9-(2-chlorobenzyl)carbazole | 88107-71-5

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吲哚及其衍生物
• 英文名称: 9-(2-chlorobenzyl)carbazole
• 英文别名: 9-(2-chlorobenzyl)-9H-carbazole；N-(2-chlorobenzyl)carbazole；9-[(2-Chlorophenyl)methyl]-9H-carbazole；9-[(2-chlorophenyl)methyl]carbazole
• CAS: 88107-71-5
• 化学式: C₁₉H₁₄ClN
• 分子量: 291.78
• InChiKey: XCNGYHQPFQLMQK-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  5.6
• 重原子数：
  21
• 可旋转键数：
  2
• 环数：
  4.0
• sp3杂化的碳原子比例：
  0.05
• 拓扑面积：
  4.9
• 氢给体数：
  0
• 氢受体数：
  0

反应信息

• 作为反应物：
  描述：

  9-(2-chlorobenzyl)carbazole 在 三氯氧磷 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 以53%的产率得到9-[(2-氯苯基)甲基]咔唑-3-甲醛
  参考文献：
  名称：

  Inhibition of nitric oxide production by the carbazole compound LCY-2-CHO via blockade of activator protein-1 and CCAAT/enhancer-binding protein activation in microglia

  摘要：

  Excessive nitric oxide (NO) production by activated microglia plays a critical role in neurodegenerative disorders. In this study, we found that 9-(2-chlorobenyl)-9H-carbazole-3-carbaldehyde (LCY-2-CHO) suppressed the NO production in lipopolysaccharide (LPS)/interferon-gamma (IFN gamma)-stimulated murine microglial N9 and BV-2 cells and in LPS-stimulated N9 cells and rat primary microglia. LCY-2-CHO had no cytotoxic effect on microglia. in activated N9 cells, LCY-2-CHO abolished the expression of inducible nitric oxide synthase (iNOS) protein and mRNA but failed to alter the stability of expressed iNOS mRNA and the enzymatic activity of expressed iNOS protein. LCY-2-CHO did not block DNA-binding activity of nuclear factor-kappa B (NF-kappa B) or cyclic AMP response element-binding protein (CREB), but abolished that of activator protein-1 (AP-1), CCAAT/enhancer-binding protein (C/EBP) and nuclear factor IL6 (NF-IL6). LCY-2-CHO attenuated the nuclear levels of c-Jun and C/EBP beta, but not those of p65, p50, C/EBP delta, signal transducer and activator of transcription-1 (STAT-1) or the nuclear expression of IFN regulatory factor-1 (IRF-1). LCY-2-CHO had no effect on the phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), MAPK-activated protein kinase-2 (MAPKAPK-2), STAT-1, CREB or c-Jun in LPS/IFN gamma-stimulated N9 cells, whereas it attenuated the phosphorylation of C/EBP beta at Ser105 and Thr235 residues, which occurred concomitantly with LCY-2-CHO inhibition of C/EBP beta expression and phosphorylation. Taken together, these results suggest that LCY-2-CHO inhibits NO production in microglia through the blockade of AP-1 and C/EBP activation. (C) 2008 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.bcp.2008.06.002
• 作为产物：
  描述：

  咔唑 、 邻氯氯苄 在 氢氧化钾 作用下， 以 四氢呋喃 为溶剂， 反应 16.0h， 以45%的产率得到9-(2-chlorobenzyl)carbazole
  参考文献：
  名称：

  Inhibition of nitric oxide production by the carbazole compound LCY-2-CHO via blockade of activator protein-1 and CCAAT/enhancer-binding protein activation in microglia

  摘要：

  Excessive nitric oxide (NO) production by activated microglia plays a critical role in neurodegenerative disorders. In this study, we found that 9-(2-chlorobenyl)-9H-carbazole-3-carbaldehyde (LCY-2-CHO) suppressed the NO production in lipopolysaccharide (LPS)/interferon-gamma (IFN gamma)-stimulated murine microglial N9 and BV-2 cells and in LPS-stimulated N9 cells and rat primary microglia. LCY-2-CHO had no cytotoxic effect on microglia. in activated N9 cells, LCY-2-CHO abolished the expression of inducible nitric oxide synthase (iNOS) protein and mRNA but failed to alter the stability of expressed iNOS mRNA and the enzymatic activity of expressed iNOS protein. LCY-2-CHO did not block DNA-binding activity of nuclear factor-kappa B (NF-kappa B) or cyclic AMP response element-binding protein (CREB), but abolished that of activator protein-1 (AP-1), CCAAT/enhancer-binding protein (C/EBP) and nuclear factor IL6 (NF-IL6). LCY-2-CHO attenuated the nuclear levels of c-Jun and C/EBP beta, but not those of p65, p50, C/EBP delta, signal transducer and activator of transcription-1 (STAT-1) or the nuclear expression of IFN regulatory factor-1 (IRF-1). LCY-2-CHO had no effect on the phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), MAPK-activated protein kinase-2 (MAPKAPK-2), STAT-1, CREB or c-Jun in LPS/IFN gamma-stimulated N9 cells, whereas it attenuated the phosphorylation of C/EBP beta at Ser105 and Thr235 residues, which occurred concomitantly with LCY-2-CHO inhibition of C/EBP beta expression and phosphorylation. Taken together, these results suggest that LCY-2-CHO inhibits NO production in microglia through the blockade of AP-1 and C/EBP activation. (C) 2008 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.bcp.2008.06.002

文献信息

• Design, synthesis and evaluation of carbazole derivatives as potential antimicrobial agents
  作者：Yi-Jie Xue、Ming-Yue Li、Xue-Jun Jin、Chang-Ji Zheng、Hu-Ri Piao

