1,2,3-tri-O-acetyl-5-O-methyl-β-D-ribofuranoside | 169274-64-0

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: 1,2,3-tri-O-acetyl-5-O-methyl-β-D-ribofuranoside
• 英文别名: 1,2,3-tri-O-acetyl-5-O-methyl-β-D-ribofuranose；[(2R,3R,4R,5S)-4,5-diacetyloxy-2-(methoxymethyl)oxolan-3-yl] acetate
• CAS: 169274-64-0
• 化学式: C₁₂H₁₈O₈
• 分子量: 290.27
• InChiKey: WKSIBZZBSUBESO-DDHJBXDOSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.6
• 重原子数：
  20
• 可旋转键数：
  8
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.75
• 拓扑面积：
  97.4
• 氢给体数：
  0
• 氢受体数：
  8

反应信息

• 作为反应物：
  描述：

  1,2,3-tri-O-acetyl-5-O-methyl-β-D-ribofuranoside 在 吡啶 、 4-二甲氨基吡啶 、 sodium methylate 、 四氯化锡 、 叔丁基二甲基氯硅烷 作用下， 以 甲醇 、 1,2-二氯乙烷 为溶剂， 反应 189.25h， 生成 1-(5'-O-methyl-β-D-ribofuranosyl)-2-methylbenzimidazole-2'-phenylphosphate
  参考文献：
  名称：

  动力学溶剂氘同位素在RNA模型酯交换中的作用。

  摘要：

  合成了2-甲基苯并咪唑核糖核苷芳基磷酸酯（1a，b）和烷基磷酸酯（2a，b），作为包含最少数量可交换质子的RNA模型化合物。在H 2 O和D 2 O溶液中在较宽的p L范围内研究了这些底物的分子内酯交换反应，研究了两种底物的碱性裂解以及中性和酸性条件下2a的裂解和异构化的明显的动力学溶剂氘同位素效应。决定。对于磷酸芳基酯1b的碱性裂解，观察到的k / k为4.9可主要归因于ΔP ķ攻击亲核试剂。2a中的烷基离去基团带来额外的1.5倍同位素效应（k / k为7.1），考虑到p L –反应的依赖性，不能用涉及质子转移的过程来解释。暂时建议将过渡态的溶剂化差异作为差异的来源。与碱性裂解相反，在中性和酸性条件下2a的裂解和异构化显示没有明显的溶剂同位素效应。文献中发现的几个例子表明，在平衡之前分子内质子从磷酸盐转移到离去基团可能不一定导致可观察到的溶剂同位素效应。由于分子内质子转移过程发生在中性和

  DOI：

  10.1002/poc.883
• 作为产物：
  描述：

  D-核糖 在 吡啶 、 盐酸 、 copper(II) sulfate 、 三氟乙酸 、 silver(l) oxide 作用下， 以 N,N-二甲基甲酰胺 、 乙腈 为溶剂， 反应 9.75h， 生成 1,2,3-tri-O-acetyl-5-O-methyl-β-D-ribofuranoside
  参考文献：
  名称：

  动力学溶剂氘同位素在RNA模型酯交换中的作用。

  摘要：

  合成了2-甲基苯并咪唑核糖核苷芳基磷酸酯（1a，b）和烷基磷酸酯（2a，b），作为包含最少数量可交换质子的RNA模型化合物。在H 2 O和D 2 O溶液中在较宽的p L范围内研究了这些底物的分子内酯交换反应，研究了两种底物的碱性裂解以及中性和酸性条件下2a的裂解和异构化的明显的动力学溶剂氘同位素效应。决定。对于磷酸芳基酯1b的碱性裂解，观察到的k / k为4.9可主要归因于ΔP ķ攻击亲核试剂。2a中的烷基离去基团带来额外的1.5倍同位素效应（k / k为7.1），考虑到p L –反应的依赖性，不能用涉及质子转移的过程来解释。暂时建议将过渡态的溶剂化差异作为差异的来源。与碱性裂解相反，在中性和酸性条件下2a的裂解和异构化显示没有明显的溶剂同位素效应。文献中发现的几个例子表明，在平衡之前分子内质子从磷酸盐转移到离去基团可能不一定导致可观察到的溶剂同位素效应。由于分子内质子转移过程发生在中性和

  DOI：

  10.1002/poc.883

文献信息

• Synthesis and Antiviral Activity of Certain 5‘-Modified Analogs of 2,5,6-Trichloro-1-(β-<scp>d</scp>-ribofuranosyl)benzimidazole
  作者：Kristjan S. Gudmundsson、John C. Drach、Linda L. Wotring、Leroy B. Townsend

