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  • 芹菜素; 芹黄素; 5,7,4'-三羟基黄酮


    芹菜素; 芹黄素; 5,7,4'-三羟基黄酮
    产品编号 CFN98843
    CAS编号 520-36-5
    分子式 = 分子量 C15H10O5 = 270.2
    产品纯度 >=98%
    物理属性 Yellow powder
    化合物类型 Flavonoids
    植物来源 The roots of Scutellaria indica L.
    产品名称 产品编号 CAS编号 包装 QQ客服
    芹菜素; 芹黄素; 5,7,4'-三羟基黄酮 CFN98843 520-36-5 10mg QQ客服:3257982914
    芹菜素; 芹黄素; 5,7,4'-三羟基黄酮 CFN98843 520-36-5 20mg QQ客服:3257982914
    芹菜素; 芹黄素; 5,7,4'-三羟基黄酮 CFN98843 520-36-5 50mg QQ客服:3257982914
    芹菜素; 芹黄素; 5,7,4'-三羟基黄酮 CFN98843 520-36-5 100mg QQ客服:3257982914
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    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

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

    PMID: 32004475

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

    PMID: 29149595

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

    PMID: 29553709

    Nature Plants. 2016 Dec 22;3: 16206.
    doi: 10.1038/nplants.2016.205.

