4-(3-(trifluoromethyl)phenoxy)butanoic acid | 87411-31-2

• 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: 4-(3-(trifluoromethyl)phenoxy)butanoic acid
• 英文别名: 4-(3-Trifluoromethyl-phenoxy)-butyric acid；4-[3-(trifluoromethyl)phenoxy]butanoic acid
• CAS: 87411-31-2
• 化学式: C₁₁H₁₁F₃O₃
• mdl: MFCD08111620
• 分子量: 248.202
• InChiKey: BROOMGSHOWKNNX-UHFFFAOYSA-N

物化性质

• 熔点：
  54-55 °C(Solv: heptane (142-82-5))
• 沸点：
  352.6±42.0 °C(Predicted)
• 密度：
  1.298±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  17
• 可旋转键数：
  5
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.363
• 拓扑面积：
  46.5
• 氢给体数：
  1
• 氢受体数：
  6

安全信息

• 危险等级：
  IRRITANT

反应信息

• 作为反应物：
  描述：

  4-(3-(trifluoromethyl)phenoxy)butanoic acid 生成 8-trifluoromethyl-3,4-dihydro-2H-benzo[b]oxepin-5-one
  参考文献：
  名称：

  FREEDMAN, JULES;STEWART, KENNETH T., J. HETEROCYCL. CHEM., 26,(1989) N, C. 1547-1554

  摘要：

  DOI：
• 作为产物：
  描述：

  间三氟甲基苯酚 在 potassium carbonate 、 sodium hydroxide 作用下， 以 二甲基亚砜 为溶剂， 生成 4-(3-(trifluoromethyl)phenoxy)butanoic acid
  参考文献：
  名称：

  含氟的α-[[（取代的苯氧基丁氧基或戊氧基）]烷基膦酸酯和2-（取代的苯氧基丁氧基）烷基-5,5-二甲基-1,3,2-二氧杂膦烷-2-酮的合成及除草活性

  摘要：

  基于我们对先导化合物I的结构修饰的先前工作，设计并合成了三组新型的含氟膦酸酯衍生物（II，III和IV）。在温室中评估了它们对某些杂草的出苗后除草活性。通过将两种亚甲基引入结构I来合成化合物II。与市售除草剂消旋杀虫剂相比，化合物Ⅱ显示出中等的除草活性，对青菜b虫（Abutilon theophrasti），普通mar菜（Amaranthus retroflexus）和白食（白色）的抑制作用为60-85％。旱莲草（Eclipta prostrate）的速率为150 g ai / ha。通过引入具有显着除草活性的开链膦酸酯来设计化合物III。尤其是，化合物III-1 – III-4，III – 6，III – 8，III – 11和III – 12与clacyfos相比，对所有测试的阔叶杂草表现出显着的除草活性（80–100％），而化合物IV具有五个碳原子的羧酸链对所有测试的杂草均无活性。结

  DOI：

  10.1016/j.jfluchem.2016.11.008

文献信息

• Small Molecule Analogs of the Nemo Binding Peptide
  申请人：THE SCRIPPS RESEARCH INSTITUTE

  公开号：US20180169078A1

  公开（公告）日：2018-06-21

  The invention is directed to a method of inhibiting, within a living cell, the interaction between NF-κB essential modulator (“NEMO”) with IκB kinase-β (IKK-β) at the NEMO binding domain (NBD), comprising exposing the cell to an effective amount or concentration of a compound of the invention, a NEMO-binding domain analog (NBDA). The invention is further directed to a method of treating a condition in a patient, wherein inhibiting the interaction between NF-κB essential modulator (“NEMO”) with IκB kinase-β (IKK-β) at the NEMO binding domain (NBD) is medically indicated, comprising administering to the patient an effective dose of a compound of the invention. Conditions that can be treated by a method of the invention includes muscular dystrophy, asthma, inflammatory bowel disease, multiple sclerosis, Parkinson's Disease, arthritis, diabetes, graft versus host disease, accelerated aging, heart ischemia, cancer, UV-induced skin damage, or an age-related pathology.

  该发明涉及一种抑制活细胞内NF-κB基本调节因子（“NEMO”）与IκB激酶-β（IKK-β）在NEMO结合结构域（NBD）上相互作用的方法，包括将细胞暴露于一种有效量或浓度的该发明化合物，即NEMO结合结构域类似物（NBDA）。该发明进一步涉及一种治疗患者病症的方法，其中在医学上指示抑制NF-κB基本调节因子（“NEMO”）与IκB激酶-β（IKK-β）在NEMO结合结构域（NBD）上的相互作用，包括向患者施用该发明化合物的有效剂量。该发明方法可治疗的病症包括肌肉萎缩症、哮喘、炎性肠病、多发性硬化症、帕金森病、关节炎、糖尿病、移植物抗宿主病、加速衰老、心脏缺血、癌症、紫外线诱导的皮肤损伤或与年龄相关的病理。
• Identification of Small Molecules Blocking the Pseudomonas aeruginosa Type III Secretion System Protein PcrV
  作者：Charlotta Sundin、Michael Saleeb、Sara Spjut、Liena Qin、Mikael Elofsson

  DOI：10.3390/biom11010055

  日期：——

  Pseudomonas aeruginosa is an opportunistic bacterial pathogen that employs its type III secretion system (T3SS) during the acute phase of infection to translocate cytotoxins into the host cell cytoplasm to evade the immune system. The PcrV protein is located at the tip of the T3SS, facilitates the integration of pore-forming proteins into the eukaryotic cell membrane, and is required for translocation of cytotoxins into the host cell. In this study, we used surface plasmon resonance screening to identify small molecule binders of PcrV. A follow-up structure-activity relationship analysis resulted in PcrV binders that protect macrophages in a P. aeruginosa cell-based infection assay. Treatment of P. aeruginosa infections is challenging due to acquired, intrinsic, and adaptive resistance in addition to a broad arsenal of virulence systems such as the T3SS. Virulence blocking molecules targeting PcrV constitute valuable starting points for development of next generation antibacterials to treat infections caused by P. aeruginosa.

