2-cyclohexyl-2,2-diphenylacetonitrile | 94684-49-8

• 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: 2-cyclohexyl-2,2-diphenylacetonitrile
• 英文别名: Diphenyl-cyclohexyl-acetonitril；α-Cyclohexyl-diphenylacetonitril；cyclohexyl-diphenyl-acetonitrile
• CAS: 94684-49-8
• 化学式: C₂₀H₂₁N
• 分子量: 275.393
• InChiKey: DFCPGSVFJAZMDA-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  5.8
• 重原子数：
  21
• 可旋转键数：
  3
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.35
• 拓扑面积：
  23.8
• 氢给体数：
  0
• 氢受体数：
  1

反应信息

• 作为反应物：
  描述：

  2-cyclohexyl-2,2-diphenylacetonitrile 在 二异丁基氢化铝 作用下， 以 环己胺 、 甲苯 为溶剂， 反应 12.0h， 以63%的产率得到2-环己基-2,2-二苯基乙醛
  参考文献：
  名称：

  氧化金催化满足光化学反应–由二炔合成苯并[ a ]芴酮

  摘要：

  AbstractDiynes bearing one terminal and one triarylmethyl‐substituted alkyne were converted into complex benzofluorenone derivatives via a one‐pot process involving a gold‐catalyzed step followed by a photocyclization/oxidation. In the first step an N‐oxide was used to position‐selectively generate an α‐oxo carbenoid at the terminal alkyne which after a regioselective 1,6‐carbene transfer along the tethered tritylalkyne and a subsequent aryl 1,2‐shift furnished tetraphenylethylene‐like derivatives. These intermediates were successfully transformed to fluorenones via oxidative photocyclization.magnified image

  DOI：

  10.1002/adsc.201400969
• 作为产物：
  描述：

  环己基苯基乙腈 在 溴 作用下， 生成 2-cyclohexyl-2,2-diphenylacetonitrile
  参考文献：
  名称：

  Hoch; Lecocq, Comptes Rendus Hebdomadaires des Seances de l'Academie des Sciences, 1957, vol. 245, p. 73

  摘要：

  DOI：

文献信息

• Triaryl methane compounds and analogues thereof useful for the treatment
  申请人：Children's Medical Center Corporation

  公开号：US06028103A1

  公开（公告）日：2000-02-22

  The present invention provides a class of chemical compounds useful as efficacious drugs in the treatment of sickle cell disease and diseases characterized by unwanted or abnormal cell proliferation. The active compounds are substituted triaryl methane compounds or analogues thereof where one or more of the aryl groups is replaced with a heteroaryl, cycloalkyl or heterocycloalkyl group and/or the tertiary carbon atom is replaced with a different atom such as Si, Ge, N or P. The compounds inhibit mammalian cell proliferation, inhibit the Gardos channel of erythrocytes, reduce sickle erythrocyte dehydration and/or delay the occurrence of erythrocyte sickling or deformation.

  本发明提供了一类化合物，可作为治疗镰状细胞病和以不需要或异常细胞增殖为特征的疾病的有效药物。这些活性化合物是取代的三芳基甲烷化合物或其类似物，其中芳基中的一个或多个被取代为杂芳基、环烷基或杂环烷基，或者第三级碳原子被硅、锗、氮或磷等不同的原子取代。这些化合物抑制哺乳动物细胞的增殖，抑制红细胞的Gardos通道，减少镰状红细胞的脱水，延迟红细胞的镰刀变形或变形的发生。
• Use of triaryl methane compounds for inhibiting unwanted cellular proliferation associated with inflammatory disease
  申请人：Ion Pharmaceuticals, Inc.

  公开号：US06331564B1

  公开（公告）日：2001-12-18

  The present invention provides a class of chemical compounds useful as efficacious drugs in the treatment of sickle cell disease and diseases characterized by unwanted or abnormal cell proliferation, and in particular inflammatory diseases associated with unwanted cellular proliferation. The active compounds are substituted triaryl methane compounds or analogues thereof where one or more of the aryl groups is replaced with a heteroaryl, cycloalkyl or heterocycloalkyl group and/or the tertiary carbon atom is replaced with a different atom such as Si, Ge, N or P, the compounds inhibit mammalian cell proliferation, inhibit the Gardos channel of erythrocytes, reduce sickle erythrocyte dehydration and/or delay the occurrence of erythrocyte sickling or deformation.

  本发明提供了一类化合物，可用作治疗镰状细胞病和以不需要或异常细胞增殖为特征的疾病的有效药物，特别是与不需要的细胞增殖相关的炎症性疾病。这些活性化合物是取代的三芳基甲烷化合物或其类似物，其中芳基之一或多个被取代为杂芳基、环烷基或杂环烷基，以及/或者第三级碳原子被其他原子如硅、锗、氮或磷所取代，这些化合物抑制哺乳动物细胞增殖，抑制红细胞的Gardos通道，减少镰状红细胞的脱水，和/或延迟红细胞的镰刀形成或变形的发生。
• EP0918514A4
  申请人：——

  公开号：EP0918514A4

  公开（公告）日：2001-05-09
• TRIARYL METHANE COMPOUNDS FOR SICKLE CELL DISEASE
  申请人：PRESIDENT AND FELLOWS OF HARVARD COLLEGE

  公开号：EP0918514A1

  公开（公告）日：1999-06-02
• TRIARYL METHANE COMPOUNDS FOR THE TREATMENT OF CANCER, ACTINIC KERATOSIS AND KAPOSI'S SARCOMA
  申请人：PRESIDENT AND FELLOWS OF HARVARD COLLEGE

  公开号：EP0918514B9

  公开（公告）日：2006-07-05