2-(4-hydroxy-3,5diiodophenyl)-2-oxoacetic acid | 76590-55-1

• 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-(4-hydroxy-3,5diiodophenyl)-2-oxoacetic acid
• 英文别名: (4-hydroxy-3,5-diiodo-phenyl)-glyoxylic acid；(4-Hydroxy-3,5-dijod-phenyl)-glyoxylsaeure；2-(4-Hydroxy-3,5-diiodophenyl)-2-oxoacetic acid
• CAS: 76590-55-1
• 化学式: C₈H₄I₂O₄
• 分子量: 417.926
• InChiKey: WJUVPHFVVBNRHU-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.3
• 重原子数：
  14
• 可旋转键数：
  2
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  74.6
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  4-羟基苯基乙醛酸 在 一氯化碘 、 溶剂黄146 作用下， 反应 1.0h， 以9%的产率得到2-(4-hydroxy-3,5diiodophenyl)-2-oxoacetic acid
  参考文献：
  名称：

  某些苯乙醛酸促进心脏中碳水化合物的氧化。

  摘要：

  描述了一系列苯乙醛酸，其中许多能够促进肌肉组织中碳水化合物的氧化，从而在提高脂肪酸利用率的情况下有利地改变碳水化合物/脂肪酸的平衡。据报道，这种情况发生在缺血性心脏病中，尤其是在心肌感染之后。为了有效地将苯乙醛酸递送至细胞内的作用部位，L-（+）-苯甘氨酸被用作前药。已知这些被氨基转移为苯乙醛酸。已选择L-（+）-2-（4-羟基苯基）甘氨酸（25，奥芬尼辛）进行临床评估。

  DOI：

  10.1021/jm00136a009

文献信息

• Promotion of carbohydrate oxidation in the heart by some phenylglyoxylic acids
  作者：Ian T. Barnish、Peter E. Cross、John C. Danilewicz、Roger P. Dickinson、David A. Stopher

  DOI：10.1021/jm00136a009

  日期：1981.4

  phenylglyoxylic acids is described, many of which are able to promote carbohydrate oxidation in muscle tissue, thereby favorably altering the carbohydrate/fatty acid balance in situations where fatty acid utilization is elevated. Such situations are reported to occur in ischemic heart disease, particularly following myocardial infection. In an attempt to effectively deliver the phenylglyoxylic acids to the

  描述了一系列苯乙醛酸，其中许多能够促进肌肉组织中碳水化合物的氧化，从而在提高脂肪酸利用率的情况下有利地改变碳水化合物/脂肪酸的平衡。据报道，这种情况发生在缺血性心脏病中，尤其是在心肌感染之后。为了有效地将苯乙醛酸递送至细胞内的作用部位，L-（+）-苯甘氨酸被用作前药。已知这些被氨基转移为苯乙醛酸。已选择L-（+）-2-（4-羟基苯基）甘氨酸（25，奥芬尼辛）进行临床评估。
• Synthesis of Arylglyoxylic Acids and Their Collision-Induced Dissociation
  作者：Kuldeep Wadhwa、Chengxi Yang、Paul R. West、Kris C. Deming、Sanjay R. Chemburkar、Rajarathnam E. Reddy

  DOI：10.1080/00397910802369554

  日期：2008.11.13

  A variety of substituted arylglyoxylic acids (2a-g) were synthesized via oxidation of the corresponding aryl-methylketones (1a-e) using selenium dioxide or Friedel-Crafts acylation of phenol (3) with ethyl chlorooxoacetate and further transformations. It was found that the arylglyoxylic acids (2) undergo facile unimolecular dissociation with loss of carbon monoxide to give the corresponding arylcarboxylic acids (7) under collisionally induced mass spectrometric conditions.
• Flumazenil abolishes midazolam-induced increase in the work of nasal breathing
  作者：Yasuko Kawauchi、Tsutomu Oshima、Yuhji Saitoh、Hidenori Toyooka

  DOI：10.1007/bf03019871

  日期：2000.12

  Purpose: To evaluate the effects of midazolam sedation followed by flumazenil antagonism on the work of nasal breathing in normal humans.Methods: We measured minute ventilation through the nasal route, respiratory frequency, nasal resistance (R-n) and the work of nasal breathing under three conditions: awake, during midazolam sedation, and after flumazenil antagonism in eight healthy human subjects. A custom-made, partitioned face mask enabled nasal and oral airflow to be measured separately. To calculate R-n and the work of nasal breathing, nasal mask and oropharyngeal pressure was also measured.Results: Total resistive work spent on the upstream segment of the nasal route per minute (W-n) (J.min(-1)) was greater during midazolam sedation (3.6 +/- 2.9) than while awake (1.6 +/- 0.9) and after flumazenil antagonism (1.7 +/- 0.6), respectively (mean +/- SD) (P < 0.05). Total resistive work spent on the upstream segment of nasal breathing (W-n/V-nE) (J.L-1) increased from 0.31 +/- 0.14 to 0.75 +/- 0.61 after midazolam administration (P < 0.05) and decreased to 0.31 +/- 0.10 after flumazenil. Following midazolam administration, a strong correlation was observed between changes in W-n/V-nE and changes in (R-n r = 0.852, P < 0.0001), whereas there was no correlation between changes in W-n and changes in (R-n = 0.159, P = 0.279).Conclusion: The work of breathing spent on the upstream segment of the nasal route increases during midazolam sedation and returns to baseline after flumazenil antagonism.