2-trifluoromethylbenzalacetone | 76293-37-3

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 肉桂酸及其衍生物
• 英文名称: 2-trifluoromethylbenzalacetone
• 英文别名: 2-Trifluormethylbenzalaceton；4-(2-Trifluoromethylphenyl)-3-buten-2-one；4-[2-(trifluoromethyl)phenyl]but-3-en-2-one
• CAS: 76293-37-3
• 化学式: C₁₁H₉F₃O
• 分子量: 214.187
• InChiKey: DNMFDFHJWALWGN-UHFFFAOYSA-N

物化性质

• 沸点：
  260.7±35.0 °C(Predicted)
• 密度：
  1.206±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.9
• 重原子数：
  15
• 可旋转键数：
  2
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.18
• 拓扑面积：
  17.1
• 氢给体数：
  0
• 氢受体数：
  4

安全信息

• 危险等级：
  IRRITANT

反应信息

• 作为反应物：
  描述：

  2-trifluoromethylbenzalacetone 在 镍 氢气 、 title compound 作用下， 以 乙酸乙酯 为溶剂， 反应 7.0h， 生成 4-(2-trifluoromethylphenyl)butan-2-one
  参考文献：
  名称：

  Aminoacetonitrile derivatives and their use for controlling parasites

  摘要：

  本发明涉及一般式（I）的化合物，其中R1，R2，X，Ar1和Ar2如权利要求1所定义，并涉及其任何对映体。该活性成分具有有利的农药性能。它们特别适用于控制温血动物中的寄生虫。

  公开号：

  US07091371B2
• 作为产物：
  描述：

  邻三氟甲基苯甲醛 、 1-三苯基膦-2-丙酮 以 四氢呋喃 为溶剂， 反应 12.0h， 生成 2-trifluoromethylbenzalacetone
  参考文献：
  名称：

  Cyclohexane 1,3-diones and their inhibition of mutant SOD1-dependent protein aggregation and toxicity in PC12 cells

  摘要：

  Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive loss of motor neurons. Currently, there is only one FDA-approved treatment for ALS (riluzole), and that drug only extends life, on average, by 2-3 months. Mutations in Cu/Zn superoxide dismutase (SOD1) are found in familial forms of the disease and have played an important role in the study of ALS pathophysiology. On the basis of their activity in a PC12-G93A-YFP high-throughput screening assay, several bioactive compounds have been identified and classified as cyclohexane-1,3-dione (CHD) derivatives. A concise and efficient synthetic route has been developed to provide diverse CHD analogs. The structural modification of the CHD scaffold led to the discovery of a more potent analog (26) with an EC(50) of 700 nM having good pharmacokinetic properties, such as high solubility, low human and mouse metabolic potential, and relatively good plasma stability. It was also found to efficiently penetrate the blood-brain barrier. However, compound 26 did not exhibit any significant life span extension in the ALS mouse model. It was found that, although 26 was active in PC12 cells, it had poor activity in other cell types, including primary cortical neurons, indicating that it can penetrate into the brain, but is not active in neuronal cells, potentially due to poor selective cell penetration. Further structural modification of the CHD scaffold was aimed at improving global cell activity as well as maintaining potency. Two new analogs (71 and 73) were synthesized, which had significantly enhanced cortical neuronal cell permeability, as well as similar potency to that of 26 in the PC12-G93A assay. These CHD analogs are being investigated further as novel therapeutic candidates for ALS. (C) 2011 Elsevier Ltd. All rights reserved.

  DOI：

  10.1016/j.bmc.2011.11.039

文献信息

• Preventive effect of ursolic acid derivative on particulate matter 2.5‐induced chronic obstructive pulmonary disease involves suppression of lung inflammation
  作者：Cuini Li、Junxian Chen、Weiwei Yuan、Wei Zhang、Hong Chen、Hongtao Tan

  DOI：10.1002/iub.2201

  日期：2020.4

  ursolic acid derivative treatment increased level of superoxide dismutase in mice with COPD. The lung injury induced by PM2.5 in mice was also prevented on treatment with ursolic acid derivative. Thus, ursolic acid derivative inhibits pulmonary tissues damage in mice through suppression of inflammatory cytokine and oxidative enzymes. Therefore, ursolic acid derivative can be of therapeutic importance

  慢性阻塞性肺病 (COPD) 等呼吸系统疾病与空气中颗粒物 2.5 (PM2.5) 的存在有关。在本研究中，在体内研究了合成的熊果酸衍生物对 PM2.5 诱导的 COPD 小鼠模型的影响。每日鼻内给予PM2.5混悬液25μL，连续1周，建立COPD小鼠模型。给予 PM2.5 后，小鼠支气管肺泡液中氧化应激标志物和炎症细胞因子（如肿瘤坏死因子-α 和白细胞介素-6）的水平显着增加。然而，熊果酸衍生物治疗以剂量依赖性方式显着抑制 PM2.5 诱导的氧化应激标志物和炎症细胞因子的增加。苏木精和伊红染色显示患有慢性阻塞性肺病的小鼠肺组织中有过度的炎症细胞浸润。用熊果酸衍生物治疗小鼠后，炎症细胞浸润受到抑制。熊果酸衍生物治疗可增加慢性阻塞性肺病小鼠的超氧化物歧化酶水平。熊果酸衍生物治疗也可以预防小鼠中由 PM2.5 引起的肺损伤。因此，熊果酸衍生物通过抑制炎症细胞因子和氧化酶来抑制小鼠肺组织损伤。因此，熊果酸衍生物对于治疗
• Primary Amine/(+)-CSA Salt-Promoted Organocatalytic Conjugate Addition of Nitro Esters to Enones
  作者：Chen Liu、Yixin Lu

  DOI：10.1021/ol1006407

  日期：2010.5.21

  The combination of 9-amino-9-deoxy-epi-cinchonine and (+)-CSA resulted in a novel primary amine-based organocatalyst for effective iminium activation of α,β-unsaturated ketones. Such a catalytic system could catalyze the conjugate addition of nitroacetate to enones in a highly enantioselective manner, affording the desired adducts in high yields and with up to 99% ee.