  DOI：10.1021/jm9604888

  日期：1997.2.1

  A series of 5'-modified 2,5,6-trichlorobenzimidazole ribonucleosides has been synthesized and tested for activity against two human herpesviruses and for cytotoxicity. The 5'-methoxy, 5'-ethoxy, and 5'-butoxy analogs of 2,5,6-trichloro-1-(beta-D-ribofuranosyl)benzimidazole (TCRB) were prepared by coupling the appropriate 5-O-alkyl-1,2,3-tri-O-acetyl-beta-D-ribose derivatives with 2,5,6-trichlorobenzimidazole followed by removal of the protecting groups. The 5'-deoxy-5'-fluoro, -5'-chloro, -5'-bromo, -5'-iodo, -5'-azido, and -5'-thiomethyl derivatives were synthesized in a similar fashion. All of these 5'-modified derivatives had significant activity against HCMV in plaque and yield reduction assays (IC50's = 0.5-14.2 mu M) but had little activity (IC50's > 100 mu M) against HSV-1. This pattern is similar to the antiviral activity profile observed for TCRB. The 5'-halogenated derivatives were more active than the other 5'-modified derivatives with antiviral activity well separated from cytotoxicity. In general, cytotoxicity of all the 5'-modified derivatives was greater in human foreskin fibroblasts (HFF cells) than in L1210 or K-B tumor cells. These results indicate that the viral target tolerates significant modifications of TCRB at the 5'-position without adversely affecting activity against HCMV, whereas the 5'-modifications increased cytotoxicity in human diploid cells.
• 5‘-<i>O</i>-Alkyl Ethers of<i> N</i>,2-Substituted Adenosine Derivatives:  Partial Agonists for the Adenosine A₁ and A₃ Receptors
  作者：Erica W. van Tilburg、Pieter A. M. van der Klein、Jacobien von Frijtag Drabbe Künzel、Miriam de Groote、Christina Stannek、Anna Lorenzen、Ad P. IJzerman

  DOI：10.1021/jm001114o

  日期：2001.8.1

  New N,5'-di- and N,2,5'-trisubstituted adenosine derivatives were synthesized in good overall yields. Appropriate 5-O-alkyl-substituted ribose moieties were coupled to 6-chloropurine or 2,6-dichloropurine via Vorbruggen's glycosylation method. Subsequent amination and deprotection of the intermediates yielded compounds 18-35. Binding affinities were determined for rat adenosine A(1) and A(2A) receptors and the human A(3) receptor. The ability of compounds 18-35 to inhibit forskolin-induced (10 muM) cyclic AMP (cAMP) production and their ability to stimulate guanosine 5'-O-(3-[S-35]thio)triphosphate ([S-35]GTP gammaS) binding, via either the adenosine A(1) receptor or the adenosine A(3) receptor, were assessed. N-Cyclopentyl-substituted adenosine derivatives displayed affinities in the low nanomolar range for the adenosine A(1) receptor, whereas N-(3-iodobenzyl)-substituted derivatives had high affinity for the adenosine A(3) receptor. Compound 22 had the highest affinity for the adenosine A(3) receptor (K-i value of 16 nM), and compounds 20 and 26 had the highest affinities for the adenosine A(3) receptor (K-i values of 4 and 3 nM, respectively). A chlorine substituent at the 2-position either did not affect or slightly increased the adenosine A(3) receptor affinity, whereas the A(3) receptor affinity was affected differently, depending on the N-substituent. Furthermore, the introduction of chlorine slightly increased the A(3)/A(1) selectivity ratio. At the 5 ' -position, an O-methyl substituent induced the highest adenosine A(1) receptor affinity, whereas an O-ethyl substituent did so for the A(3) receptor. All compounds showed partial agonistic effects in both the cAMP and [S-35]GTP gammaS assays, although more marked in the latter assay. In general, the 2-chloro derivatives seemed to have lower intrinsic activities compared to the 2-H-substituted compounds on both the adenosine A(1) and the adenosine A(3) receptors. The compounds with an N-(3-iodobenzyl) substituent displayed the lowest intrinsic activities. Finally, all compounds also showed partially antagonistic behavior in the [S-35]GTP gammaS assay.
• US5589467A
  申请人：——

  公开号：US5589467A

  公开（公告）日：1996-12-31
• [EN] A METHOD OF TREATING DISORDERS RELATED TO CYTOKINES IN MAMMALS<br/>[FR] PROCEDE DE TRAITEMENT D'AFFECTIONS ASSOCIEES AUX CYTOKINES CHEZ LES MAMMIFERES
  申请人：NOVO NORDISK A/S

  公开号：WO1997033590A1

  公开（公告）日：1997-09-18

  (EN) A method of treating disorders related to cytokines such as TNF$g(a) in mammals. The disorder is an autoimmune disorder, inflammation, arthritis, type I or type II diabetes, multiple sclerosis, stroke, osteoporosis, septic shock or menstrual complications.(FR) Procédé de traitement d'affections associées aux cytokines telles que le facteur de nécrose des tumeurs $g(a) (TNF$g(a)) chez les mammifères. Cette affection peut être une affection autoimmune, une inflammation, l'arthrite, le diabète de type I ou II, la sclérose en plaques, une attaque, l'ostéoporose, un choc septique ou des complications menstruelles.