MC2211 | 1023694-53-2

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: MC2211
• 英文别名: N-(2-aminophenyl)-4-[(6-oxo-4-phenyl-1H-pyrimidin-2-yl)sulfanylmethyl]benzamide
• CAS: 1023694-53-2
• 化学式: C₂₄H₂₀N₄O₂S
• 分子量: 428.514
• InChiKey: DDFXLJZLWDEHBH-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.5
• 重原子数：
  31
• 可旋转键数：
  6
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.04
• 拓扑面积：
  122
• 氢给体数：
  3
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  4-((6-oxo-4-phenyl-1,6-dihydropyrimidin-2-ylthio)methyl)benzoic acid 、 邻苯二胺 在 (benzotriazo-1-yloxy)tris(dimethylamino)phosphonium hexafluorophosphate 、 三乙胺 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 0.5h， 以58%的产率得到MC2211
  参考文献：
  名称：

  Novel uracil-based 2-aminoanilide and 2-aminoanilide-like derivatives: Histone deacetylase inhibition and in-cell activities

  摘要：

  A novel series of non-hydroxamate HDAC inhibitors (HDACi) showing a uracil group at the left and a 2-aminoanilide/2-aminoanilide- like portion at the right head have been reported. In particular, the new compounds incorporating a 2-aminoanilide moiety behaved as class I-selective HDACi. Compound 8, the most potent and class I-selective, showed weak apoptosis (higher than MS-275) joined to cytodifferentiating activity on U937 cells. Surprisingly, the highest differentiation was observed with 13, through an effect that seems to be unrelated to HDAC inhibition. (c) 2008 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmcl.2008.03.055

文献信息

• TREATMENT OF RETROVIRAL RESERVOIRS EXPLOITING OXIDATIVE STRESS
  申请人：Savarino Andrea

  公开号：US20110305774A1

  公开（公告）日：2011-12-15

  Activation of HIV-1 replication causes oxidative stress, which in turn potentiates HIV-1 replication. The common basis for the compounds of the present invention is: A) the capacity of reactivating HIV-1 from latency, and B) the ability to counteract the cellular machinery which activates in order to limit the effects of oxidative stress. In this way, oxidative stress can be potentiated and a “chain reaction” is sparked. This “chain reaction” induces a more efficient reactivation of HIV-1 from latency and, in some cases, induces selective killing of the infected cells. Actions A) and B) can either be carried out by one drug exerting both effects, or obtained by the combined use of distinct drugs. There are two main cellular machineries counteracting oxidative stress, i.e. the thioredoxin (Trx) thioredoxin reductase (TrxR) system and glutathione. Herein, we present drug strategies capable of exerting action B) by blocking either of the two machineries.

  HIV-1复制的激活会引起氧化应激，从而加强HIV-1的复制。本发明化合物的共同基础是：A）重新激活HIV-1潜伏感染的能力，和B）对抗细胞机制，以限制氧化应激的影响。通过这种方式，氧化应激可以被增强并引发“连锁反应”。这种“连锁反应”诱导更有效的HIV-1潜伏感染的重新激活，并在某些情况下诱导感染细胞的选择性杀死。行动A）和B）可以由一种药物实现两种效果，也可以通过联合使用不同药物获得。对抗氧化应激的两种主要细胞机制是硫氧还蛋白（Trx）硫氧还蛋白还原酶（TrxR）系统和谷胱甘肽。在此，我们提出了能够通过阻断这两种机制之一来实现B）行动的药物策略。
• TREATMENT OF LATENT HIV-1 INFECTIONS USING AURANOFIN OR ARSENIC TRIOXIDE
  申请人：Istituto Superiore di Sanità

  公开号：EP2349245B1

  公开（公告）日：2016-08-03
• US8785493B2
  申请人：——

  公开号：US8785493B2

  公开（公告）日：2014-07-22
• [EN] TREATMENT OF RETROVIRAL RESERVOIRS EXPLOITING OXIDATIVE STRESS<br/>[FR] TRAITEMENT DE RÉSERVOIRS RÉTROVIRAUX EXPLOITANT LE STRESS OXYDATIF
  申请人：IST SUPERIORE SANITA

  公开号：WO2010049182A2

  公开（公告）日：2010-05-06

  Activation of HIV-1 replication causes oxidative stress, which in turn potentiates HIV-1 replication. The common basis for the compounds of the present invention is: A) the capacity of reactivating HIV-1 from latency, and B) the ability to counteract the cellular machinery which activates in order to limit the effects of oxidative stress. In this way, oxidative stress can be potentiated and a "chain reaction" is sparked. This "chain reaction" induces a more efficient reactivation of HIV-1 from latency and, in some cases, induces selective killing of the infected cells. Actions A) and B) can either be carried out by one drug exerting both effects, or obtained by the combined use of distinct drugs. There are two main cellular machineries counteracting oxidative stress, i.e. the thioredoxin (Trx) thioredoxin reductase (TrxR) system and glutathione. Herein, we present drug strategies capable of exerting action B) by blocking either of the two machineries.
• Novel uracil-based 2-aminoanilide and 2-aminoanilide-like derivatives: Histone deacetylase inhibition and in-cell activities
  作者：Antonello Mai、Andrea Perrone、Angela Nebbioso、Dante Rotili、Sergio Valente、Maria Tardugno、Silvio Massa、Floriana De Bellis、Lucia Altucci

  DOI：10.1016/j.bmcl.2008.03.055

  日期：2008.4

  A novel series of non-hydroxamate HDAC inhibitors (HDACi) showing a uracil group at the left and a 2-aminoanilide/2-aminoanilide- like portion at the right head have been reported. In particular, the new compounds incorporating a 2-aminoanilide moiety behaved as class I-selective HDACi. Compound 8, the most potent and class I-selective, showed weak apoptosis (higher than MS-275) joined to cytodifferentiating activity on U937 cells. Surprisingly, the highest differentiation was observed with 13, through an effect that seems to be unrelated to HDAC inhibition. (c) 2008 Elsevier Ltd. All rights reserved.