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    金合欢素; 刺槐素

    Acacetin

    金合欢素; 刺槐素
    产品编号 CFN98744
    CAS编号 480-44-4
    分子式 = 分子量 C16H12O5 = 284.3
    产品纯度 >=98%
    物理属性 Yellow powder
    化合物类型 Flavonoids
    植物来源 The barks of Acacia farnesiana.
    ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用
    提供自定义包装
    产品名称 产品编号 CAS编号 包装 QQ客服
    金合欢素; 刺槐素 CFN98744 480-44-4 10mg QQ客服:2932563308
    金合欢素; 刺槐素 CFN98744 480-44-4 20mg QQ客服:2932563308
    金合欢素; 刺槐素 CFN98744 480-44-4 50mg QQ客服:2932563308
    金合欢素; 刺槐素 CFN98744 480-44-4 100mg QQ客服:2932563308
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    ChemFaces的产品在许多优秀和顶级科学期刊中被引用

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.
    IF=36.216(2019)

    PMID: 29328914

    Cell Metab. 2020 Mar 3;31(3):534-548.e5.
    doi: 10.1016/j.cmet.2020.01.002.
    IF=22.415(2019)

    PMID: 32004475

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.
    IF=14.548(2019)

    PMID: 29149595

    ACS Nano. 2018 Apr 24;12(4): 3385-3396.
    doi: 10.1021/acsnano.7b08969.
    IF=13.903(2019)

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.
    IF=13.297(2019)

    PMID: 28005066

    Sci Adv. 2018 Oct 24;4(10): eaat6994.
    doi: 10.1126/sciadv.aat6994.
    IF=12.804(2019)

