N^α-(N-benzyloxycarbonyl-β-alanyl)-histidine methyl ester | 21612-27-1

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 肽模拟物
• 英文名称: N^α-(N-benzyloxycarbonyl-β-alanyl)-histidine methyl ester
• 英文别名: N^α-(N-benzyloxycarbonyl-β-alanyl)-L-histidine-methyl ester；N^α-(N-Benzyloxycarbonyl-β-alanyl)-L-histidin-methylester；Z-beta-Ala-His-OCH3；methyl (2S)-3-(1H-imidazol-5-yl)-2-[3-(phenylmethoxycarbonylamino)propanoylamino]propanoate
• CAS: 21612-27-1
• 化学式: C₁₈H₂₂N₄O₅
• 分子量: 374.396
• InChiKey: TWUVQBFXFRTPJP-HNNXBMFYSA-N

物化性质

• 熔点：
  103-104 °C(Solv: ethanol (64-17-5); ligroine (8032-32-4))
• 沸点：
  696.7±55.0 °C(Predicted)
• 密度：
  1.281±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  0.8
• 重原子数：
  27
• 可旋转键数：
  11
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.33
• 拓扑面积：
  122
• 氢给体数：
  3
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  N^α-(N-benzyloxycarbonyl-β-alanyl)-histidine methyl ester 生成 L-carnosine methyl ester
  参考文献：
  名称：

  NAGAI, KANEHSIRO

  摘要：

  DOI：
• 作为产物：
  描述：

  L-组氨酸甲酯 生成 N^α-(N-benzyloxycarbonyl-β-alanyl)-histidine methyl ester
  参考文献：
  名称：

  NAGAI, KANEHSIRO

  摘要：

  DOI：

文献信息

• Substituted tetrapeptides
  申请人：Ciba-Geigy Corporation

  公开号：US04595677A1

  公开（公告）日：1986-06-17

  Tetrapeptides of the formula I, ##STR1## in which R.sup.1 represents hydrogen or acyl, R.sup.2 represents alkyl or aralkyl, R.sup.3 represents free or functionally modified hydroxy, R.sup.4 represents free or substituted amino or free or etherified hydroxy, and -Pro-, -Phe- and -His- respectively represent the bivalent radicals of the amino acids proline, phenylalanine and histidine or the (D)-isomers thereof, salts of such compounds having salt-forming groups, and processes for their manufacture. The compounds inhibit the action of the enzyme renin and can be used as antihypertensives and for the treatment of cardiac insufficiency.

  公式I的四肽，其中R.sup.1代表氢或酰基，R.sup.2代表烷基或芳基烷基，R.sup.3代表自由或功能性修饰的羟基，R.sup.4代表自由或取代氨基或自由或醚化羟基，-Pro-，-Phe-和-His-分别代表脯氨酸，苯丙氨酸和组氨酸的二价基团或其(D)异构体，具有形成盐的基团的这些化合物的盐以及它们的制造过程。这些化合物抑制酶肾素的作用，可用作降压剂和治疗心力衰竭。
• Neuroprotective effects of a novel carnosine-hydrazide derivative on hippocampal CA1 damage after transient cerebral ischemia
  作者：Kei Noguchi、Taha F.S. Ali、Junko Miyoshi、Kimihiko Orito、Tetsuya Negoto、Tanima Biswas、Naomi Taira、Ryoko Koga、Yoshinari Okamoto、Mikako Fujita、Masami Otsuka、Motohiro Morioka

  DOI：10.1016/j.ejmech.2018.11.060

  日期：2019.2

  Ischemia-reperfusion injuries produce reactive oxygen species that promote the peroxide lipid oxidation process resulting in the production of an endogenic lipid peroxide, 4-hydroxy-trans-2-nonenal (4-HNE), a highly cytotoxic aldehyde that induces cell death. We synthesized a novel 4-HNE scavenger a carnosine-hydrazide derivative, L-carnosine hydrazide (CNN) - and examined its neuroprotective effect in a model of transient ischemia.PC-12 cells were pre-incubated with various doses (0-50 mmol/L) of CNN for 30 min, followed by incubation with 4-HNE (250 mu M). An MIT assay was performed 24 h later to examine cell survival. Transient ischemia was induced by bilateral common carotid artery occlusion (BCCO) in the Mongolian gerbil. Animals were assigned to sham-operated (n = 6), placebo-treated (n = 12), CNN pre-treated (20 mg/kg; n = 12), CNN post-treated (100 mg/kg; n = 11), and histidyl hydrazide (a previously known 4-HNE scavenger) post-treated (100 mg/kg; n = 7) groups. Heat shock protein 70 immunoreactivity in the hippocampal CM region was evaluated 24 h later, while delayed neuronal death using 4-HNE staining was evaluated 7 days later.Pre-incubation with 30 mmol/L CNN completely inhibited 4-HNE-induced cell toxicity. CNN prevented delayed neuronal death by >60% in the pre-treated group (p < 0.001) and by >40% in the post-treated group (p <0.01). Histidyl hydrazide post-treatment elicited no protective effect. CNN pre-treatment resulted in high heat shock protein 70 and low 4-HNE immunoreactivity in CAl pyramidal neurons. Higher 4-HNE immunoreactivity was also found in the placebo-treated animals than in the CNN pretreated animals.Our novel compound, CNN, elicited highly effective 4-HNE scavenging activity in vitro. Furthermore, CNN administration both pre- and post-BCCO remarkably reduced delayed neuronal death in the hippocampal CAl region via its induction of heat shock protein 70 and scavenging of 4-HNE. (C) 2018 The Authors. Published by Elsevier Masson SAS. This is an open access article under the CC BY-NC-ND license.
• Davis, Journal of Biological Chemistry, 1956, vol. 223, p. 935,945
  作者：Davis

  DOI：——

  日期：——
• Davis; Smith, Biochemical Preparations, 1955, vol. 4, p. 38,40,42
  作者：Davis、Smith

  DOI：——

  日期：——