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  • 花旗松素

    Taxifolin

    花旗松素
    产品编号 CFN98734
    CAS编号 480-18-2
    分子式 = 分子量 C15H12O7 = 304.3
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Flavonoids
    植物来源 The barks of Pinus yunnanensis.
    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
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    产品名称 产品编号 CAS编号 包装 QQ客服
    花旗松素 CFN98734 480-18-2 10mg QQ客服:1413575084
    花旗松素 CFN98734 480-18-2 20mg QQ客服:1413575084
    花旗松素 CFN98734 480-18-2 50mg QQ客服:1413575084
    花旗松素 CFN98734 480-18-2 100mg QQ客服:1413575084
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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
  • University of Lodz (Poland)
  • Universiti Malaysia Pahang (Malaysia)
  • University of Zurich (Switzerland)
  • Mahatma Gandhi University (India)
  • Instytut Nawozów Sztucznych w Pu?awach (Poland)
  • Technical University of Denmark (Denmark)
  • University of Bordeaux (France)
  • University of Maryland (USA)
  • Wroclaw Medical University (Poland)
  • University of Canterbury (New Zealand)
  • Tokyo Woman's Christian University (Japan)
  • Guangzhou Institutes of Biomedicine and Health (China)
  • Warszawski Uniwersytet Medyczny (Poland)
  • Melbourne University (Australia)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • J Biol Chem.2014, 289(3):1723-31
  • Pharmacogn Mag.2015, 11:S585-91
  • BMC Complement Altern Med.2016, 16:213
  • J Pharm Anal.2016, 6(6):363-373
  • Polytechnic University of Catalonia2017, 105826
  • Molecular & Cellular Toxicology2017, 13(3):271-278
  • BMC Complement Altern Med.2017, 17(1):393
  • J Ethnopharmacol.2017, 198:205-213
  • Biol Pharm Bull.2017, 40(6):797-806
  • Food Res Int.2018, 106:909-919
  • Int J Mol Sci.2018, 19(9):E2601
  • Molecules.2018, 23(3):E615
  • Phytomedicine.2018, 38:12-23
  • Journal of Ginseng Research2019, 10.1016
  • BMC Complement Altern Med.2019, 19(1):325
  • Spectrochim Acta A2019, 210:372-380
  • J Ethnopharmacol.2019, 235:406-414
  • Molecules.2019, 24(1):E159
  • Molecules.2019, 24(16):E2985
  • Molecules.2019, 24(2):E343
  • Saudi Pharm J.2019, 27(1):145-153
  • Ann Transl Med.2019, 7(23):731
  • Biomolecules.2019, 9(11):E696
  • ...
  • 生物活性
    Description: Taxifolin exhibits important anti-tyrosinase activity, it also exhibits significant inhibitory activity against collagenase with an IC50 value of 193.3 μM.Taxifolin has anti-oxidant, anti-melanogenic, chemopreventive, anti-inflammatory, and cardioprotective effects. Taxifolin promotes osteoblast differentiation in MC3T3-E1 cells and also inhibit osteoclastogenesis in RAW264.7 cells, it also can enhance andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.
    Targets: EGFR | PI3K | COX | PGE | Akt | NADPH-oxidase | ROS | Caspase | STAT | JAK | NOS | NO | NF-kB
    In vitro:
    Cancer Prev Res (Phila). 2012 Sep;5(9):1103-14.
    Taxifolin suppresses UV-induced skin carcinogenesis by targeting EGFR and PI3K.[Pubmed: 22805054 ]
    Skin cancer is one of the most commonly diagnosed cancers in the United States. Taxifolin reportedly exerts multiple biologic effects, but the molecular mechanisms and direct target(s) of Taxifolin in skin cancer chemoprevention are still unknown.
    METHODS AND RESULTS:
    In silico computer screening and kinase profiling results suggest that the EGF receptor (EGFR), phosphoinositide 3-kinase (PI3K), and Src are potential targets for Taxifolin. Pull-down assay results showed that EGFR, PI3K, and Src directly interacted with Taxifolin in vitro, whereas Taxifolin bound to EGFR and PI3K, but not to Src in cells. ATP competition and in vitro kinase assay data revealed that Taxifolin interacted with EGFR and PI3K at the ATP-binding pocket and inhibited their kinase activities. Western blot analysis showed that Taxifolin suppressed UVB-induced phosphorylation of EGFR and Akt, and subsequently suppressed their signaling pathways in JB6 P+ mouse skin epidermal cells. Expression levels and promoter activity of COX-2 and prostaglandin E(2) (PGE(2)) generation induced by UVB were also attenuated by Taxifolin. The effect of Taxifolin on UVB-induced signaling pathways and PGE(2) generation was reduced in EGFR knockout murine embryonic fibroblasts (MEF) compared with EGFR wild-type MEFs. Taxifolin also inhibited EGF-induced cell transformation. Importantly, topical treatment of Taxifolin to the dorsal skin significantly suppressed tumor incidence, volume, and multiplicity in a solar UV (SUV)-induced skin carcinogenesis mouse model. Further analysis showed that the Taxifolin-treated group had a substantial reduction in SUV-induced phosphorylation of EGFR and Akt in mouse skin.
    CONCLUSIONS:
    These results suggest that Taxifolin exerts chemopreventive activity against UV-induced skin carcinogenesis by targeting EGFR and PI3K.