    PMID: 30417089
    我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
  • Institute of Pathophysiology Medical University of Vienna (Austria)
  • Universit?t Basel (Switzerland)
  • University of Vienna (Austria)
  • Lodz University of Technology (Poland)
  • University of Cincinnati (USA)
  • University of Stirling (United Kingdom)
  • Max Rubner-Institut (MRI) (Germany)
  • University of Lodz (Poland)
  • Srinakharinwirot University (Thailand)
  • University of Limpopo (South Africa)
  • Auburn University (USA)
  • Martin Luther University of Halle-Wittenberg (Germany)
  • Donald Danforth Plant Science Center (USA)
  • Korea Intitute of Science and Technology (KIST) (Korea)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • Food Research International2016, 106-113
  • J Basic Clin Physiol Pharmacol.2016, 27(1):1-8
  • Kor. J. Pharmacogn.2016, 47(1):62-72
  • J Ethnopharmacol.2017, 197:157-164
  • LWT-Food Science and Technology2017, 75:488-496
  • Sci Rep. 2017, 8207(7)
  • Drug Test Anal.2018, 10(10):1579-1589
  • Int J Biol Macromol.2018, 112:1093-1103
  • Malaysian J of Fundamental and Applied Sciences 2018, 14(3):368-373
  • Evid Based Complement Alternat Med.2018, 2018:8565132
  • Exp Neurobiol.2018, 27(3):200-209
  • Sci Adv.2018, 4(10)
  • J Sep Sci.2018, 41(11):2488-2497
  • Oncology Letters2018, 4690-4696
  • J Ethnopharmacol.2019, 228:132-141
  • Planta Med.2019, 85(3):217-224
  • Drug Des Devel Ther.2020, 14:61-71
  • Antioxidants (Basel).2020, 9(2):E120
  • Metabolites.2020, 11(1):E11.
  • Toxins (Basel).2020, 12(4):210.
  • Food Chem.2020, 332:127412
  • J of l. Chroma.&Related Tech2020, 43(11-12):414-423.
  • J Formos Med Assoc.2020, S0929-6646(20)30425-3
  • ...
  • 生物活性
    Description: Acacetin is an atrium-selective agent that prolongs the atrial effective refractory period without prolonging the corrected QT interval and effectively prevents atrial fibrillation (AF) in anesthetized dogs after intraduodenal administration. Acacetin has anti-cancer, anti-mutagenic, spasmolytic and antinociceptive, anti-inflammatory and anti-peroxidative effects.
    Targets: NF-kB | IkB | Akt | Bcl-2/Bax | COX | PI3K | VEGFR | STAT | NOS | MMP(e.g.TIMP) | Calcium Channel | p38MAPK | JNK | IL Receptor | Potassium Channel | EGFR | IKK
    In vitro:
    Cancer Prev Res (Phila). 2013 Oct;6(10):1128-39.
    Acacetin inhibits in vitro and in vivo angiogenesis and downregulates Stat signaling and VEGF expression.[Pubmed: 23943785]
    Angiogenesis is an effective target in cancer control. The antiangiogenic efficacy and associated mechanisms of acacetin, a plant flavone, are poorly known.
    METHODS AND RESULTS:
    In the present study, acacetin inhibited growth and survival (up to 92%; P < 0.001), and capillary-like tube formation on Matrigel (up to 98%; P < 0.001) by human umbilical vein endothelial cells (HUVEC) in regular condition, as well as VEGF-induced and tumor cells conditioned medium-stimulated growth conditions. It caused retraction and disintegration of preformed capillary networks (up to 91%; P < 0.001). HUVEC migration and invasion were suppressed by 68% to 100% (P < 0.001). Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC. It also suppressed nuclear localization of pStat-3 (Tyr705). Acacetin strongly inhibited capillary sprouting and networking from rat aortic rings and fertilized chicken egg chorioallantoic membrane (CAM; ∼71%; P < 0.001). Furthermore, it suppressed angiogenesis in Matrigel plugs implanted in Swiss albino mice. Acacetin also inhibited tyrosine phosphorylation of Stat-1 and -3, and expression of VEGF in cancer cells.
    CONCLUSIONS:
    Overall, acacetin inhibits Stat signaling and suppresses angiogenesis in vitro, ex vivo, and in vivo, and therefore, it could be a potential agent to inhibit tumor angiogenesis and growth.
    J Cell Mol Med. 2015 Aug;19(8):1910-5.
    Acacetin inhibits expression of matrix metalloproteinases via a MAPK-dependent mechanism in fibroblast-like synoviocytes.[Pubmed: 25856795]
    It is well known that rheumatoid arthritis (RA) is an autoimmune joint disease in which fibroblast-like synoviocytes (FLSs) play a pivotal role.
    METHODS AND RESULTS:
    In this study, we investigated the anti-arthritic properties of acacetin in FLSs. The expression of matrix metalloproteinase (MMP)-1, MMP-3 and MMP-13 were investigated by quantitative RT-PCR and western blot at gene and protein levels. At the same time, the phosphorylation of mitogen-activated protein kinases (MAPK) was investigated. The DNA-binding activity of NF-κB was investigated by electrophoretic mobility shift assay. We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1β-induced FLSs.
    CONCLUSIONS:
    Our results suggest that acacetin has antiarthritic effects in FLSs. Thus, acacetin should be further studied for the treatment of arthritis.
    Circulation. 2008 May 13;117(19):2449-57.
    Acacetin, a natural flavone, selectively inhibits human atrial repolarization potassium currents and prevents atrial fibrillation in dogs.[Pubmed: 18458165 ]

