S-ethyl 2-oxopropanethioate

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 硫代羧酸及其衍生物
• 英文名称: S-ethyl 2-oxopropanethioate
• 英文别名: 2-oxopropanethioic acid S-ethyl ester；S-ethyl oxopropanethioate
• 化学式: C₅H₈O₂S
• 分子量: 132.183
• InChiKey: OEJFCBZISPMDIA-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.9
• 重原子数：
  8
• 可旋转键数：
  3
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.6
• 拓扑面积：
  59.4
• 氢给体数：
  0
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  以75%的产率得到S-ethyl 2-oxopropanethioate
  参考文献：
  名称：

  在固液体系中某些由α-磺酰基或α-亚磺酰基活化的羧酸衍生物的PTC磺酰化

  摘要：

  摘要 报道了使用固体 K2CO3、S-甲基甲硫代磺酸盐和 TEBA 对 α-磺酰基取代的内酯和硫酯以及 α-亚磺酰基取代的酯和硫酯进行磺酰化。将结果与均相和非催化两相体系中的结果进行比较。

  DOI：

  10.1080/10426509708044209

文献信息

• EOP, a Newly Synthesized Ethyl Pyruvate Derivative, Attenuates the Production of Inflammatory Mediators via p38, ERK and NF-κB Pathways in Lipopolysaccharide-Activated BV-2 Microglial Cells
  作者：Soon Min、Sandeep More、Ju-Young Park、Sae-Bom Jeon、Shin Park、Eun-Jung Park、Sung-Hwa Yoon、Dong-Kug Choi

  DOI：10.3390/molecules191219361

  日期：——

  Microglia-induced neuroinflammation is an important pathological mechanism influencing various neurodegenerative disorders. Excess activation of microglia produces a myriad of proinflammatory mediators that decimate neurons. Hence, therapeutic strategies aimed to suppress the activation of microglia might lead to advancements in the treatment of neurodegenerative diseases. In this study, we synthesized a novel ethyl pyruvate derivative, named EOP (S-ethyl 2-oxopropanethioate) and studied its effects on lipopolysaccharide (LPS)-induced production of nitric oxide (NO) in rat primary microglia and mouse BV-2 microglia. EOP significantly decreased the production of NO, inducible nitric oxide synthase, cyclooxygenase and other proinflammatory cytokines, such as interleukin (IL)-6, IL-1β and tumor necrosis factor-α, in LPS-stimulated BV-2 microglia. The phosphorylation levels of extracellular regulated kinase, p38 mitogen-activated protein kinase, and nuclear translocation of NF-κB were also inhibited by EOP in LPS-activated BV-2 microglial cells. Overall, our observations indicate that EOP might be a promising therapeutic agent to diminish the development of neurodegenerative diseases associated with microglia activation.

  小胶质细胞诱导的神经炎症是影响各种神经退行性疾病的重要病理机制。小胶质细胞的过度激活会产生大量促炎介质，导致神经元衰竭。因此，旨在抑制小胶质细胞活化的治疗策略可能会推动神经退行性疾病的治疗。在这项研究中，我们合成了一种新型丙酮酸乙酯衍生物，命名为 EOP（S-乙基 2-氧代丙烷硫酸盐），并研究了它对大鼠原代小胶质细胞和小鼠 BV-2 小胶质细胞中脂多糖（LPS）诱导的一氧化氮（NO）产生的影响。在 LPS 刺激的 BV-2 小胶质细胞中，EOP 能明显减少 NO、诱导型一氧化氮合酶、环氧化酶和其他促炎细胞因子（如白细胞介素（IL）-6、IL-1β 和肿瘤坏死因子-α）的产生。在 LPS 激活的 BV-2 小胶质细胞中，细胞外调节激酶、p38 丝裂原活化蛋白激酶的磷酸化水平和 NF-κB 的核转位也受到 EOP 的抑制。总之，我们的观察结果表明，EOP可能是一种很有前景的治疗药物，可以减少与小胶质细胞活化相关的神经退行性疾病的发展。
• Substances and Pharmaceutical Compositions for the Inhibition of Glyoxalases and Their Use As Anti-Fungal Agents
  申请人：Huse Klaus

  公开号：US20080300303A1

  公开（公告）日：2008-12-04

  The present invention pertains to substances of the formula (I) wherein X is O or S; and R1-R4 are defined in the claims as inhibitors of glyoxalase I and/or II, pharmaceutical compositions comprising one or more compounds according to formula (I) and the use of one or more compounds according to formula (I) for the treatment of diseases associated with increased glycolytic metabolism. In one embodiment, the disease is a fungal infection.

  本发明涉及式（I）的物质，其中X是O或S; R1-R4在权利要求中定义为乙醛酸酯酶I和/或II的抑制剂，包含一个或多个式（I）化合物的制药组合物以及使用一个或多个式（I）化合物治疗与增加的糖酵解代谢相关的疾病。在一种实施方式中，该疾病是真菌感染。
• PTC SULFANYLATION OF SOME CARBOXYLIC ACIDS DERIVATIVES ACTIVATed BY α-SULFONYL OR α-SULFINYL GROUP, In SOLID-LIQUID SYSTEM
  作者：Blanka Wladislaw、Liliana Marzorati、Claudio L. Donnici、Francisco C. Biaggio、Regina M.A. Neves、Nelson F. Claro

  DOI：10.1080/10426509708044209

  日期：1997.4.1

  Abstract The sulfanylation of α-sulfonyl substituted lactone and thioesters and α-sulfinyl-substituted esters and thioesters, employing solid K2CO3, S-methyl methanethiosulfonate and TEBA, is reported. The results are compared with those in the homogeneous phase and in the non-catalytic two-phase system.

  摘要 报道了使用固体 K2CO3、S-甲基甲硫代磺酸盐和 TEBA 对 α-磺酰基取代的内酯和硫酯以及 α-亚磺酰基取代的酯和硫酯进行磺酰化。将结果与均相和非催化两相体系中的结果进行比较。