which demonstrates the cartilage protective effect of 5,7,3',4'-Tetramethoxyflavone (TMF) by decreasing the concentration of IL-1β, TNF-α and PGE2 in the knee synovial fluid in OA rat models in vivo. In vitro, after induced by PGE2, the apoptosis rate of chondrocytes was significantly increased. In addition, PGE2 increased the expression of cAMP/PKA signaling pathway in chondrocytes, stabilized and accumulated β-catenin, and activated the expression of β-catenin signaling pathway. These activities were counteracted by TMF dose-dependently. Collectively, TMF is a potential compound with chondroprotective activity by inhibiting both EP/cAMP/PKA signaling pathway and β-catenin signaling pathway.
Reversal of P-glycoprotein-mediated multidrug resistance by 5,6,7,3',4'-pentamethoxyflavone (Sinensetin)
Biochem Biophys Res Commun 2002 Jul 26;295(4):832-40.PMID:12127970DOI:10.1016/s0006-291x(02)00755-6.
Multidrug resistance (MDR) cells can be sensitized to anticancer drugs when treated concomitantly with chemosensitizers. In this study, chemosensitizing effects of 5,6,7,3',4'-pentamethoxyflavone (sinensetin) and its analogs were investigated with respect to in vitro efficacy and structure-activity relationship. Sinensetin reversed the resistance of P-glycoprotein (Pgp)-overexpressing AML-2/D100 to vincristine in a concentration-dependent manner. Chemosensitizing effect of sinensetin was 10- and 18-fold higher than those of 5,7,3',4'-Tetramethoxyflavone and 3,7-dihydroxy-3',4'-dimethoxyflavone, respectively. Sinensetin cytotoxicity in AML-2/D100 was not changed by the complete inhibition of Pgp, suggesting that it is not a substrate for Pgp. Flow cytometry showed that sinensetin increased drug accumulation in the AML-2/D100 in a concentration-dependent manner. Unlike verapamil and cyclosporin A, the maximum non-cytotoxic concentrations of sinensetin were found to decrease the Pgp levels. Azidopine-binding assay showed that cyclosporin A or verapamil inhibited azidopine binding on Pgp partially but sinensetin did not. Taken together, these results suggest that sinensetin has a chemosensitizing effect in reversing Pgp-mediated MDR by increasing the intracellular accumulation of drugs without competition in a binding site of azidopine. Thus, sinensetin is anticipated as a novel and highly potent second-generation flavonoid chemosensitizer, since sinensetin has significant advantages of having a high therapeutic index, of being a non-transportable inhibitor, and of effecting no induction of Pgp.