  铜绿假单胞菌是一种机会性细菌病原体，它在感染的急性阶段利用其III型分泌系统（T3SS）将细胞毒素转运到宿主细胞胞质中，以逃避免疫系统。PcrV蛋白位于T3SS的顶端，促进孔形成蛋白与真核细胞膜的整合，并且需要将细胞毒素转运到宿主细胞中。在这项研究中，我们使用表面等离子共振筛选识别PcrV的小分子结合物。随后进行的结构-活性关系分析得出了能在基于P. aeruginosa细胞的感染实验中保护巨噬细胞的PcrV结合物。治疗P. aeruginosa感染具有挑战性，因为除了广泛的毒力系统（如T3SS）外，还存在获得性、固有性和适应性抗性。针对PcrV的毒力阻断分子为开发下一代抗菌剂治疗由铜绿假单胞菌引起的感染提供了宝贵的起点。
• Synthesis and herbicidal activity of α-[(substituted phenoxybutyryloxy or valeryoxy)]alkylphosphonates and 2-(substituted phenoxybutyryloxy)alkyl-5,5-dimethyl-1,3,2-dioxaphosphinan-2-one containing fluorine
  作者：Wei Wang、Yuan Zhou、Hao Peng、Hong-Wu He、Xing-Tao Lu

  DOI：10.1016/j.jfluchem.2016.11.008

  日期：2017.1

  modification of the lead compound I, three series of novel fluorine-containing phosphonates derivatives (II, III and IV) were designed and synthesized. Their post-emergence herbicidal activities against some species of weeds were evaluated in a green house. The compounds II were synthesized by introducing of two methylene into the structure I. Compared with the commercial herbicidal clacyfos, compounds II showed

  基于我们对先导化合物I的结构修饰的先前工作，设计并合成了三组新型的含氟膦酸酯衍生物（II，III和IV）。在温室中评估了它们对某些杂草的出苗后除草活性。通过将两种亚甲基引入结构I来合成化合物II。与市售除草剂消旋杀虫剂相比，化合物Ⅱ显示出中等的除草活性，对青菜b虫（Abutilon theophrasti），普通mar菜（Amaranthus retroflexus）和白食（白色）的抑制作用为60-85％。旱莲草（Eclipta prostrate）的速率为150 g ai / ha。通过引入具有显着除草活性的开链膦酸酯来设计化合物III。尤其是，化合物III-1 – III-4，III – 6，III – 8，III – 11和III – 12与clacyfos相比，对所有测试的阔叶杂草表现出显着的除草活性（80–100％），而化合物IV具有五个碳原子的羧酸链对所有测试的杂草均无活性。结
• 바르비투르산 유도체 화합물을 유효성분으로 포함하는 살충제
  申请人：서울대학교산학협력단

  公开号：KR20220066701A

  公开（公告）日：2022-05-24

  본 발명은 저항성 해충의 발달, 인축에 대한 독성, 환경오염, 잔류문제 등 다양한 부작용을 낳고 있는 유기합성 농약을 대체할 수 있는 새로운 살충제 원제 개발에 활용 가능한 바르비투르산 유도체 화합물, 이를 유효성분으로 함유하는 살충제 조성물을 제공한다.

  本发明提供了一种可以用于开发新的杀虫剂原料，以替代产生多种副作用，如抗性害虫的发展，对人畜的毒性，环境污染和残留问题等有机合成农药的巴比妥酸诱导体化合物，以及包含其作为有效成分的杀虫剂组合物。
• Small molecule analogs of the nemo binding peptide
  申请人：THE SCRIPPS RESEARCH INSTITUTE

  公开号：US10758522B2

  公开（公告）日：2020-09-01

  The invention is directed to a method of inhibiting, within a living cell, the interaction between NF-κB essential modulator (“NEMO”) with IκB kinase-β (IKK-β) at the NEMO binding domain (NBD), comprising exposing the cell to an effective amount or concentration of a compound of the invention, a NEMO-binding domain analog (NBDA). The invention is further directed to a method of treating a condition in a patient, wherein inhibiting the interaction between NF-κB essential modulator (“NEMO”) with IκB kinase-β (IKK-β) at the NEMO binding domain (NBD) is medically indicated, comprising administering to the patient an effective dose of a compound of the invention. Conditions that can be treated by a method of the invention includes muscular dystrophy, asthma, inflammatory bowel disease, multiple sclerosis, Parkinson's Disease, arthritis, diabetes, graft versus host disease, accelerated aging, heart ischemia, cancer, UV-induced skin damage, or an age-related pathology.

  本发明涉及一种在活细胞内抑制NF-κB基本调节剂（"NEMO"）与IκB激酶-β（IKK-β）在NEMO结合结构域（NBD）处相互作用的方法，包括将细胞暴露于有效量或有效浓度的本发明化合物--NEMO结合结构域类似物（NBDA）。本发明进一步涉及一种治疗患者病症的方法，其中抑制 NF-κB 基本调节剂（"NEMO"）与 IκB 激酶-β（IKK-β）在 NEMO 结合结构域（NBD）处的相互作用具有医学指征，包括向患者施用有效剂量的本发明化合物。本发明方法可治疗的疾病包括肌肉萎缩症、哮喘、炎症性肠病、多发性硬化症、帕金森病、关节炎、糖尿病、移植物抗宿主疾病、加速衰老、心脏缺血、癌症、紫外线引起的皮肤损伤或与年龄相关的病理。