    METHODS AND RESULTS:
    The effects of Acacetin on human atrial ultrarapid delayed rectifier K(+) current (I(Kur)) and other cardiac ionic currents were studied with a whole-cell patch technique. Acacetin suppressed I(Kur) and the transient outward K(+) current (IC(50) 3.2 and 9.2 mumol/L, respectively) and prolonged action potential duration in human atrial myocytes. The compound blocked the acetylcholine-activated K(+) current; however, it had no effect on the Na(+) current, L-type Ca(2+) current, or inward-rectifier K(+) current in guinea pig cardiac myocytes. Although Acacetin caused a weak reduction in the hERG and hKCNQ1/hKCNE1 channels stably expressed in HEK 293 cells, it did not prolong the corrected QT interval in rabbit hearts. In anesthetized dogs, Acacetin (5 mg/kg) prolonged the atrial effective refractory period in both the right and left atria 1 to 4 hours after intraduodenal administration without prolongation of the corrected QT interval, whereas sotalol at 5 mg/kg prolonged both the atrial effective refractory period and the corrected QT interval. Acacetin prevented AF induction at doses of 2.5 mg/kg (50%), 5 mg/kg (85.7%), and 10 mg/kg (85.7%). Sotalol 5 mg/kg also prevented AF induction (60%).
    CONCLUSIONS:
    The present study demonstrates that the natural compound Acacetin is an atrium-selective agent that prolongs the atrial effective refractory period without prolonging the corrected QT interval and effectively prevents AF in anesthetized dogs after intraduodenal administration. These results indicate that oral Acacetin is a promising atrium-selective agent for the treatment of AF.
    In vivo:
    PLoS One. 2014 Feb 10;9(2):e88644.
    Acacetin inhibits glutamate release and prevents kainic acid-induced neurotoxicity in rats.[Pubmed: 24520409]
    An excessive release of glutamate is considered to be a molecular mechanism associated with several neurological diseases that causes neuronal damage. Therefore, searching for compounds that reduce glutamate neurotoxicity is necessary.
    METHODS AND RESULTS:
    In this study, the possibility that the natural flavone acacetin derived from the traditional Chinese medicine Clerodendrum inerme (L.) Gaertn is a neuroprotective agent was investigated. The effect of acacetin on endogenous glutamate release in rat hippocampal nerve terminals (synaptosomes) was also investigated. The results indicated that acacetin inhibited depolarization-evoked glutamate release and cytosolic free Ca(2+) concentration ([Ca(2+)]C) in the hippocampal nerve terminals. However, acacetin did not alter synaptosomal membrane potential. Furthermore, the inhibitory effect of acacetin on evoked glutamate release was prevented by the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channel blocker known as ω-conotoxin MVIIC. In a kainic acid (KA) rat model, an animal model used for excitotoxic neurodegeneration experiments, acacetin (10 or 50 mg/kg) was administrated intraperitoneally to the rats 30 min before the KA (15 mg/kg) intraperitoneal injection, and subsequently induced the attenuation of KA-induced neuronal cell death and microglia activation in the CA3 region of the hippocampus.
    CONCLUSIONS:
    The present study demonstrates that the natural compound, acacetin, inhibits glutamate release from hippocampal synaptosomes by attenuating voltage-dependent Ca(2+) entry and effectively prevents KA-induced in vivo excitotoxicity. Collectively, these data suggest that acacetin has the therapeutic potential for treating neurological diseases associated with excitotoxicity.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.5174 mL 17.5871 mL 35.1741 mL 70.3482 mL 87.9353 mL
    5 mM 0.7035 mL 3.5174 mL 7.0348 mL 14.0696 mL 17.5871 mL
    10 mM 0.3517 mL 1.7587 mL 3.5174 mL 7.0348 mL 8.7935 mL
    50 mM 0.0703 mL 0.3517 mL 0.7035 mL 1.407 mL 1.7587 mL
    100 mM 0.0352 mL 0.1759 mL 0.3517 mL 0.7035 mL 0.8794 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    部分图片展示
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    4',5,6,7-四甲氧基黄酮; 4',5,6,7-Tetramethoxyflavone CFN91034 1168-42-9 C19H18O6 = 342.4 5mg QQ客服:1413575084
    4,5,7,8,-四甲氧基黄酮; 6-Demethoxytangeretin CFN93255 6601-66-7 C19H18O6 = 342.4 5mg QQ客服:1413575084
    石吊兰甲素; Lysionotin CFN99787 152743-19-6 C18H16O7 = 344.32 20mg QQ客服:2056216494
    栀子黄素B; Gardenin B CFN93144 2798-20-1 C19H18O7 = 358.4 10mg QQ客服:1413575084
    桔皮素; Tangeretin CFN90240 481-53-8 C20H20O7 = 372.37 20mg QQ客服:2932563308
    5,4'-二羟基黄酮; 4',5-Dihydroxyflavone CFN97137 6665-67-4 C15H10O4 = 254.2 5mg QQ客服:2932563308
    芹菜素; 芹黄素; 5,7,4'-三羟基黄酮; Apigenin CFN98843 520-36-5 C15H10O5 = 270.2 20mg QQ客服:2932563308
    芫花素; Genkwanin CFN98670 437-64-9 C16H12O5 = 284.3 20mg QQ客服:3257982914
    黄花夹竹桃黄酮; Thevetiaflavone CFN96124 29376-68-9 C16H12O5 = 284.3 5mg QQ客服:1413575084
    野黄芩素; Scutellarein CFN98557 529-53-3 C15H10O6 = 286.24 20mg QQ客服:2056216494

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