    PLoS One. 2013;8(1):e54577.
    Taxifolin enhances andrographolide-induced mitotic arrest and apoptosis in human prostate cancer cells via spindle assembly checkpoint activation.[Pubmed: 23382917]
    Andrographolide (Andro) suppresses proliferation and triggers apoptosis in many types of cancer cells. Taxifolin (Taxi) has been proposed to prevent cancer development similar to other dietary flavonoids.
    METHODS AND RESULTS:
    In the present study, the cytotoxic and apoptotic effects of the addition of Andro alone and Andro and Taxi together on human prostate carcinoma DU145 cells were assessed. Andro inhibited prostate cancer cell proliferation by mitotic arrest and activation of the intrinsic apoptotic pathway. Although the effect of Taxi alone on DU145 cell proliferation was not significant, the combined use of Taxi with Andro significantly potentiated the anti-proliferative effect of increased mitotic arrest and apoptosis by enhancing the cleavage of poly(ADP-ribose) polymerase, and caspases-7 and -9. Andro together with Taxi enhanced microtubule polymerization in vitro, and they induced the formation of twisted and elongated spindles in the cancer cells, thus leading to mitotic arrest. In addition, we showed that depletion of MAD2, a component in the spindle assembly checkpoint (SAC), alleviated the mitotic block induced by the two compounds, suggesting that they trigger mitotic arrest by SAC activation.
    CONCLUSIONS:
    This study suggests that the anti-cancer activity of Andro can be significantly enhanced in combination with Taxi by disrupting microtubule dynamics and activating the SAC.
    In vivo:
    Food Chem Toxicol. 2014 Jan;63:221-32.
    Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis.[Pubmed: 24269735]
    Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy.
    METHODS AND RESULTS:
    The objective of this study was to investigate the potential protective effects and mechanisms of taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that taxifolin inhibited 33 mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm.
    CONCLUSIONS:
    In conclusion, taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy.
    Phytother Res. 2008 Sep;22(9):1200-7.
    Flavonoids, taxifolin and luteolin attenuate cellular melanogenesis despite increasing tyrosinase protein levels.[Pubmed: 18729255 ]
    Flavonoids are a group of polyphenolic compounds widely distributed in plants. Their potent bio-activities and relatively low toxicity have rendered them useful ingredients in functional cosmetics. The purpose of the present study was to examine their potential effects on cellular melanogenesis. When tested in murine melanoma B16F10 cells activated by alpha-melanocyte stimulating hormone (alpha-MSH), taxifolin and luteolin inhibited the cellular melanogenesis as effectively as arbutin, one of the most widely used hypopigmenting agents in cosmetics. As opposed to their antimelanogenic effects, taxifolin and luteolin rather increased the tyrosinase protein levels in the absence and presence of alpha-MSH. However, these flavonoids effectively inhibited tyrosinase-catalysed oxidation of l-dihydroxyphenylalanine in cell-free extracts and in living cells. Furthermore, they attenuated cell pigmentation induced by expression of exogenous human tyrosinase. Therefore, the antimelanogenic effects of taxifolin and luteolin are attributed to their inhibitory effects on tyrosinase enzymatic activity, despite their effects on increasing tyrosinase protein levels.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.2862 mL 16.4312 mL 32.8623 mL 65.7246 mL 82.1558 mL
    5 mM 0.6572 mL 3.2862 mL 6.5725 mL 13.1449 mL 16.4312 mL
    10 mM 0.3286 mL 1.6431 mL 3.2862 mL 6.5725 mL 8.2156 mL
    50 mM 0.0657 mL 0.3286 mL 0.6572 mL 1.3145 mL 1.6431 mL
    100 mM 0.0329 mL 0.1643 mL 0.3286 mL 0.6572 mL 0.8216 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
    刺槐亭; Dihydrorobinetin CFN98671 4382-33-6 C15H12O7 = 304.3 20mg QQ客服:215959384
    蛇葡萄素; 二氢杨梅素; Ampelopsin CFN98326 27200-12-0 C15H12O8 = 320.3 20mg QQ客服:1413575084
    Sepinol; Sepinol CFN97204 72061-63-3 C16H14O7 = 318.3 5mg QQ客服:3257982914
    6-甲基二氢槲皮素; Cedeodarin CFN97912 31076-39-8 C16H14O7 = 318.3 5mg QQ客服:215959384
    雪松素; Cedrin CFN97872 75513-81-4 C16H14O8 = 334.3 5mg QQ客服:2159513211
    (-)-二氢槲皮素; (-)-Dihydroquercetin CFN92413 111003-33-9 C15H12O7 = 304.3 5mg QQ客服:3257982914
    花旗松素; Taxifolin CFN98734 480-18-2 C15H12O7 = 304.3 20mg QQ客服:2159513211
    李属素; Padmatin CFN97280 80453-44-7 C16H14O7 = 318.3 5mg QQ客服:1148253675
    雪松素 ; Deodarin CFN96563 33788-39-5 C16H14O7 = 318.29 5mg QQ客服:1148253675
    2',3,5,6',7-四羟基二氢黄烷酮; 2',3,5,6',7-Pentahydroxyflavanone CFN97277 80366-15-0 C15H12O7 = 304.3 5mg QQ客服:2159513211

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