4-fluoro-2-nitrophenyl 3,4-dimethoxybenzoate | 1049032-96-3

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 缩酚酸和缩酚酸环醚类
• 英文名称: 4-fluoro-2-nitrophenyl 3,4-dimethoxybenzoate
• CAS: 1049032-96-3
• 化学式: C₁₅H₁₂FNO₆
• 分子量: 321.262
• InChiKey: OTBUZLHOYZZVSC-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  None
• 重原子数：
  None
• 可旋转键数：
  None
• 环数：
  None
• sp3杂化的碳原子比例：
  None
• 拓扑面积：
  None
• 氢给体数：
  None
• 氢受体数：
  None

反应信息

• 作为反应物：
  描述：

  4-fluoro-2-nitrophenyl 3,4-dimethoxybenzoate 在 5%-palladium/activated carbon 、 氢气 作用下， 以 乙醇 为溶剂， 反应 3.0h， 生成
  参考文献：
  名称：

  强效抗肿瘤药2-（3,4-二甲氧基苯基）-5-氟苯并噻唑的苯并噻唑，苯并恶唑和chromen-4-one类似物的合成和生物学特性（PMX 610，NSC 721648）。

  摘要：

  已经合成了新的氟化的2-芳基-苯并噻唑，-苯并恶唑和-铬-4-酮，与有效的抗肿瘤苯并噻唑5相比，它们对MCF-7和MDA 468乳腺癌细胞系具有活性。 12a，d在两种细胞系中产生亚微摩尔GI 50值；然而，就抗肿瘤效力而言，新化合物均未达到5。对于5，似乎必须结合芳基烃受体，但不足以抑制生长。

  DOI：

  10.1021/jm800418z
• 作为产物：
  描述：

  2-硝基-4-氟苯酚 、 3,4-二甲氧基苯甲酰氯 在 吡啶 作用下， 反应 48.0h， 以0.63 g的产率得到4-fluoro-2-nitrophenyl 3,4-dimethoxybenzoate
  参考文献：
  名称：

  强效抗肿瘤药2-（3,4-二甲氧基苯基）-5-氟苯并噻唑的苯并噻唑，苯并恶唑和chromen-4-one类似物的合成和生物学特性（PMX 610，NSC 721648）。

  摘要：

  已经合成了新的氟化的2-芳基-苯并噻唑，-苯并恶唑和-铬-4-酮，与有效的抗肿瘤苯并噻唑5相比，它们对MCF-7和MDA 468乳腺癌细胞系具有活性。 12a，d在两种细胞系中产生亚微摩尔GI 50值；然而，就抗肿瘤效力而言，新化合物均未达到5。对于5，似乎必须结合芳基烃受体，但不足以抑制生长。

  DOI：

  10.1021/jm800418z

文献信息

• Molecular Engineering of Conotoxins: The Importance of Loop Size to α-Conotoxin Structure and Function
  作者：Ai-Hua Jin、Norelle L. Daly、Simon T. Nevin、Ching-I A. Wang、Sebastien Dutertre、Richard J. Lewis、David J. Adams、David J. Craik、Paul F. Alewood

  DOI：10.1021/jm800278k

  日期：2008.9.25

  alpha-Conotoxins are competitive antagonists of nicotinic acetylcholine receptors (nAChRs). The majority of currently characterized alpha-conotoxins have a 4/7 loop size, and the major features of neuronal alpha-conotoxins include a globular disulfide connectivity and a helical structure centered around the third of their four cysteine residues. In this study, a novel "molecular pruning" approach was undertaken to define the relationship between loop size, structure, and function of a-conotoxins. This involved the systematic truncation of the second loop in the a-conotoxin [A10L]PnIA [4/7], a potent antagonist of the alpha 7 nAChR. The penalty for truncation was found to be decreased conformational stability and increased susceptibility to disulfide bond scrambling. Truncation down to 4/4[A10L]PnIA maintained helicity and did not significantly reduce electrophysiological activity at alpha 7 nAChRs, whereas 4/3[AIOL]PnIA lost both alpha 7 nAChR activity and helicity. In contrast, all truncated analogues lost similar to 100-fold affinity at the AMP, a model protein for the extracellular domain of the nAChR. Docking simulations identified several hydrogen bonds lost upon truncation that provide an explanation for the reduced affinities observed at the alpha 7 nAChR and AChBP.
• Antimicrobial cyclic decapeptides with anticancer activity
  作者：Lidia Feliu、Glòria Oliveras、Anna D. Cirac、Emili Besalú、Cristina Rosés、Ramon Colomer、Eduard Bardají、Marta Planas、Teresa Puig

  DOI：10.1016/j.peptides.2010.07.027

  日期：2010.11

  Antimicrobial peptides have been considered as potential candidates for cancer therapy We report here the cytotoxicity of a library of 66 antibacterial cyclodecapeptides on human carcinoma cell lines and their effects on apoptosis [as assessed by cleavage of poly(ADP-ribose) polymerase (PARP)] and cell signaling proteins (p53 and ERK1/2) in cultured human cervical carcinoma cells A design of experiments approach permitted to analyze the results of a subset of 16 peptides and define rules for high anticancer activity against MDA-MB-231 breast carcinoma cells Eight peptides were identified with IC50 values ranging from 18 5 to 57 5 mu M against the five cell lines tested being HeLa cells the most sensitive Among these sequences BPC88 BPC96 BPC98 and BPC194 displayed specificity and high cytotoxicity against HeLa cells (IC50 of 22 5-385 mu M) showed low hemolytic activity and low cytotoxicity to non-malignant fibroblasts and were stable to proteases in human serum Induction of apoptosis by these peptides was observed and the apoptotic effect of BPC88 and BPC96 caused a marked decrease on the activated form of ERK1/2 kinase and an induction of p53 We further showed that BPC96 at low doses synergized the cytotoxic effect of cisplatin These findings suggest that cyclic decapeptides may represent novel anticancer agents providing a new strategy in cancer therapy (C) 2010 Elsevier Inc All rights reserved