CAS: 545380-34-5; N4-(4-Phenoxyphenethyl)Quinazoline-4,6-Diamine

该化合物是一种合成有机化合物,其特点是五氯基核心结构,这是一种双环化合物,含有苯环,并附着于一个火利米丁环;该化合物在五氯环的4和6个位置上有两个地雷组,有助于其作为药理剂的潜力;乙基联系器中附着的四苯基组的存在,增强了其亲脂性并可能影响其生物活动;通常,这种性质的化合物由于其潜在的治疗用途,特别是肿瘤学或作为动脉抑制剂,受到调查,因为其潜在的治疗用途与生物目标发生相互作用的结构模型;分子结构表明,它可能具有诸如有机溶剂溶性以及标准实验室条件下的中度稳定性等特性;与许多合成化合物一样,需要实验性地确定具体特性,包括溶解性,熔点和再活性.

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物理性质

MSDS等安全信息

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C&L通报

上下游产品

6-nitro-4-(4-phenoxyphenylethylamino)quinazoline 4-chloro-6-nitro-quinazoline 6-nitroquinazolone 2-amino-5-nitrobenzamide

合成工艺路线路线简述

    📜N-Boc-酪胺置于吡啶,Palladium On Activated Charcoal,氢气,Copper Diacetate,三乙胺,三氟乙酸体系中,用 四氢呋喃 作为反应溶剂,化学反应生成 N4-[2-(4-苯氧基苯基)乙基]-4,6-喹唑啉二胺
    参考文献:一种新型的基于喹唑啉的类似物通过ros依赖性机制诱导人a549肺癌细胞中的g2 / M细胞周期阻滞和凋亡.
    标题:一种新型的基于喹唑啉的类似物通过ros依赖性机制诱导人a549肺癌细胞中的g2 / M细胞周期阻滞和凋亡.
    摘要:6-氨基-4-(4-苯氧基苯基乙基氨基)喹唑啉(qnz)是一种出色的含喹唑啉的nf-Kb抑制剂,也可作为新型抗癌药.考虑到喹唑啉支架的药用价值和亲电子基抗氧化剂策略中以michael受体为中心的药效基团的可调功能,我们通过在喹唑啉的6位引入一个michael受体单元,设计了一种新颖的qnz亲电子分子qnz-A.在qnz响.我们的结果确定了qnz-A是一种有前途的针对a549细胞的选择性细胞毒剂.qnz-A通过其迈克尔受体单元诱导了与a549细胞中氧化还原缓冲系统崩溃相关的活性氧(ros)积累.这导致p53诱导的p21上调和氧化还原敏感的cdc25C以及细胞周期蛋白b1 / Cdk1的下调,导致g2 / M细胞周期停滞和最终细胞凋亡.相反,缺乏迈克尔受体单元的qnz-A的还原产物qnz-B不能诱导ros的产生以及所有这些与细胞周期有关的事件.总之,这项工作为通过ros促进策略设计qnz定向抗
    DOI:10.1016/j.Bbrc.2017.03.034

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    专利信息


    专利号:US-2014255341-A1
    优先权日:2011-07-22
    标题:Tumor Selective Chemokine Modulation
    发明人：KALINSKI PAWEL; MUTHUSWAMY RAVIKUMAR
    权利人:KALINSKI PAWEL; MUTHUSWAMY RAVIKUMAR
    摘要:Therapies effective for the treatment and prevention of cancer and other diseases are disclosed. These methods include the administration of therapeutically effective amounts of agents that increase the local production of effector cell-attracting chemokines within tumor lesions, with concomitant suppression of local production of undesirable chemokines that attract regulatory T(reg) cells. These methods include administering to the subject therapeutically effective amounts of a Toll-like receptor (TLR) agonist or other activator of NF-KB pathway in combination with a blocker of prostaglandin synthesis or a blocker of prostaglandin signaling, in combination with a type-1 interferon, or in combination with both a blocker of prostaglandin synthesis or signaling and with a type-1 interferon. Alternatively, the methods derived from the same paradigms, but aimed to treat or prevent autoimmune disease, chronic inflammatory disease, transplant rejection or GvR, include the combination of a Toll-like receptor (TLR) agonist in combination with a prostaglandin or other cAMP-activator.

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    主要参考文献


    1: Nekrasov ED, Vigont VA, Klyushnikov SA, Lebedeva OS, Vassina EM, Bogomazova AN, Chestkov IV, Semashko TA, Kiseleva E, Suldina LA, Bobrovsky PA, Zimina OA, Ryazantseva MA, Skopin AY, Illarioshkin SN, Kaznacheyeva EV, Lagarkova MA, Kiselev SL. Manifestation of Huntington's disease pathology in human induced pluripotent stem cell-derived neurons. Mol Neurodegener. 2016 Apr 14;11:27. doi: 10.1186/s13024-016-0092-5.
    2: Wu J, Ryskamp DA, Liang X, Egorova P, Zakharova O, Hung G, Bezprozvanny I. Enhanced Store-Operated Calcium Entry Leads to Striatal Synaptic Loss in a Huntington's Disease Mouse Model. J Neurosci. 2016 Jan 6;36(1):125-41. doi: 10.1523/JNEUROSCI.1038-15.2016.
    3: Vigont V, Kolobkova Y, Skopin A, Zimina O, Zenin V, Glushankova L, Kaznacheyeva E. Both Orai1 and TRPC1 are Involved in Excessive Store-Operated Calcium Entry in Striatal Neurons Expressing Mutant Huntingtin Exon 1. Front Physiol. 2015 Nov 24;6:337. doi: 10.3389/fphys.2015.00337. eCollection 2015.

    合成参考文献


    参考文献:10.1016/s0092-8674(00)81318-5
    摘要:Baeuerle PA, Baltimore D. NF-kappa B: ten years after. Cell. 1996 Oct 04;87(1):13–20. doi: 10.1016/s0092-8674(00)81318-5.
    参考文献:10.1186/1476-9255-7-1
    摘要:Hoareau L, Bencharif K, Rondeau P, Murumalla R, Ravanan P, Tallet F, Delarue P, Cesari M, Roche R, Festy F. Signaling pathways involved in LPS induced TNFalpha production in human adipocytes. Journal of Inflammation. 2010 Jan 08;7(1):1. doi: 10.1186/1476-9255-7-1.
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