(4-hydroxy-phenyl)-acetic acid-(4-benzyloxy-3-methoxy-phenethylamide) | 14383-18-7

• 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-hydroxy-phenyl)-acetic acid-(4-benzyloxy-3-methoxy-phenethylamide)
• 英文别名: (4-Hydroxy-phenyl)-essigsaeure-(4-benzyloxy-3-methoxy-phenaethylamid)；N-(4-Benzyloxy-3-methoxy-phenaethyl)-4-hydroxy-phenyl-acetamid
• CAS: 14383-18-7
• 化学式: C₂₄H₂₅NO₄
• 分子量: 391.467
• InChiKey: LMRFOOLEFBUPJP-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  3.88
• 重原子数：
  29.0
• 可旋转键数：
  9.0
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.21
• 拓扑面积：
  67.79
• 氢给体数：
  2.0
• 氢受体数：
  4.0

反应信息

• 作为反应物：
  描述：

  (4-hydroxy-phenyl)-acetic acid-(4-benzyloxy-3-methoxy-phenethylamide) 、 氯甲酸乙酯 在 sodium hydroxide 作用下， 生成 (4-ethoxycarbonyloxy-phenyl)-acetic acid-(4-benzyloxy-3-methoxy-phenethylamide)
  参考文献：
  名称：

  Kametani et al., Chemical and pharmaceutical bulletin, 1966, vol. 14, p. 974,979

  摘要：

  DOI：
• 作为产物：
  描述：

  4-苄氧基-3-甲氧基苯乙胺 、 4-羟基苯乙酸甲酯 生成 (4-hydroxy-phenyl)-acetic acid-(4-benzyloxy-3-methoxy-phenethylamide)
  参考文献：
  名称：

  Kametani et al., Chemical and pharmaceutical bulletin, 1966, vol. 14, p. 974,979

  摘要：

  DOI：

文献信息

• Bilateral crossed cerebello-cerebral diaschisis and mutism after surgery for cerebellar medulloblastoma
  作者：Takao Sagiuchi、Katsumi Ishii、Yuki Aoki、Sirichi Kan、Satoshi Utsuki、Ryuusui Tanaka、Kiyotaka Fujii、Kazushige Hayakawa

  DOI：10.1007/bf02988609

  日期：2001.4

  A 7-year-old boy developed mutism after surgery for cerebellar medulloblastoma. Postoperative magnetic resonance imaging (MRI) showed atrophy of the cerebellar vermis and both cerebellar hemispheres, predominantly on the right side. Single photon emission computed tomography (SPECT) with technetium-99m-ethyl cysteinate dimer (Tc-99m ECD) revealed decreased cerebral blood flow (CBF) in the bilateral thalami, bilateral medial frontal lobes, and left temporal lobe in addition to the cerebellar vermis and both cerebellar hemispheres when mutism was manifest, indicating the existence of bilateral crossed cerebello-cerebral diaschisis (BCCCD). Circulatory disturbance in both cerebellar hemispheres secondary to tumor resection probably caused BCCCD in both cerebral hemispheres, predominantly in the left, via the dentatothalamocortical pathway (DTCP). With recovery of his mutism, CBF increased in the right thalamus, bilateral medial frontal lobes and left temporal lobe. Thus BCCCD was improved, with only a slight decrease in CBF still persisting in the left thalamus. The mechanism of mutism may have involved damage to the cerebellar vermis (the site of incision at operation), the left dentate nucleus (heavily infiltrated by the tumor) and the right dentate nucleus of the cerebellum (affected by circulatory disturbance secondary to acute postoperative edema). The SPECT findings suggested that mutism was associated with BCCCD-induced cerebral circulatory and metabolic hypofunction in the supplementary motor area mediated via the DTCP.