N-adamantyl-4-methylthiazol-2-amine | 1497249-95-2

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 唑类
• 英文名称: N-adamantyl-4-methylthiazol-2-amine
• 英文别名: N-(1-adamantyl)-4-methyl-1,3-thiazol-2-amine
• CAS: 1497249-95-2
• 化学式: C₁₄H₂₀N₂S
• 分子量: 248.392
• InChiKey: JMRLYCMPIVIOSE-UHFFFAOYSA-N

物化性质

• 沸点：
  371.9±35.0 °C(Predicted)
• 密度：
  1.253±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  4.3
• 重原子数：
  17
• 可旋转键数：
  2
• 环数：
  5.0
• sp3杂化的碳原子比例：
  0.79
• 拓扑面积：
  53.2
• 氢给体数：
  1
• 氢受体数：
  3

制备方法与用途

KHG26693是一种抗炎和抗氧化剂，能够通过显著降低血糖、甘油三酯和胆固醇水平，并提高胰岛素敏感性来发挥作用。

反应信息

• 作为产物：
  描述：

  异硫氰酸1-金刚烷酯 在 氨 作用下， 以 乙醇 为溶剂， 反应 24.0h， 生成 N-adamantyl-4-methylthiazol-2-amine
  参考文献：
  名称：

  2-Amino-1,3-thiazoles Suppressed Lipopolysaccharide-Induced IL-β and TNF-α

  摘要：

  DOI：

  10.5012/bkcs.2013.34.1.271

文献信息

• 10.1007/s11696-024-03572-6
  作者：Ahmed, Atteeque、Channar, Pervaiz Ali、Ejaz, Syeda Abida、Saeed, Aamer、Saleem, Muhammad、Shamim, Tahira、Wani, Tanveer A.、Hussain, Jabir、Gul, Nadeem、Khan, Siraj、Zargar, Seema、Li, Chen

  DOI：10.1007/s11696-024-03572-6

  日期：——

  compound 6f, 6k, 6j was considerably high against carbonic anhydrase, with their IC50 values of 3.02 ± 0.31 µM, 4.5 ± 0.041 µM and 2.7 ± 0.004 µM, respectively, as compared to acetazolamide with an IC50 value of IC50 0.12 ± 0.03 µM. The molecular docking of the active compounds docked in the active site of urease, α-glucosidase enzyme and carbonic anhydrase and depicted a good-binding score for all active

  本研究旨在合成一系列金刚烷连接的氨基噻唑衍生物(6a-)并评估其酶抑制活性。这些衍生物是根据已知酶抑制剂的结构特征合成的，并使用各种光谱技术（包括 FTIR、 1 H NMR、 13 C NMR 和质谱）对其结构进行了表征。进一步评估了合成的化合物对脲酶、α-葡萄糖苷酶和碳酸酐酶的抑制活性。酶抑制活性结果表明，化合物6c、6g和6k具有优异的脲酶抑制活性，IC 50 值分别为18.07±0.11、13.05±0.2和17.12±0.1μM。这些值显着低于标准抑制剂硫脲的 IC 50 值 (21,021 ± 0.02 µM)。此外，化合物6c和6e表现出良好的α-葡萄糖苷酶抑制活性。因此，化合物6c和6e对α-葡萄糖苷酶具有优异的IC 50 值，分别为18.4±0.11和58.01±0.8μM，并且与已知的α-葡萄糖苷酶抑制剂（即，阿卡波糖的 IC 50 值为 883.93 ± 2.18 µ
• Anti-inflammatory mechanisms of N-adamantyl-4-methylthiazol-2-amine in lipopolysaccharide-stimulated BV-2 microglial cells
  作者：Eun-A Kim、A Reum Han、Jiyoung Choi、Jee-Yin Ahn、Soo Young Choi、Sung-Woo Cho