  DOI：10.1080/14756366.2020.1850713

  日期：2021.1.1

  Five series of novel carbazole derivatives containing an aminoguanidine, dihydrotriazine, thiosemicarbazide, semicarbazide or isonicotinic moiety were designed, synthesised and evaluated for their antimicrobial activities. Most of the compounds exhibited potent inhibitory activities towards different bacterial strains (including one multidrug-resistant clinical isolate) and one fungal strain with minimum

  设计、合成了五种含有氨基胍、二氢三嗪、氨基硫脲、氨基脲或异烟碱部分的新型咔唑衍生物，并对其抗菌活性进行了评估。大多数化合物对不同的细菌菌株（包括一种耐多药临床分离株）和一种真菌菌株表现出有效的抑制活性，最低抑制浓度（MIC）在 0.5 和 16 µg/ml 之间。化合物 8f 和 9d 显示出最有效的抑制活性（MIC 为 0.5-2 µg/ml）。此外，具有抗菌活性的化合物 8b、8d、8f、8k、9b 和 9e 对人胃癌细胞系（SGC-7901 和 AGS）或正常人肝细胞系（L-02）没有细胞毒性。构效关系分析和对接研究表明，二氢三嗪基团可增加抗菌效力并降低咔唑化合物的毒性。体外酶活性测定表明，与二氢叶酸还原酶结合的化合物 8f 可能是抗菌作用的原因。
• Trivalent Organostibines: Sb,N Ligands in Double N-Arylation of Primary Amines toward Functionalized Carbazoles
  作者：Lifen Peng、Yanting Zhao、Jiayi Chen、Hao Lu、Zilong Tang、Yi Chen、Shuang-Feng Yin、Nobuaki Kambe、Renhua Qiu

  DOI：10.1021/acs.joc.3c01863

  日期：2024.1.5

  A Sb,N ligand (L-Sb) for Pd-catalyzed double N-arylation of primary amines was developed. This trivalent ligand L-Sb, containing a 5,6,7,12-tetrahydrodibenzo[c,f][1,5]azastibocine skeleton and stable under air and moisture, could be synthesized facilely on a gram scale from chlorostibine (1) and cyclopentylmagnesium bromide. L-Sb showed excellent catalytic performance in Pd2(dba)3-catalyzed double

  开发了一种用于 Pd 催化伯胺双 N-芳基化的 Sb,N 配体 ( L-Sb )。这种三价配体L-Sb含有 5,6,7,12-四氢二苯并[ c , f ][1,5]氮杂替博辛骨架，在空气和湿气下稳定，可以从氯锑碱轻松合成克级 ( 1 )和环戊基溴化镁。 L-Sb在 Pd 2 (dba) 3催化的 2,2'-二溴-1,1'-联苯 ( 2 ) 与伯胺 ( 3 ) 的双 N-芳基化反应中表现出优异的催化性能，以良好的产率提供官能化咔唑。该Pd 2 (dba) 3 / L-Sb催化的双N-芳基化反应是三价有机锑化合物作为配体应用于N-芳基化反应的首例，具有催化剂负载量小、官能团耐受性广、化学稳定性好等优点。产率以及克级合成的简易性。
• CN116874409
  申请人：——

  公开号：——

  公开（公告）日：——
• Inhibition of nitric oxide production by the carbazole compound LCY-2-CHO via blockade of activator protein-1 and CCAAT/enhancer-binding protein activation in microglia
  作者：Ling-Chu Chang、Lo-Ti Tsao、Chi-Sen Chang、Chun-Jung Chen、Li-Jiau Huang、Sheng-Chu Kuo、Ruey-Hseng Lin、Jih-Pyang Wang

  DOI：10.1016/j.bcp.2008.06.002

  日期：2008.8

  Excessive nitric oxide (NO) production by activated microglia plays a critical role in neurodegenerative disorders. In this study, we found that 9-(2-chlorobenyl)-9H-carbazole-3-carbaldehyde (LCY-2-CHO) suppressed the NO production in lipopolysaccharide (LPS)/interferon-gamma (IFN gamma)-stimulated murine microglial N9 and BV-2 cells and in LPS-stimulated N9 cells and rat primary microglia. LCY-2-CHO had no cytotoxic effect on microglia. in activated N9 cells, LCY-2-CHO abolished the expression of inducible nitric oxide synthase (iNOS) protein and mRNA but failed to alter the stability of expressed iNOS mRNA and the enzymatic activity of expressed iNOS protein. LCY-2-CHO did not block DNA-binding activity of nuclear factor-kappa B (NF-kappa B) or cyclic AMP response element-binding protein (CREB), but abolished that of activator protein-1 (AP-1), CCAAT/enhancer-binding protein (C/EBP) and nuclear factor IL6 (NF-IL6). LCY-2-CHO attenuated the nuclear levels of c-Jun and C/EBP beta, but not those of p65, p50, C/EBP delta, signal transducer and activator of transcription-1 (STAT-1) or the nuclear expression of IFN regulatory factor-1 (IRF-1). LCY-2-CHO had no effect on the phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), MAPK-activated protein kinase-2 (MAPKAPK-2), STAT-1, CREB or c-Jun in LPS/IFN gamma-stimulated N9 cells, whereas it attenuated the phosphorylation of C/EBP beta at Ser105 and Thr235 residues, which occurred concomitantly with LCY-2-CHO inhibition of C/EBP beta expression and phosphorylation. Taken together, these results suggest that LCY-2-CHO inhibits NO production in microglia through the blockade of AP-1 and C/EBP activation. (C) 2008 Elsevier Inc. All rights reserved.