3-(2,3,4-trifluorophenyl)propionic acid | 377084-05-4

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 苯丙酸
• 英文名称: 3-(2,3,4-trifluorophenyl)propionic acid
• 英文别名: 3-(2,3,4-Trifluorophenyl)propanoic acid
• CAS: 377084-05-4
• 化学式: C₉H₇F₃O₂
• 分子量: 204.149
• InChiKey: ANWNVMXSGRKDIA-UHFFFAOYSA-N

物化性质

• 沸点：
  272.7±35.0 °C(Predicted)
• 密度：
  1.398±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2
• 重原子数：
  14
• 可旋转键数：
  3
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.22
• 拓扑面积：
  37.3
• 氢给体数：
  1
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  3-(2,3,4-trifluorophenyl)propionic acid 在 aluminum (III) chloride 、 草酰氯 、 N,N-二甲基甲酰胺 作用下， 以 二氯甲烷 为溶剂， 反应 2.0h， 生成 4,5,6-trifluoro-2,3-dihydro-1H-inden-1-one
  参考文献：
  名称：

  1-茚酮通过乙烯插入碳-碳键的双碳环扩展

  摘要：

  据报道，铑催化乙烯直接插入 1-茚满酮中相对无应变的碳-碳键，为制备七元环酮提供了一种双碳扩环策略。由于许多 1-茚满酮可商购获得且乙烯价格低廉，因此该策略简化了苯并环庚烯酮的合成，苯环庚烯酮是生物活性化合物的宝贵合成中间体，但在其他方面制备具有挑战性。此外，该反应无副产物，氧化还原中性，并且可以耐受多种官能团，这可能对制备复杂环状分子的非常规战略键断开产生影响。

  DOI：

  10.1021/jacs.9b07445
• 作为产物：
  描述：

  丙二酸环(亚)异丙酯 、 2,3,4-三氟苯甲醛 在 甲酸 、 三乙胺 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 5.0h， 生成 3-(2,3,4-trifluorophenyl)propionic acid
  参考文献：
  名称：

  1-茚酮通过乙烯插入碳-碳键的双碳环扩展

  摘要：

  据报道，铑催化乙烯直接插入 1-茚满酮中相对无应变的碳-碳键，为制备七元环酮提供了一种双碳扩环策略。由于许多 1-茚满酮可商购获得且乙烯价格低廉，因此该策略简化了苯并环庚烯酮的合成，苯环庚烯酮是生物活性化合物的宝贵合成中间体，但在其他方面制备具有挑战性。此外，该反应无副产物，氧化还原中性，并且可以耐受多种官能团，这可能对制备复杂环状分子的非常规战略键断开产生影响。

  DOI：

  10.1021/jacs.9b07445

文献信息

• [EN] YAP1 INHIBITORS THAT TARGET THE INTERACTION OF YAP1 WITH OCT4<br/>[FR] INHIBITEURS DE YAP1 CIBLANT L'INTERACTION DE YAP1 AVEC OCT4
  申请人：H LEE MOFFITT CANCER CT & RES

  公开号：WO2018053446A1

  公开（公告）日：2018-03-22

  Binding of the transcriptional co-activator, YAP1, to the transcription factor Oct4, induces Sox2, which is a transcription actor necessary for the self-renewal of stem-like cells from non-small cell lung cancer. The WW domain of YAP1 binds to the PPxY motif of Oct4 to induce Sox2. Delivering a peptide corresponding to the WW domain could prevent the induction of Sox2 and stemness. Similarly, peptides and mimetics of the PPxY motif would be able to inhibit stemness. Disclosed are compounds that affect the Yap1:Oct4 interaction.

  转录共激活因子YAP1与转录因子Oct4的结合诱导Sox2，Sox2是非小细胞肺癌干细胞自我更新所必需的转录因子。YAP1的WW结构域与Oct4的PPxY基序结合以诱导Sox2。提供与WW结构域相对应的肽段可以阻止Sox2和干细胞特性的诱导。类似地，PPxY基序的肽段和模拟物能够抑制干细胞特性。揭示了影响Yap1:Oct4相互作用的化合物。
• YAP1 inhibitors that target the interaction of YAP1 with OCT4
  申请人：H. LEE MOFFITT CANCER CENTER AND RESEARCH INSTITUTE, INC.

  公开号：US10906874B2

  公开（公告）日：2021-02-02

  Binding of the transcriptional co-activator, YAP1, to the transcription factor Oct4, induces Sox2, which is a transcription actor necessary for the self-renewal of stem-like cells from non-small cell lung cancer. The WW domain of YAP1 binds to the PPxY motif of Oct4 to induce Sox2. Delivering a peptide corresponding to the WAV domain could prevent the induction of Sox2 and stemness. Similarly, peptides and mimetics of the PPxY motif would be able to inhibit stemness. Disclosed are compounds that affect the Yap1:Oct4 interaction.

