N-(2-furoyl)tryptamine

• 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-furoyl)tryptamine
• 英文别名: N-(2-(1H-indol-3-yl)ethyl)furan-2-carboxamide；tripfuroila；N(b)-2-furancarbonyltryptamine；N-[2-(1H-indol-3-yl)ethyl]furan-2-carboxamide
• 化学式: C₁₅H₁₄N₂O₂
• 分子量: 254.288
• InChiKey: DRMVPEKPNDBZMT-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.9
• 重原子数：
  19
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.13
• 拓扑面积：
  58
• 氢给体数：
  2
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  N-(2-furoyl)tryptamine 在 三乙基硅烷 、 三氟乙酸 作用下， 反应 1.0h， 以97%的产率得到N(b)-2-furanecarbonyl-2,3-dihydrotryptamine
  参考文献：
  名称：

  Synthesis of Nb-Acyltryptamines and Their 1-Hydroxy-tryptamine Derivatives as New α2-Blockers

  摘要：

  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.

  DOI：

  10.3987/com-08-s(d)29
• 作为产物：
  描述：

  呋喃甲酰氯 、 色胺 在 sodium hydroxide 作用下， 以 氯仿 、 水 为溶剂， 以31%的产率得到N-(2-furoyl)tryptamine
  参考文献：
  名称：

  The Plasmodium falciparum eIK1 kinase (PfeIK1) is central for melatonin synchronization in the human malaria parasite. Melatotosil blocks melatonin action on parasite cell cycle

  摘要：

  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.

  DOI：

  10.1111/jpi.12685