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  • 毛蕊异黄酮

    Calycosin

    毛蕊异黄酮
    产品编号 CFN99140
    CAS编号 20575-57-9
    分子式 = 分子量 C16H12O5 = 284.26
    产品纯度 >=98%
    物理属性 Yellow powder
    化合物类型 Flavonoids
    植物来源 The herbs of Astragalus membranaceus Bge. var. mongholicus.
    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
    毛蕊异黄酮 CFN99140 20575-57-9 10mg QQ客服:2056216494
    毛蕊异黄酮 CFN99140 20575-57-9 20mg QQ客服:2056216494
    毛蕊异黄酮 CFN99140 20575-57-9 50mg QQ客服:2056216494
    毛蕊异黄酮 CFN99140 20575-57-9 100mg QQ客服:2056216494
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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
  • Kazusa DNA Research Institute (Japan)
  • Universidad de Ciencias y Artes de Chiapas (Mexico)
  • Amity University (India)
  • Universite Libre de Bruxelles (Belgium)
  • The Institute of Cancer Research (United Kingdom)
  • Universitas islam negeri Jakarta (Indonesia)
  • Instytut Nawozów Sztucznych w Pu?awach (Poland)
  • Wroclaw Medical University (Poland)
  • Complutense University of Madrid (Spain)
  • Martin Luther University of Halle-Wittenberg (Germany)
  • Universidade Federal de Santa Catarina (Brazil)
  • Srinakharinwirot University (Thailand)
  • Fraunhofer-Institut für Molekularbiologie und Angewandte ?kologie IME (Germany)
  • Northeast Normal University Changchun (China)
  • More...
  • 国外学术期刊发表的引用ChemFaces产品的部分文献
  • BMC Plant Biol.2018, 18(1):122
  • Trop J Pharm Res.2023, 22(3):283-288.
  • The Catharanthus Genome2022,35-83.
  • ACS Chem Biol.2019, 14(5):873-881
  • Phytomedicine.2019, 62:152962
  • Vietnam Journal of Science2022,64(2):69-75.
  • Separations2021, 8(7),90.
  • BMC Microbiol.2019, 19(1):78
  • Nutrients.2021, 13(10):3414.
  • Biol Pharm Bull.2020, 43(10):1534-1541.
  • Pak J Pharm Sci.2018, 31:311-315
  • GxABT2022, 2268.2:15515.
  • J of Essential Oil Research2019, 1677272
  • Evid Based Complement Alternat Med.2018, 2018:3610494
  • UDC.2020, 19(4).
  • Horticulture Research2022, uhac276.
  • Research Square2021, 10.21203.
  • ACS Omega2020, 5,33,20825-20830
  • Phytother Res.2022, 35844057.
  • Eur J Neurosci.2021, 53(11):3548-3560.
  • Applied Biological Chemistry 2022, 65,5(2022).
  • Bioorg Med Chem.2020, 28(12):115553.
  • Indian J Pharm Sci.2022, 84(4): 874-882.
  • ...
  • 生物活性
    Description: Calycosin, a selective estrogen receptor modulator, is also a vasorelaxant and a noncompetitive Ca(2+) channel blocker. It has anti-oxidative, anti-inflammatory, hepatoprotective,antineoplastic, and effective skin-lightening activities. Calycosin exhibited tyrosinase inhibitory activity with an IC(50) value of 38.4 microM, it suppressed breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways.
    Targets: Bcl-2/Bax | Caspase | Akt | FXR | STAT | p38MAPK | ERK | JNK | PI3K | IGF-1R | Calcium Channel
    In vitro:
    Cell Physiol Biochem. 2015;35(2):722-8.
    Calycosin and Genistein Induce Apoptosis by Inactivation of HOTAIR/p-Akt Signaling Pathway in Human Breast Cancer MCF-7 Cells.[Pubmed: 25613518]
    Calycosin and genistein are the two main components of isoflavones. Previously, we reported that these compounds display antitumor activities in the breast cancer cell lines MCF-7 and T47D. In the present study, we investigated the mechanism of action of calycosin and genistein, and their respective efficacies as potential therapies for the treatment of breast carcinoma in the clinic.
