Ac-N(Me)Ile-Gly-N(Me)Leu-Met-N(Me)Val-Gly-NH2 | 960324-14-5

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 英文名称: Ac-N(Me)Ile-Gly-N(Me)Leu-Met-N(Me)Val-Gly-NH2
• 英文别名: (2S,3S)-2-[acetyl(methyl)amino]-N-[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[(2-amino-2-oxoethyl)amino]-3-methyl-1-oxobutan-2-yl]-methylamino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]-methylamino]-2-oxoethyl]-3-methylpentanamide
• CAS: 960324-14-5
• 化学式: C₃₁H₅₇N₇O₇S
• 分子量: 671.902
• InChiKey: IJPVZZGYUGQONC-RMRWLJQJSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.6
• 重原子数：
  46
• 可旋转键数：
  20
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.77
• 拓扑面积：
  217
• 氢给体数：
  4
• 氢受体数：
  8

反应信息

• 作为产物：
  描述：

  Fmoc-甘氨酸 、 Fmoc-N-甲基-L-亮氨酸 、 乙酸酐 、 Fmoc-L-蛋氨酸 、 Fmoc-N-甲基-L-缬氨酸 、 Fmoc-N-甲基-L-异亮氨酸 在 N,N-二异丙基乙胺 、 Methanaminium,N-[(dimethylamino)(3H-1,2,3-triazolo[4,5-b]pyridin-3-yloxy)methylene]-N-methyl-, hexafluorophosphate(1-) 、 哌啶 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 生成 Ac-N(Me)Ile-Gly-N(Me)Leu-Met-N(Me)Val-Gly-NH2
  参考文献：
  名称：

  Poly-N-methylated Amyloid β-Peptide (Aβ) C-Terminal Fragments Reduce Aβ Toxicity in Vitro and in Drosophila melanogaster

  摘要：

  Alzheimer's disease (AD), an age related neurodegenerative disorder, threatens to become a major health-economic problem. Assembly of 40- or 42-residue amyloid beta-peptides (A beta) into neurotoxic oligo-/polymeric beta-sheet structures is an important pathogenic feature in AD, thus, inhibition of this process has been explored to prevent or treat AD. The C-terminal part plays an important role in A beta aggregation, but most A beta aggregation inhibitors have targeted the central region around residues 16-23. Herein, we synthesized hexapeptides with varying extents of N-methylation based on residues 32-37 of A beta to target its C-terminal region. We measured the peptides abilities to retard beta-sheet and fibril formation of A beta and to reduce A beta neurotoxicity. A penta-N-methylated peptide was more efficient than peptides with 0, 2, or 3 N-methyl groups. This penta-N-methylated peptide moreover increased life span and locomotor activity in Drosophila melanogaster flies overexpressing human A beta(1-42).

  DOI：

  10.1021/jm901092h

文献信息

• Poly-<i>N</i>-methylated Amyloid β-Peptide (Aβ) C-Terminal Fragments Reduce Aβ Toxicity in Vitro and in <i>Drosophila melanogaster</i>
  作者：Partha Pratim Bose、Urmimala Chatterjee、Charlotte Nerelius、Thavendran Govender、Thomas Norström、Adolf Gogoll、Anna Sandegren、Emmanuelle Göthelid、Jan Johansson、Per I. Arvidsson

  DOI：10.1021/jm901092h

  日期：2009.12.24

  Alzheimer's disease (AD), an age related neurodegenerative disorder, threatens to become a major health-economic problem. Assembly of 40- or 42-residue amyloid beta-peptides (A beta) into neurotoxic oligo-/polymeric beta-sheet structures is an important pathogenic feature in AD, thus, inhibition of this process has been explored to prevent or treat AD. The C-terminal part plays an important role in A beta aggregation, but most A beta aggregation inhibitors have targeted the central region around residues 16-23. Herein, we synthesized hexapeptides with varying extents of N-methylation based on residues 32-37 of A beta to target its C-terminal region. We measured the peptides abilities to retard beta-sheet and fibril formation of A beta and to reduce A beta neurotoxicity. A penta-N-methylated peptide was more efficient than peptides with 0, 2, or 3 N-methyl groups. This penta-N-methylated peptide moreover increased life span and locomotor activity in Drosophila melanogaster flies overexpressing human A beta(1-42).