  9-氨基-9-脱氧-表-辛可宁和（+）-CSA的组合产生了一种新型的基于伯胺的有机催化剂，可以有效地亚胺激活α，β-不饱和酮。这种催化系统可以以高对映选择性的方式催化硝基乙酸与烯酮的共轭加成，从而以高收率和高达99％的ee提供所需的加合物。
• Organocatalyzed [4 + 2] cycloaddition of α,β-unsaturated ketones and isatylidene malononitrile: accessing spiro[3-arylcyclohexanone]oxindole derivatives
  作者：Baliram R. Patil、Chandrakant B. Nichinde、Suryakant S. Chaudhari、Gamidi Rama Krishna、Anil K. Kinage

  DOI：10.1039/d3ra07652k

  日期：——

  Herein, we developed a series of compounds featuring spiro[3-arylcyclohexanone]oxindoles through Barbas [4 + 2] cycloaddition reactions between isatylidene malononitrile and α,β-unsaturated ketones using L-proline as an organocatalyst. The reported methodology offers many advantages such as mild reaction conditions, diverse substrate scope with high yields, easy reaction setup, and use of easily synthesizable

  在此，我们以L-脯氨酸为有机催化剂，通过异亚叉基丙二腈与α,β-不饱和酮之间的Barbas [4 + 2]环加成反应，开发了一系列以螺[3-芳基环己酮]羟吲哚为特征的化合物。所报道的方法具有许多优点，例如温和的反应条件、高产率的多样化底物范围、简单的反应设置以及使用易于合成的起始材料。
• Antimalarial drugs. 64. Synthesis and antimalarial properties of 1-imino derivatives of 7-chloro-3-substituted-3,4-dihydro-1,9(2H,10H)-acridinediones and related structures
  作者：Stephen J. Kesten、Margaret J. Degnan、Jocelyn Hung、Dennis J. McNamara、Daniel F. Ortwine、Susan E. Uhlendorf、Leslie M. Werbel

  DOI：10.1021/jm00097a001

  日期：1992.9

  To improve upon the activity and properties of the 3-aryl-7-chloro-3,4-dihydro-1,9(2H,10H)-acridinediones, a variety of 1-[(alkylamino)alkylene]imino derivatives (3) were prepared and shown to be highly active antimalarial agents in both rodents and primates. Among structural modifications prepared, including N-10-alkyl and C2-substituted analogs, removal of the C-9 oxygen, and introduction of an imino side chain at C-9, the imines of the N-10-H acridinediones were the most active compounds obtained. The [3-(NN-dimethylamino)propyl]imino derivative of 7-chloro-3-(2,4-dichlorophenyl)-3,4-dihydro-1,9(2H,10H)-acridinedione (9aa) proved to be highly active in advanced studies in primates.
• Cyclohexane 1,3-diones and their inhibition of mutant SOD1-dependent protein aggregation and toxicity in PC12 cells
  作者：Wei Zhang、Radhia Benmohamed、Anthony C. Arvanites、Richard I. Morimoto、Robert J. Ferrante、Donald R. Kirsch、Richard B. Silverman

  DOI：10.1016/j.bmc.2011.11.039

  日期：2012.1

  Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive loss of motor neurons. Currently, there is only one FDA-approved treatment for ALS (riluzole), and that drug only extends life, on average, by 2-3 months. Mutations in Cu/Zn superoxide dismutase (SOD1) are found in familial forms of the disease and have played an important role in the study of ALS pathophysiology. On the basis of their activity in a PC12-G93A-YFP high-throughput screening assay, several bioactive compounds have been identified and classified as cyclohexane-1,3-dione (CHD) derivatives. A concise and efficient synthetic route has been developed to provide diverse CHD analogs. The structural modification of the CHD scaffold led to the discovery of a more potent analog (26) with an EC(50) of 700 nM having good pharmacokinetic properties, such as high solubility, low human and mouse metabolic potential, and relatively good plasma stability. It was also found to efficiently penetrate the blood-brain barrier. However, compound 26 did not exhibit any significant life span extension in the ALS mouse model. It was found that, although 26 was active in PC12 cells, it had poor activity in other cell types, including primary cortical neurons, indicating that it can penetrate into the brain, but is not active in neuronal cells, potentially due to poor selective cell penetration. Further structural modification of the CHD scaffold was aimed at improving global cell activity as well as maintaining potency. Two new analogs (71 and 73) were synthesized, which had significantly enhanced cortical neuronal cell permeability, as well as similar potency to that of 26 in the PC12-G93A assay. These CHD analogs are being investigated further as novel therapeutic candidates for ALS. (C) 2011 Elsevier Ltd. All rights reserved.