N-(2-(1H-indol-3-yl)ethyl)cyclohexanecarboxamide | 19462-22-7

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吲哚及其衍生物
• 英文名称: N-(2-(1H-indol-3-yl)ethyl)cyclohexanecarboxamide
• 英文别名: N(b)-cyclohexanecarbonyltryptamine；N-cyclohexylcarbonyltryptamine；tripcicloexila；N-cyclohexylcarbonyl-tryptamine；N-Cyclohexylcarbonyltryptamin；N-[2-(1H-indol-3-yl)ethyl]cyclohexanecarboxamide
• CAS: 19462-22-7
• 化学式: C₁₇H₂₂N₂O
• mdl: MFCD00716923
• 分子量: 270.374
• InChiKey: IKDNYMADROKAPP-UHFFFAOYSA-N

物化性质

• 熔点：
  108.5-109 °C(Solv: chloroform (67-66-3))
• 沸点：
  541.3±29.0 °C(Predicted)
• 密度：
  1.144±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  3.9
• 重原子数：
  20
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.47
• 拓扑面积：
  44.9
• 氢给体数：
  2
• 氢受体数：
  1

反应信息

• 作为反应物：
  描述：

  N-(2-(1H-indol-3-yl)ethyl)cyclohexanecarboxamide 在 劳森试剂 、 对硝基溴化苄 作用下， 以 乙二醇二甲醚 、 乙腈 为溶剂， 反应 18.0h， 生成 1-Cyclohexyl-4,9-dihydro-3H-β-carboline; hydrobromide
  参考文献：
  名称：

  A new method for the preparation of 3,4-dihydro - and 1,2,3,4-tetrahydro-.BETA.-carbolines.

  摘要：

  N-烷基硫羰基色氨酸（2a-i）和色氨酸（2j-m）衍生物可以在温和条件下通过烷基化或酰基化剂转化为相应的3, 4-二氢-β-氨基吲哚（3）。1, 3-二取代的3, 4-二氢-β-氨基吲哚（3a-i）经过NaBH4还原，得到了具有满意立体选择性的顺式（5）或反式-1, 2, 3, 4-四氢-β-氨基吲哚（6）。本文还描述了外消旋活性3a, b和5a, b的合成。

  DOI：

  10.1248/cpb.33.3237
• 作为产物：
  描述：

  色胺 、 环己甲酰氯 在 三乙胺 作用下， 以 二氯甲烷 为溶剂， 反应 1.0h， 以59%的产率得到N-(2-(1H-indol-3-yl)ethyl)cyclohexanecarboxamide
  参考文献：
  名称：

  通过基于结构和配体的虚拟佐剂发现疫苗佐剂，合理设计了新型的类收费受体4（TLR4）色胺相关激动剂。

  摘要：

  为了识别人类通行费样受体4（hTLR4）调制的新颖的铅结构，已经进行了由千万亿次规模的超级计算机进行的虚拟高通量筛选。根据计算机研究，合理设计了一系列与色胺有关的12种化合物，以保留合适的分子几何结构以与hTLR4结合位点相互作用，并满足药物相似性的一般原则。合成了拟议的化合物，并通过体外和离体实验进行了测试，结果表明它们中的几种能够在体外刺激hTLR4，其单磷酰脂质A的活性最高可达25％。体外最有效的物质的特异性亲和力为经表面等离振子共振直接结合实验证实。而且，

  DOI：

  10.3390/molecules23010102

文献信息

• Azepino [1,2,3-lm]-.beta.-carboline compounds and pharmaceutical
  申请人：Tanabe Seiyaku Co., Ltd.

  公开号：US04228168A1

  公开（公告）日：1980-10-14

  An azepino[1,2,3-lm]-.beta.-carboline compound of the formula: ##STR1## wherein R.sup.1 is hydrogen, cycloalkyl of 3 to 7 carbon atoms, phenyl, hydroxy, alkoxycarbonyl of 2 or 3 carbon atoms or alkanoyl of 2 or 3 carbon atoms, and A is single bond or straight or branched alkylene of one to 5 carbon atoms. Several methods of preparing the compound [I] are disclosed. The compound [I] and a pharmaceutical acceptable acid addition salt thereof have a potent anti-anoxic activity.

  一种azepino[1,2,3-lm]-β-咔啉类化合物，化学式如下：##STR1##其中R.sup.1为氢、3至7个碳原子的环烷基、苯基、羟基、2或3个碳原子的烷氧羰基或2或3个碳原子的烷酰基，A为单键或一至5个碳原子的直链或支链烷基。公开了制备化合物[I]的几种方法。化合物[I]及其药用可接受的酸加盐具有强效的抗缺氧活性。
• Asymmetric transfer hydrogenation of imines and iminiums catalyzed by a water-soluble catalyst in water
  作者：Jiashou Wu、Fei Wang、Yaping Ma、Xin Cui、Linfeng Cun、Jin Zhu、Jingen Deng、Bangliang Yu

  DOI：10.1039/b600496b

  日期：——

  The first asymmetric transfer hydrogenation of cyclic imines and iminiums in water was successfully performed in high yields and enantioselectivities with sodium formate as the hydrogen source and CTAB as an additive catalyzed by a water-soluble and recyclable ruthenium(II) complex of the ligand (R,R)-2.

