6,6'-dibromo-6,6'-dideoxy-α,α-trehalose | 50257-14-2

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: 6,6'-dibromo-6,6'-dideoxy-α,α-trehalose
• 英文别名: 6,6'-Dibrom-6,6'-dideoxy-α,α-trehalose；6,6'-Dibrom-6,6'-didesoxy-trehalose
• CAS: 50257-14-2
• 化学式: C₁₂H₂₀Br₂O₉
• 分子量: 468.093
• InChiKey: HZKIXDWIXNRYES-LIZSDCNHSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -2.59
• 重原子数：
  23.0
• 可旋转键数：
  4.0
• 环数：
  2.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  149.07
• 氢给体数：
  6.0
• 氢受体数：
  9.0

反应信息

• 作为反应物：
  描述：

  6,6'-dibromo-6,6'-dideoxy-α,α-trehalose 、 乙酸酐 在 吡啶 作用下， 生成 2,3,4,2',3',4'-hexa-O-acetyl-6,6'-dibromo-6,6'-dideoxy-α,α-trehalose
  参考文献：
  名称：

  在未保护的碳水化合物或糖苷中伯醇的区域选择性溴化的新协议。

  摘要：

  在干燥的DMF中，在四丁基溴化铵（TBAB）存在下，使用（氯-苯硫基-亚甲基）二甲基氯化铵（CPMA）成功地实现了未保护的碳水化合物或糖苷中伯羟基的区域选择性和有效溴化。

  DOI：

  10.1002/cjoc.201200211
• 作为产物：
  描述：

  海藻糖 在 四丁基溴化铵 、 (chloro(phenylthio)methylene)dimethylammonium chloride 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 反应 48.0h， 生成 6,6'-dibromo-6,6'-dideoxy-α,α-trehalose
  参考文献：
  名称：

  在未保护的碳水化合物或糖苷中伯醇的区域选择性溴化的新协议。

  摘要：

  在干燥的DMF中，在四丁基溴化铵（TBAB）存在下，使用（氯-苯硫基-亚甲基）二甲基氯化铵（CPMA）成功地实现了未保护的碳水化合物或糖苷中伯羟基的区域选择性和有效溴化。

  DOI：

  10.1002/cjoc.201200211

文献信息

• Trehalose–Carnosine Prevents the Effects of Spinal Cord Injury Through Regulating Acute Inflammation and Zinc(II) Ion Homeostasis
  作者：Irene Paterniti、Alessia Filippone、Irina Naletova、Valentina Greco、Sebastiano Sciuto、Emanuela Esposito、Salvatore Cuzzocrea、Enrico Rizzarelli

  DOI：10.1007/s10571-022-01273-w

  日期：——

  Spinal cord injury (SCI) leads to long-term and permanent motor dysfunctions, and nervous system abnormalities. Injury to the spinal cord triggers a signaling cascade that results in activation of the inflammatory cascade, apoptosis, and Zn(II) ion homeostasis. Trehalose (Tre), a nonreducing disaccharide, and l-carnosine (Car), (β-alanyl-l-histidine), one of the endogenous histidine dipeptides have been recognized to suppress early inflammatory effects, oxidative stress and to possess neuroprotective effects. We report on the effects of the conjugation of Tre with Car (Tre–car) in reducing inflammation in in vitro and in vivo models. The in vitro study was performed using rat pheochromocytoma cells (PC12 cell line). After 24 h, Tre–car, Car, Tre, and Tre + Car mixture treatments, cells were collected and used to investigate Zn²⁺ homeostasis. The in vivo model of SCI was induced by extradural compression of the spinal cord at the T6–T8 levels. After treatments with Tre, Car and Tre–Car conjugate 1 and 6 h after SCI, spinal cord tissue was collected for analysis. In vitro results demonstrated the ionophore effect and chelating features of l-carnosine and its conjugate. In vivo, the Tre–car conjugate treatment counteracted the activation of the early inflammatory cascade, oxidative stress and apoptosis after SCI. The Tre–car conjugate stimulated neurotrophic factors release, and influenced Zn²⁺ homeostasis. We demonstrated that Tre–car, Tre and Car treatments improved tissue recovery after SCI. Tre–car decreased proinflammatory, oxidative stress mediators release, upregulated neurotrophic factors and restored Zn²⁺ homeostasis, suggesting that Tre–car may represent a promising therapeutic agent for counteracting the consequences of SCI.

  标题：摘要 脊髓损伤（SCI）会导致长期和永久的运动功能障碍和神经系统异常。脊髓损伤会触发信号级联反应，导致炎症级联反应、细胞凋亡和Zn（II）离子稳态失衡。特雷哈罗斯（Tre）是一种非还原二糖，而β-丙氨酸- L-组氨酸（Car）是内源性组氨酸二肽之一，已被认为可以抑制早期炎症效应、氧化应激并具有神经保护作用。我们报告了Tre与Car（Tre-car）的结合对于体外和体内模型中减少炎症的影响。体外研究使用大鼠嗜铬细胞瘤细胞（PC12细胞系）进行，24小时后，Tre-car、Car、Tre和Tre+Car混合物处理后，收集细胞并用于研究Zn2+稳态。SCI的体内模型是通过在T6-T8水平压迫脊髓引起的。SCI后1小时和6小时给予Tre、Car和Tre-Car结合物治疗后，收集脊髓组织进行分析。体外结果表明了L-肉碱的离子载体效应和螯合特性及其结合物。在体内，Tre-car结合物治疗对抗了SCI后早期炎症级联反应、氧化应激和细胞凋亡。Tre-car结合物刺激神经营养因子的释放，并影响了Zn2+稳态。我们证明了Tre-car、Tre和Car治疗可以改善SCI后的组织恢复。Tre-car减少了促炎症、氧化应激介质的释放，上调了神经营养因子并恢复了Zn2+稳态，表明Tre-car可能是一种有前途的治疗剂，可以对抗SCI的后果。
• α,α-Trehalose derivatives bearing guanidino groups as inhibitors to HIV-1 Tat–TAR RNA interaction in human cells
  作者：Min Wang、Zhidong Xu、Pengfei Tu、Xiaolin Yu、Sulong Xiao、Ming Yang

  DOI：10.1016/j.bmcl.2004.02.073

  日期：2004.5

  Replication of HIV-1 requires specific interactions of Tat protein with TAR RNA. Disruption of Tat TAR RNA interaction could inhibit HIV-1 replication. Here four target compounds were designed and synthesized to bind to TAR RNA for blocking the interaction of Tat-TAR RNA. The core molecule 6,6'-diamino-6,6'-dideoxy-alpha,alpha-trehalose was obtained from selective bromination of, alpha,alpha-trehalose at C-6,6', followed by acetylation, azide displacement, deacetylation, and reduction. Coupling of the core molecule with the protected amino acid, then deprotection and guanidinylation generated the novel alpha,alpha-trehalose derivatives. Their abilities to inhibit Tat-TAR RNA interaction in human cells were determined by a Tat-dependent HIV-1 LTR-driven CAT assays. (C) 2004 Elsevier Ltd. All rights reserved.
• Toward Point-of-Care Detection of <i>Mycobacterium tuberculosis</i>: A Brighter Solvatochromic Probe Detects Mycobacteria within Minutes
  作者：Mireille Kamariza、Samantha G. L. Keyser、Ashley Utz、Benjamin D. Knapp、Christopher Ealand、Green Ahn、C. J. Cambier、Teresia Chen、Bavesh Kana、Kerwyn Casey Huang、Carolyn R. Bertozzi

  DOI：10.1021/jacsau.1c00173

  日期：2021.9.27