2-(3-bromo-4-hydroxybenzylidene)-1H-indene-1,3(2H)-dione | 25315-16-6

• 分子结构分类: 有机化合物 - 苯类化合物 - 茚满类
• 英文名称: 2-(3-bromo-4-hydroxybenzylidene)-1H-indene-1,3(2H)-dione
• 英文别名: IDD-24；2-[(3-bromo-4-hydroxyphenyl)methylidene]indene-1,3-dione
• CAS: 25315-16-6
• 化学式: C₁₆H₉BrO₃
• 分子量: 329.15
• InChiKey: HEUZOZXAJYAJIF-UHFFFAOYSA-N

物化性质

• 沸点：
  495.4±45.0 °C(Predicted)
• 密度：
  1.697±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  3.8
• 重原子数：
  20
• 可旋转键数：
  1
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  54.4
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  1,3-茚满二酮 、 3-溴-4-羟基苯甲醛 在 盐酸 、 溶剂黄146 作用下， 以 水 为溶剂， 以75.1%的产率得到2-(3-bromo-4-hydroxybenzylidene)-1H-indene-1,3(2H)-dione
  参考文献：
  名称：

  嵌合化合物的体外抗黑色素生成作用，具有 β-苯基-α，β-不饱和二羰基支架的 2-（取代亚苄基）-1,3-茚满二酮衍生物

  摘要：

  酪氨酸酶被认为是黑色素生成的关键因素，因此医疗和美容目的需要安全、有效的酪氨酸酶抑制剂来治疗皮肤色素沉着过度和防止水果和蔬菜褐变。根据我们在酪氨酸酶抑制剂上积累的 SAR 数据，无论是E还是Z构型的 β-苯基-α,β-不饱和羰基支架，都可以赋予强大的酪氨酸酶抑制活性。在这项研究中，合成了十二种茚满二酮衍生物作为嵌合化合物，带有 β-苯基-α,β-不饱和二羰基支架。这些衍生物中的两个，即化合物2和3（分别为 85% 和 96% 的抑制），50 μM 对蘑菇酪氨酸酶的抑制显着高于曲酸（49% 的抑制）。对接研究预测化合物2和3都竞争性地抑制酪氨酸酶，这些发现得到 Lineweaver-Burk 图的支持。此外，这两种化合物比曲酸更能抑制 B16F10 细胞中的酪氨酸酶活性和黑色素含量，而没有明显的细胞毒性。这些结果支持这样的观点，即具有 β-苯基-α,β-不饱和二羰基支架的嵌合化合物代表了开发强效酪氨酸酶抑制剂的有希望的起点。

  DOI：

  10.1016/j.bioorg.2021.104688

文献信息

• Benzylidine indane-1,3-diones: As novel urease inhibitors; synthesis, in vitro, and in silico studies
  作者：Bilquees Bano、Kanwal、Khalid Mohammed Khan、Farida Begum、Muhammad Arif Lodhi、Uzma Salar、Ruqaiya Khalil、Zaheer Ul-Haq、Shahnaz Perveen

  DOI：10.1016/j.bioorg.2018.09.030

  日期：2018.12

  Current study deals with the evaluation of indane-1,3-dione based compounds as new class of urease inhibitors. For that purpose, benzylidine indane-1,3-diones (1-30) were synthesized and fully characterized by different spectroscopic techniques including EI-MS, HREI-MS, H-1, and C-13 NMR. All synthetic molecules 1-30 were evaluated for urease inhibitory activity and showed good to moderate inhibitory potential within the range of (IC50 = 11.60 +/- 0.3-257.05 +/- 0.7 mu M) as compared to the standard acetohydroxamic acid (IC50 = 27.0 +/- 0.5 mu M). Compound 1 (IC50 = 11.60 +/- 0.3 mu M) was found to be most potent inhibitor amongst all derivatives. The key binding interactions of most active compounds within the enzyme pocket were evaluated through in silico studies.
• A new indanedione derivative alleviates symptoms of diabetes by modulating RAGE-NF-kappaB pathway in db/db mice
  作者：Gulnaz Khan、Meha Fatima Aftab、Bilquees Bano、Khalid Mohammed Khan、Munazza Murtaza、Sonia Siddiqui、M.Hafizur Rehman、Rizwana Sanaullah Waraich

  DOI：10.1016/j.bbrc.2018.05.043

  日期：2018.7

  Accumulating evidence indicates that a number of tissues are damaged due to build-up of abnormal amount of Advanced Glycation End products (AGEs) in several diseases including diabetes. Currently AGE inhibitors are scarce in clinical use indicating a need for development of new anti-AGE agents. The aim of the current study is to identify the new AGE inhibitors and to decipher their mechanism of action for alleviating symptoms of diabetes in mice. Among several derivatives, one of the derivatives of indanedione, IDD-24 demonstrated highest inhibition of AGE formation and AGE mediated reactive oxygen species production in HepG-2 and mature 313-L1 adipocytes. In mice treated with IDD-24, reduction in serum AGE formation and expression of Receptor for AGEs (RAGE) was seen in IDD-24 treated db/db mice. In vivo, glycogen synthesis was also increased in muscle tissue. In adipocytes, anti-AGE agent restored AGEs' induced diminished glucose uptake in fat cells. Mice treated with IDD-24 exhibited increased glucose tolerance, increaed serum adiponectin levels and decreased insulin resistance. Deciphering mechanism of IDD-24 in diabetic mice, it was observed that nuclear factor-kappa B (NF-kappa B) and serine phosphorylation of Insulin receptor substrate-1 (IRS-1) declined, while diminished activation of c-Jun NH2-terminal kinase (JNK) appears to be partly responsible for restoration of insulin signaling. We conclude that IDD-24 can be a possible treatment target to address symptoms of diabetes. (C) 2018 Elsevier Inc. All rights reserved.