  以甲酸钠为氢源，CTAB 为添加剂，在配体 (R,R)-2 的水溶性可回收钌 (II) 复合物催化下，首次成功地在水中对环状亚胺和亚胺进行了不对称转移加氢反应，并获得了较高的产率和对映选择性。
• Asymmetric Synthesis of Sterically Hindered 1-Substituted Tetrahydro-β-carbolines Enabled by Imine Reductase: Enzyme Discovery, Protein Engineering, and Reaction Development
  作者：Yitong Li、Xiaoping Yue、Zhining Li、Zedu Huang、Fener Chen

  DOI：10.1021/acs.orglett.3c00147

  日期：2023.3.3

  We report the discovery of a new imine reductase (IRED), named AtIRED, by genome mining. Site-saturation mutagenesis on AtIRED generated two single mutants M118′L and P120′G and the double mutant M118′L/P120′G with improved specific activity toward sterically hindered 1-substituted dihydro-β-carbolines. The synthetic potential of these engineered IREDs was showcased by the preparative-scale synthesis

  我们报告了通过基因组挖掘发现了一种名为At IRED 的新亚胺还原酶 (IRED)。At IRED上的定点饱和诱变产生了两个单突变体 M118'L 和 P120'G 以及双突变体 M118'L/P120'G，它们对位阻 1-取代的二氢-β-咔啉具有更高的比活性。九种手性 1-取代四氢-β-咔啉 (THβC) 的制备规模合成展示了这些工程 IRED 的合成潜力，包括 (S)-1-t-丁基-THβC和( S )-1- t -戊基-THβC，分离产率为 30–87%，具有出色的光学纯度 (98–99% ee)。
• Synthesis of Nb-Acyltryptamines and Their 1-Hydroxy-tryptamine Derivatives as New α2-Blockers
  作者：Masanori Somei、Koji Yamada、Yoshio Tanaka

  DOI：10.3987/com-08-s(d)29

  日期：——

  N-b-Acyl- and N-b-acyl-1-hydroxytryptamines are found to be novel and structurally simple alpha(2)-blocker for the treatment of erectile dysfunction.
• The <i>Plasmodium falciparum</i> eIK1 kinase (PfeIK1) is central for melatonin synchronization in the human malaria parasite. Melatotosil blocks melatonin action on parasite cell cycle
  作者：Bárbara K.M. Dias、Myna Nakabashi、Marina Rangel Rodrigues Alves、Danielle Pagliaminuto Portella、Benedito Matheus Santos、Fahyme Costa da Silva Almeida、Ramira Yuri Ribeiro、Desiree C. Schuck、Alessandro Kappel Jordão、Celia R.S. Garcia

  DOI：10.1111/jpi.12685

  日期：2020.10

  AbstractMelatonin and its indoles derivatives are central in the synchronization of malaria parasites. In this research, we discovered that melatonin is unable to increase the parasitemia in the human malaria Plasmodium falciparum that lacks the kinase PfeIK1. The PfeIK1 knockout strain is a valuable tool in the screening of indol‐related compound that blocks the melatonin effect in wild‐type (WT) parasite development. The assays were performed by using flow cytometry with simultaneous labeling for mitochondria viability with MitoTracker Deep Red and nucleus staining with SYBR Green. We found that Melatotosil leads to an increase in parasitemia in P. falciparum and blocks melatonin effect in the WT parasite. Using microscopy imaging system, we found that Melatotosil at 500 nM is able to induce cytosolic calcium rise in transgenic PfGCaMP3 parasites. On the contrary, the compound Triptiofen blocks P. falciparum cell cycle with IC50 9.76 µM ± 0.6, inhibits melatonin action, and does not lead to a cytosolic calcium rise in PfGCaMP3 parasites. We also found that the synthetic indol‐related compounds arrested parasite cycle for PfeIK1 knockout and (WT) P. falciparum (3D7) in 72 hours culture assays with the IC50 values slighting lower for the WT strain. We concluded that the kinase PfeIK1 is central for melatonin downstream signaling pathways involved in parasite cell cycle progression. More importantly, the indol‐related compounds block its cycle as an upstream essential mechanism for parasite survival. Our data clearly show that this class of compounds emerge as an alternative for the problem of resistance with the classical antimalarials.