    METHODS AND RESULTS:
    MCF-7 cells were treated with calycosin or genistein. Cell proliferation and apoptosis were measured using CCK8 assay and Hoechst 33258. The expression level of phosphorylated Akt protein was determined by western blotting. Expression level of HOTAIR was quantified by real-time PCR. Both calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with calycosin. Treatment of MCF-7 cells with calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR.
    CONCLUSIONS:
    Calycosin is more effective in inhibiting breast cancer growth in comparison with genistein, through its regulation of Akt signaling pathways and HOTAIR expression.
    PLoS One. 2014 Mar 11;9(3):e91245.
    Calycosin suppresses breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways.[Pubmed: 24618835]
    We previously reported that calycosin, a natural phytoestrogen structurally similar to estrogen, successfully triggered apoptosis of estrogen receptor (ER)-positive breast cancer cell line, MCF-7.
    METHODS AND RESULTS:
    To better understand the antitumor activities of calycosin against breast cancer, besides MCF-7 cells, another ER-positive cell line T-47D was analyzed here, with ER-negative cell lines (MDA-231, MDA-435) as control. Notably, calycosin led to inhibited cell proliferation and apoptosis only in ER-positive cells, particularly in MCF-7 cells, whereas no such effect was observed in ER-negative cells. Then we investigated whether regulation of ERβ, a subtype of ER, contributed to calycosin-induced apoptosis in breast cancer cells. The results showed that incubation of calycosin resulted in enhanced expression ERβ in MCF-7 and T-47D cells, rather than MDA-231 and MDA-435 cells. Moreover, with the upregulation of ERβ, successive changes in downstream signaling pathways were found, including inactivation of insulin-like growth factor 1 receptor (IGF-1R), then stimulation of p38 MAPK and suppression of the serine/threonine kinase (Akt), and finally poly(ADP-ribose) polymerase 1 (PARP-1) cleavage. However, the other two members of the mitogen-activated protein kinase (MAPK) family, extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK), were not consequently regulated by downregulated IGF-1R, indicating ERK 1/2 and JNK pathways were not necessary to allow proliferation inhibition by calycosin.
    CONCLUSIONS:
    Taken together, our results indicate that calycosin tends to inhibit growth and induce apoptosis in ER-positive breast cancer cells, which is mediated by ERβ-induced inhibition of IGF-1R, along with the selective regulation of MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt pathways.
    In vivo:
    J Neurol Sci. 2014 Apr 15;339(1-2):144-8.
    Downregulated RASD1 and upregulated miR-375 are involved in protective effects of calycosin on cerebral ischemia/reperfusion rats.[Pubmed: 24548484 ]
    Isoflavone calycosin is a typical phytoestrogen extracted from Chinese medical herb Radix Astragali. It has been reported that estrogens could provide neuroprotective effects, and dietary intake of phytoestrogens could reduce stroke injury in cerebral ischemia/reperfusion (I/R) animal models.
    METHODS AND RESULTS:
    In the present study, we investigate the molecular mechanisms underlying the neuroprotective effects of calycosin on middle cerebral artery occlusion (MCAO) rats. Focal cerebral ischemia was induced in male rats by MCAO, neurological deficits and brain edema was evaluated after 24h of reperfusion. The results shown calycosin significantly reduced the infarcted volume and the brain water content, and improved the neurological deficit. To provide insight into the functions of estrogen receptor (ER)-mediated signaling pathway in neuroprotection by calycosin, the expression of miR-375, ER-α, RASD1 (Dexamethasone-induced Ras-related protein 1) and Bcl-2 was determined by RT-PCR or western blot assay. Calycosin exhibited a downregulation of RASD1, and an upregulation of ER-α, miR-375 and Bcl-2.
    CONCLUSIONS:
    Our finding illustrated that calycosin had been shown neuroprotective effects in cerebral ischemia/reperfusion rats, and the molecular mechanisms may correlate with the positive feedback between ER-α and miR-375, along with the regulation of downstream targets.