  转录共激活因子YAP1与转录因子Oct4结合可诱导Sox2，Sox2是非小细胞肺癌干样细胞自我更新所必需的转录因子。YAP1的WW结构域与Oct4的PPxY基序结合，诱导Sox2。输送与WAV结构域相对应的多肽可阻止Sox2的诱导和干性。同样，PPxY基团的多肽和模拟物也能抑制干性。已公开的化合物会影响Yap1与Oct4的相互作用。
• Small molecule inhibitors of the nuclear translocation of androgen receptor for the treatment of castration-resistant prostate cancer
  申请人：University of Pittsburgh—Of the Commonwealth System of Higher Education

  公开号：US10980806B2

  公开（公告）日：2021-04-20

  A compound, or a pharmaceutically acceptable salt or ester thereof, according to formula I: R20—(Z)b—(Y)c—(R21)a—(X)d—R22—R23 wherein R20 is aryl, substituted aryl, heteroaryl, substituted heteroaryl, cycloalkyl, substituted cycloalkyl, heterocycloalkyl, substituted heterocycloalkyl, alkoxy, aryloxy, a thio-containing group, or a seleno-containing group; Z is alkanediyl, substituted alkanediyl, cycloalkanediyl, or substituted cycloalkanediyl; Y is S, O, S(═O), —S(═O)(═O)—, or NR10, wherein R10 is H or alkyl; R21 is alkanediyl, substituted alkanediyl, cycloalkanediyl, substituted cycloalkanediyl, alkadienyl, substituted alkadienyl, cycloalkenediyl, substituted cycloalkenediyl, alkatrienyl, substituted alkatrienyl; X is —C(═O)—, —S(═O)(═O)—, or —N(H)C(═O)—; R22 includes at least one divalent amino radical; R23 is aryl, substituted aryl, heteroaryl, substituted heteroaryl, cycloalkyl, substituted cycloalkyl, heterocycloalkyl, substituted heterocycloalkyl, alkoxy, aryloxy, a thio-containing group, or a seleno-containing group; a, b, c, and d independently are 0 or 1.

  一种符合式 I 的化合物或其药学上可接受的盐或酯： R20-(Z)b-(Y)c-(R21)a-(X)d-R22-R23 其中 R20 是芳基、取代的芳基、杂芳基、取代的杂芳基、环烷基、取代的环烷基、杂环烷基、取代的杂环烷基、烷氧基、芳氧基、含硫基的基团或含硒基的基团；Z 是烷二基、取代的烷二基、环烷二基或取代的环烷二基； Y 是 S、O、S(═O)、-S(═O)(═O)- 或 NR10，其中 R10 是 H 或烷基；R21是烷二基、取代的烷二基、环烷二基、取代的环烷二基、烷二烯基、取代的烷二烯基、环烷二基、取代的环烷二基、烷三烯基、取代的烷三烯基；X是-C(═O)-、-S(═O)(═O)-或-N(H)C(═O)-；R22 包括至少一个二价氨基； R23 是芳基、取代的芳基、杂芳基、取代的杂芳基、环烷基、取代的环烷基、杂环烷基、取代的杂环烷基、烷氧基、芳氧基、含硫醚基团或含硒基团；a、b、c 和 d 独立地为 0 或 1。
• YAP1 inhibitors that target the interaction of YAP1 with Oct4
  申请人：H. LEE MOFFITT CANCER CENTER AND RESEARCH INSTITUTE, INC.

  公开号：US11530182B2

  公开（公告）日：2022-12-20

  Binding of the transcriptional co-activator, YAP1, to the transcription factor Oct4, induces Sox2, which is a transcription actor necessary for the self-renewal of stem-like cells from non-small cell lung cancer. The WW domain of YAP1 binds to the PPxY motif of Oct4 to induce Sox2. Delivering a peptide corresponding to the WW domain could prevent the induction of Sox2 and stemness. Similarly, peptides and mimetics of the PPxY motif would be able to inhibit sternness. Disclosed are compounds that affect the Yap1:Oct4 interaction.

  转录共激活因子YAP1与转录因子Oct4结合可诱导Sox2，Sox2是非小细胞肺癌干样细胞自我更新所必需的转录因子。YAP1的WW结构域与Oct4的PPxY基序结合，诱导Sox2。输送与WW结构域相对应的多肽可以阻止Sox2的诱导和干性。同样，PPxY基团的多肽和模拟物也能抑制干性。已公开的化合物会影响 Yap1:Oct4 的相互作用。
• Cell-Permeable and Plasma-Stable Peptidomimetic Inhibitors of the Postsynaptic Density-95/<i>N</i>-Methyl-<scp>d</scp>-Aspartate Receptor Interaction
  作者：Anders Bach、Jonas N. N. Eildal、Nicolai Stuhr-Hansen、Rasmus Deeskamp、Marie Gottschalk、Søren W. Pedersen、Anders S. Kristensen、Kristian Strømgaard

  DOI：10.1021/jm1013924

  日期：2011.3.10

  The protein protein interaction between the NMDA receptor and its intracellular scaffolding protein, PSD-95, is a potential target for treating ischemic brain diseases, neuropathic pain, and Alzheimer's disease. We have previously demonstrated that N-alkylated tetrapeptides are potent inhibitors of this interaction, and here, this template is exploited for the development of blood plasma-stable and cell-permeable inhibitors. Initially, we explored both the amino acid sequence of the tetrapeptide and the nature of the N-alkyl groups, which consolidated N-cyclohexylethyl-ETAV (1) as the most potent and selective compound. Next, the amide moieties of N-methylated ETAV were systematically replaced with thioamides, demonstrating that one of three amide bonds could be :replaced without compromising the affinity. Subsequent optimization of the N-alkyl groups and evaluation of cell permeability led to identification of N-cyclohexylethyl-ETA(s)V (54) as the most potent, plasma-stable and cell-permeable inhibitor, which is a promising tool in unraveling the therapeutic potential of the PSD-95/NMDA receptor interaction.