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  • Lonidamine
  • DICA;Diclondazolic Acid;AF1890;氯尼达明
  • 货号: abs813282
    CAS号: 50264-69-2
    分子式: C15H10Cl2N2O2
    分子量: 321.16
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    货号-规格 货期 价格 数量
    abs813282-5mg 1-2周 ¥546.00
    - +
    abs813282-10mg 1-2周 ¥945.00
    - +
    abs813282-50mg 1-2周 ¥3191.00
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    大包装询价
    产品描述
    描述

    Lonidamine是一种有效的小分子己糖激酶抑制剂,IC50为0.85 mM。

    纯度
    98%
    储存/保存方法
    store at -20℃ for one year(Powder);
    in DMSO or others solvent store at 2-4℃ for two weeks, at -20℃ for six months.
    基本信息
    别名
    DICA;Diclondazolic Acid;AF1890;氯尼达明
    外观
    白色或类白色粉末
    可溶性/溶解性
    Ethanol :1.6 mg/mL (5 mM)

    DMSO :32.1 mg/mL (100 mM)
    生物活性
    靶点
    hexokinase
    In vitro(体外研究)
    Lonidamine reduces the oxygen consumption in both normal and neoplastic cells, while it increases the aerobic glycolysis of normal cells but inhibited that of tumor cells. Lonidamine induces the permeabilization of ANT proteoliposomes in a cell-free system, yet has no effect on protein-free liposomes. Lonidamine adds to synthetic planar lipid bilayers containing ANT, eliciting ANT channel activities with clearly distinct conductance levels. Lonidamine provokes a disruption of the mitochondrial transmembrane potential which precedes signs of nuclear apoptosis and cytolysis. Lonidamine causes the dissipation of the mitochondrial inner transmembrane potential and the release of apoptogenic factors capable of inducing nuclear apoptosis in vitro. Lonidamine (50 mg/mL) induces apoptosis in adriamycin and nitrosourea-resistant cells (MCF-7 ADR(r) human breast cancer cell line, and LB9 glioblastoma multiform cell line), as demonstrated by sub-G1 peaks in DNA content histograms, condensation of nuclear chromatin, and internucleosomal DNA fragmentation. Lonidamine has a stronger effect on glioblastoma cell proliferation and metabolism in vitro than did either agent used alone.
    In vivo(体内研究)
    Lonidamine (160 mg/kg) combined with Diazepam is significantly more effective in reducing glioblastoma tumor growth than either drug alone in mice, this tumor growth retardation is maintained as long as treatment is given.
    参考文献
    参考文献
    Increased apoptotic efficacy of lonidamine plus arsenic trioxide combination in human leukemia cells. Reactive oxygen species generation and defensive protein kinase (MEK/ERK, Akt/mTOR) modulation.
    Calviño E, et al. Biochem Pharmacol. 2011 Dec 1;82(11):1619-29. PMID: 21889928.
    Lonidamine: efficacy and safety in clinical trials for the treatment of solid tumors.
    Di Cosimo S, et al. Drugs Today (Barc). 2003 Mar;39(3):157-74. PMID: 12730701.
    Mechanism of lonidamine inhibition of the CFTR chloride channel.
    Gong X, et al. Br J Pharmacol. 2002 Nov;137(6):928-36. PMID: 12411425.
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