    PMID: 28005066

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

    PMID: 30417089
  • University of Bordeaux (France)
  • Instituto de Investigaciones Agropecuarias (Chile)
  • The Ohio State University (USA)
  • Universiti Malaysia Pahang (Malaysia)
  • University of Pretoria (South Africa)
  • Tohoku University (Japan)
  • The Vancouver Prostate Centre (VPC) (Canada)
  • Agricultural Research Organization (ARO) (Israel)
  • Charles University in Prague (Czech Republic)
  • Universidad Veracuzana (Mexico)
  • Medical University of Gdansk (Poland)
  • University of Lodz (Poland)
  • Shanghai University of TCM (China)
  • University of Wuerzburg (Germany)
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  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • The University of Manitoba2021, 35690.
  • J Med Food.2022, 25(3):272-280.
  • Clin Transl Oncol.2019, 10.1007
  • Acta Chromatographica2021, 00960.
  • TCI CO.2019, US20190151281A1
  • Food and Fermentation Industries2018, 44(371)
  • Molecules. 2013, 18(11):14105-21
  • Mol Pharm.2017, 14(9):3164-3177
  • Green Chemistry2021, ISSUE 2.
  • Fitoterapia.2021, 153:104995.
  • J Biol Chem.2014, 289(3):1723-31
  • Plant Direct.2021, 5(4):e00318.
  • Korean Herb. Med. Inf.2020, 8(2):243-254.
  • Analytical Letters.2020, doi 10.1008
  • Kor. J. Herbol.2019, 34(2):59-66
  • Antioxidants (Basel).2021, 10(11): 1802.
  • J Ethnopharmacol.2017, 206:327-336
  • J of the Korean Society of Cosmetics and Cosmetology2019, 225-231
  • J Drug Delivery Science and Tech.2022, 67:102957.
  • Phytomedicine.2022, 110:154597.
  • Plants (Basel).2023, 12(22):3877.
  • J Appl Pharm Sci.2022, 12(04):044-053
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  • ...
  • 生物活性
    Description: Apigenin is a potent inhibitor of CYP2C9, which has anti-inflammatory, antiangiogenic, and anti-cancer effects, it may inhibit EV71 replication through suppressing viral IRES activity and modulating cellular JNK pathway.
    Targets: GSK-3 | TNF-α | IL Receptor | Akt | ROS | JNK | TGF-β/Smad | VEGFR | FAK | Src | CYP2C9
    In vitro:
    Antiviral Res. 2014 Sep;109:30-41.
    Apigenin inhibits enterovirus 71 replication through suppressing viral IRES activity and modulating cellular JNK pathway.[Pubmed: 24971492]
    Enterovirus 71 (EV71) is a member of genus Enterovirus in Picornaviridae family, which is one of the major causative agents for hand, foot and mouth disease (HFMD), and sometimes associated with severe central nervous system diseases in children. Currently there are no effective therapeutic medicines or vaccines for the disease.
    In this report, we found that apigenin and luteolin, two flavones that differ only in the number of hydroxyl groups could inhibit EV71-mediated cytopathogenic effect (CPE) and EV71 replication with low cytotoxicity. Both molecules also showed inhibitory effect on the viral polyprotein expression. They prevented EV71-induced cell apoptosis, intracellular reactive oxygen species (ROS) generation and cytokines up-regulation. Time-of-drug addition study demonstrated that apigenin and luteolin acted after viral entry. We examined the effect of apigenin and luteolin on 2A(pro) and 3C(pro) activity, two viral proteases responsible for viral polyprotein processing, and found that they showed less inhibitory activity on 2A(pro) or 3C(pro). Further studies demonstrated that apigenin, but not luteolin could interfere with viral IRES activity. Also, apigenin inhibited EV71-induced c-Jun N-terminal kinase (JNK) activation which is critical for viral replication, in contrast to luteolin that did not.
    This study demonstrated that apigenin may inhibit EV71 replication through suppressing viral IRES activity and modulating cellular JNK pathway. It also provided evidence that one hydroxyl group difference in the B ring between apigenin and luteolin resulted in the distinct antiviral mechanisms. This study will provide the basis for better drug development and further identification of potential drug targets.
    In vivo:
    Br J Nutr. 2015 Feb 28;113(4):618-26.
    Intestinal anti-inflammatory activity of apigenin K in two rat colitis models induced by trinitrobenzenesulfonic acid and dextran sulphate sodium.[Pubmed: 25654996]
    Flavonoids are polyphenolic compounds that are widespread in nature, and consumed as part of the human diet in significant amounts. The aim of the present study was to test the intestinal anti-inflammatory activity of apigenin K, a soluble form of apigenin, in two models of rat colitis, namely the trinitrobenzenesulfonic acid (TNBS) model and the dextran sulphate sodium (DSS) model.
    Apigenin K (1, 3 and 10 mg/kg; by the oral route; n 4-6 per group) was administered as a pre-treatment to rats with TNBS and DSS colitis, and colonic status was checked by macroscopic and biochemical examination. Apigenin K pre-treatment resulted in the amelioration of morphological signs and biochemical markers in the TNBS model. The results demonstrated a reduction in the inflamed area, as well as lower values of score and colonic weight:length ratio compared with the TNBS group. Myeloperoxidase (MPO) activity was reduced by 30 % (P< 0·05). Moreover, apigenin K pre-treatment ameliorated morphological signs and biochemical markers in the DSS model. Thus, macroscopic damage was significantly reduced and the colonic weight:length ratio was lowered by approximately 10 %, while colonic MPO and alkaline phosphatase activities were decreased by 35 and 21 %, respectively (P< 0·05). Apigenin K pre-treatment also tended to normalise the expression of a number of colonic inflammatory markers (e.g. TNF-α, transforming growth factor-β, IL-6, intercellular adhesion molecule 1 or chemokine (C-C motif) ligand 2).
    In conclusion, apigenin K is found to have anti-inflammatory effects in two preclinical models of inflammatory bowel disease.
    Evid Based Complement Alternat Med . 2017;2017:2590676.
    Apigenin Attenuates Adriamycin-Induced Cardiomyocyte Apoptosis via the PI3K/AKT/mTOR Pathway[Pubmed: 28684964]
    Treatment with Adriamycin (ADR) is one of the major causes of chemotherapy-induced cardiotoxicity and therefore is the principal limiting factor in the effectiveness of chemotherapy for cancer patients. Apigenin (API) has been shown to play a cardioprotective role. The present study examined the effect of API on ADR-induced cardiotoxicity in mice. Sixty male Kunming mice were randomly divided into 4 groups: a control group, ADR model group, low-dose API treatment group (125 mg·kg-1), and high-dose API treatment group (250 mg·kg-1). Blood samples were taken to evaluate a spectrum of myocardial enzymes. Cardiomyocyte apoptosis was measured using a TUNEL assay, and cardiomyocyte autophagy was observed using electron microscopy. Moreover, apoptosis-related proteins, such as Bax and Bcl-2, autophagy-related proteins, including Beclin1 and LC3B, and PI3K/AKT/mTOR pathway-related proteins were examined with western blot. Our results demonstrate that ADR caused an increase in the serum levels of cardiac injury markers and enhanced cardiomyocyte apoptosis and autophagy. API administration prevented the effects associated with ADR-induced cardiotoxicity in mice and inhibited ADR-induced apoptosis and autophagy. API also promoted PI3K/AKT/mTOR pathway activity in ADR-treated mice. In conclusion, API may have a protective effect against ADR-induced cardiotoxicity by inhibiting apoptosis and autophagy via activation of the PI3K/AKT/mTOR pathway.
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.701 mL 18.5048 mL 37.0096 mL 74.0192 mL 92.5241 mL
    5 mM 0.7402 mL 3.701 mL 7.4019 mL 14.8038 mL 18.5048 mL
    10 mM 0.3701 mL 1.8505 mL 3.701 mL 7.4019 mL 9.2524 mL
    50 mM 0.074 mL 0.3701 mL 0.7402 mL 1.4804 mL 1.8505 mL
    100 mM 0.037 mL 0.185 mL 0.3701 mL 0.7402 mL 0.9252 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.
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    5,4'-二羟基黄酮; 4',5-Dihydroxyflavone CFN97137 6665-67-4 C15H10O4 = 254.2 20mg QQ客服:215959384
    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:2159513211
    芫花素; Genkwanin CFN98670 437-64-9 C16H12O5 = 284.3 20mg QQ客服:2159513211
    黄花夹竹桃黄酮; Thevetiaflavone CFN96124 29376-68-9 C16H12O5 = 284.3 5mg QQ客服:2159513211
    野黄芩素; Scutellarein CFN98557 529-53-3 C15H10O6 = 286.24 20mg QQ客服:215959384
    高车前素; Hispidulin CFN99491 1447-88-7 C16H12O6 = 300.3 20mg QQ客服:2159513211
    蓟黄素; Cirsimaritin CFN97126 6601-62-3 C17H14O6 = 314.3 10mg QQ客服:1413575084
    8-羟基芹菜素; Isoscutellarein CFN91491 41440-05-5 C15H10O6 = 286.2 5mg QQ客服:2159513211
    4'-羟基汉黄芩素; 4'-Hydroxywogonin CFN98960 57096-02-3 C16H12O6 = 300.3 10mg QQ客服:3257982914
    5,8-二羟基-2-(4-羟基苯基)-6,7-二甲氧基-4H- 1-苯并吡喃-4-酮; Isothymusin CFN97562 98755-25-0 C17H14O7 = 330.3 5mg QQ客服:3257982914





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