    Acta Pharmacol. Sin., 2006, 27(8):1007–12.
    Calcium channel blocking activity of calycosin, a major active component of Astragali Radix, on rat aorta.[Pubmed: 16867251]
    To investigate the vasoactivity of calycosin, a major active component of Astragali Radix.
    METHODS AND RESULTS:
    Experiments were performed on isolated rat thoracic aortic rings pre-contracted with phenylephrine (PHE) or KCl. Calycosin produced a concentration-dependent relaxation on the tissue pre-contracted using PHE with 4.46+/-0.13 of pD(2) and 95.85%+/-2.67% of E(max); or using KCl with 4.27+/-0.05 of pD2 and 99.06%+/-2.15% of Emax, and displaced downwards the concentration-response curves of aortic rings to PHE or KCl. The relaxant effect of calycosin on denuded endothelium aortic rings was the same as on intact endothelium aortic rings, and its vasorelaxant effect was not influenced by L-NAME or indomethacin. In Ca(2+)-free solution, calycosin (30 micromol/L) did not have an effect on PHE (1 micromol/L)-induced aortic ring contraction. The effects of calycosin and nifedipine where somewhat different; calycosin decreased aortic ring contractions induced by the two agonists, but nifedipine displayed a more potent inhibitory effect on KCl-induced contractions than on PHE-induced contractions, and the vascular relaxing effects of calycosin and nifidipine were additive on PHE-induced contraction but not KCl-induced.
    CONCLUSIONS:
    Calycosin is a vasorelaxant. Its action is endothelium-independent and is unrelated to intracellular Ca(2+) release. It is a noncompetitive Ca(2+) channel blocker. The effect of calycosin on Ca(2+) channel blockade may be different from that of dihydropyridines. This study demonstrated a novel pharmacological activity of calycosin, and supplied a theoretic foundation for Astragali Radix application.
    制备储备液(仅供参考)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.5179 mL 17.5895 mL 35.1791 mL 70.3581 mL 87.9477 mL
    5 mM 0.7036 mL 3.5179 mL 7.0358 mL 14.0716 mL 17.5895 mL
    10 mM 0.3518 mL 1.759 mL 3.5179 mL 7.0358 mL 8.7948 mL
    50 mM 0.0704 mL 0.3518 mL 0.7036 mL 1.4072 mL 1.759 mL
    100 mM 0.0352 mL 0.1759 mL 0.3518 mL 0.7036 mL 0.8795 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
    3',4',7-三羟基异黄酮; 3',4',7-Trihydroxyisoflavone CFN70376 485-63-2 C15H10O5 = 270.2 5mg QQ客服:1413575084
    毛蕊异黄酮; Calycosin CFN99140 20575-57-9 C16H12O5 = 284.26 20mg QQ客服:2056216494
    3'-甲氧基大豆黄素; 3'-Methoxydaidzein CFN96186 21913-98-4 C16H12O5 = 284.3 5mg QQ客服:215959384
    3',4',5,7-四羟基异黄酮; Orobol CFN98737 480-23-9 C15H10O6 = 286.2 5mg QQ客服:2159513211
    3'-O-甲基香豌豆苷元; 3'-O-Methylorobol CFN98492 36190-95-1 C16H12O6 = 300.3 5mg QQ客服:215959384
    7,3'-二-O-甲基奥洛波尔; 7,3'-Di-O-methylorobol CFN96518 104668-88-4 C17H14O6 = 314.30 5mg QQ客服:3257982914
    红车轴草素; Pratensein CFN90805 2284-31-3 C16H12O6 = 300.3 5mg QQ客服:3257982914
    5-Hydroxypseudobaptigenin; 5-Hydroxypseudobaptigenin CFN91501 40624-03-1 C16H10O6 = 298.3 5mg QQ客服:215959384
    刺桐素 H; Erythrinin H CFN96559 1616592-62-1 C17H12O7 = 328.28 5mg QQ客服:3257982914
    次野鸢尾黄素; Irisflorentin CFN99788 41743-73-1 C20H18O8 = 386.35 20mg QQ客服:3257982914

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