  DOI：10.1016/j.intimp.2014.06.022

  日期：2014.9

  The activation of microglia is crucially associated with the neurodegeneration observed in many neuroinflammatory pathologies, such as multiple sclerosis, Parkinson's disease, and Alzheimer's disease. We have examined various thiazole derivatives with the goal of developing new anti-neuroinflammatory drugs. Thiazole derivatives are attractive candidates for drug development, because they are efficiently synthesized and active against a number of disease organisms and conditions, including neurodegenerative disorders. The present study investigated the effects of a new compound, N-adamantyl-4-methylthiazol-2-amine (KHG26693), against lipopolysaccharide (LPS)-induced inflammation in cultured BV-2 microglial cells. KHG26693 suppressed several inflammatory responses in LPS-activated cells, as evidenced by decreased levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), hydrogen peroxide (H(2)O(2)), reactive oxygen species (ROS), nitric oxide (NO), and lipid peroxidation. These anti-inflammatory/antioxidative actions occurred as a result of the downregulation of NADPH oxidase (NOX), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) content, but not as a result of the upregulation of superoxide dismutase (SOD) or catalase activity. The pharmacological properties of KHG26693 were also facilitated via inhibition of both the cluster of differentiation 14 (CD14)/toll-like receptor 4 (TLR4)-dependent nuclear factor kappa B (NF-κB) signaling pathway and extracellular signal-regulated kinase (ERK) phosphorylation. Furthermore, KHG26693 successfully blocked the migration of LPS-activated microglia, most likely by modulating the ERK pathway. Taken together, these results demonstrate that the anti-inflammatory and antioxidative actions of KHG26693 are mediated, at least in part, through the control of microglial activation.
• Effects of N-adamantyl-4-methylthiazol-2-amine on hyperglycemia, hyperlipidemia and oxidative stress in streptozotocin-induced diabetic rats
  作者：Seung-Ju Yang、Woo Je Lee、Eun-A Kim、Kee Dal Nam、Hoh-Gyu Hahn、Soo Young Choi、Sung-Woo Cho

  DOI：10.1016/j.ejphar.2014.04.031

  日期：2014.8

  Thiazole derivatives are attractive candidates for drug development because they can be efficiently synthesized and are active against a number of diseases and conditions, including diabetes. In our present study, we investigated the anti-inflammatory and antioxidant properties of N-adamantyl-4-methylthiazol-2-amine (KHG26693), a new thiazole derivative, in a streptozotocin (STZ)-induced model of diabetes mellitus. STZ-induced diabetic rats were intraperitoneally administered KHG26693 (3 mg/kg-body weight/day) for 4 weeks. KHG26693 administration significantly decreased blood glucose, triglycerides, and cholesterol and increased insulin. KHG26693 also suppressed several inflammatory responses in STZ-induced diabetic rats, as evidenced by decreased levels of serum tumor necrosis factor-alpha, interleukin-1 beta, and nitric oxide. Additionally, KHG26693 significantly modulated hepatic lipid peroxidation, catalase and superoxide dismutase activity, and the nonenzymatic antioxidant status (e.g., vitamins C and E), and reduced the glutathione content. These anti-inflammatory/antioxidative actions occurred as a result of the downregulation of inducible nitric oxide synthase and nuclear factor-kappa B. Taken together, our results suggest that KHG26693 successfully reduces the production of oxidative stress in STZ-induced diabetic rats by regulating the oxidation reduction system, specifically increasing antioxidant capacity. Furthermore, KHG26693 treatment significantly reverted the key enzymes of glucose metabolism, such as glucokinase, glucose-6-phosphatase, glycogen synthase, glycogen phosphorylase, and fructose-1,6-bisphosphatase, to near-normal levels in liver tissues. These results indicate that KHG26693 normalizes disturbed glucose metabolism by enhancing glucose utilization and decreasing liver glucose production via insulin release, suggesting the possibility of future diabetes treatments. (C) 2014 Elsevier B.V. All rights reserved.
• 2-Amino-1,3-thiazoles Suppressed Lipopolysaccharide-Induced IL-β and TNF-α
  作者：Kee Dal Nam、Minsoo Han、Jun Yoon、Eun-A Kim、Sung-Woo Cho、Hoh-Gyu Hahn

  DOI：10.5012/bkcs.2013.34.1.271

  日期：2013.1.20