(3E,5E)-3,5-bis(4-hydroxybenzylidene)-tetrahydropyran-4-one | 1268636-56-1

• 分子结构分类: 有机化合物 - 苯类化合物 - 酚类
• 英文名称: (3E,5E)-3,5-bis(4-hydroxybenzylidene)-tetrahydropyran-4-one
• 英文别名: (3E,5E)-3,5-Bis(4-hydroxybenzylidene)oxan-4-one；(3E,5E)-3,5-bis[(4-hydroxyphenyl)methylidene]oxan-4-one
• CAS: 1268636-56-1
• 化学式: C₁₉H₁₆O₄
• 分子量: 308.334
• InChiKey: HNXHPBJNEBJVDO-KAVGSWPWSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.7
• 重原子数：
  23
• 可旋转键数：
  2
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.11
• 拓扑面积：
  66.8
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  四氢吡喃酮 、 对羟基苯甲醛 在 盐酸 、 溶剂黄146 作用下， 以 乙醇 为溶剂， 以60%的产率得到(3E,5E)-3,5-bis(4-hydroxybenzylidene)-tetrahydropyran-4-one
  参考文献：
  名称：

  新型姜黄素类似物作为潜在抗肺癌药物的设计、合成和评价

  摘要：

  摘要 姜黄素是一种来源于植物姜黄的多酚化合物，其结构不稳定性限制了其进一步的临床应用。在这项研究中，制备并评估了 11 种具有更稳定支架的姜黄素类似物。结果表明，最佳化合物Y-11对包括H460和H1650在内的肺癌细胞表现出最强的抗增殖活性。进一步的研究表明，Y-11可能抑制 hDHODH，诱导细胞周期停滞和细胞凋亡，并下调 H1650 细胞中关键信号通路蛋白的表达。总之，新设计的姜黄素类似物Y-11可能适用于肺癌治疗的进一步发展。

  DOI：

  10.1080/10286020.2022.2095264

文献信息

• COMPOUNDS AND MATRICES FOR USE IN BONE GROWTH AND REPAIR
  申请人：HUMAN BIOMOLECULAR RESEARCH INSTITUTE

  公开号：US20160038641A1

  公开（公告）日：2016-02-11

  Compositions of small molecules, matrices, and isolated cells including methods of preparation, and methods for differentiation, transdifferentiation, and proliferation of animal cells into the osteoblast blast cell lineage were described. Examples of osteogenic materials that were administered to cells or co-cultured with cells are represented by compounds of Formula II, IV, and VI independently or preferably in combination with a matrix to afford bone cells. Small molecule-stimulated cells were also combined with a matrix, placed with a cellular adhesive or material carrier and implanted to a site in an animal for bone repair. Matrix pretreated with compounds of Formula II, IV, and VI were also used to cause cells to migrate to the matrix that is of use for therapeutic purposes.

  描述了由小分子、基质和孤立细胞组成的组合物，包括制备方法，以及动物细胞分化、转分化和增殖成骨母细胞谱系的方法。给细胞施加的或与细胞共培养的成骨材料的示例由独立或首选与基质组合的Formula II、IV和VI化合物代表。受小分子刺激的细胞还与基质结合，与细胞粘合剂或材料载体一起植入到动物体内的部位进行骨修复。预先用Formula II、IV和VI化合物处理的基质也被用于导致细胞迁移到用于治疗目的的基质上。
• SMALL MOLECULE IMMUNOMODULATORS FOR ALZHEIMER'S DISEASE
  申请人：Cashman John R.

  公开号：US20120040976A1

  公开（公告）日：2012-02-16

  Disclosed are methods for identifying individuals suffering from a CNS disorder (including Alzheimer's Disease, ALS, behavioral disorders, and the like) that could be treated with a CNS drug with greater therapeutic efficacy and lower side effects and the compounds useful for such treatment. Also disclosed are methods for predicting the efficacy of a drug candidate for the treatment of a CNS disorder. The technology is also applicable to drug discovery for evaluation in animal models of neurodegenerative diseases.

  本发明涉及识别患有中枢神经系统疾病（包括阿尔茨海默病、肌萎缩性侧索硬化症、行为障碍等）的个体，这些个体可以通过使用中枢神经系统药物进行治疗，其治疗效果更好，副作用更小，以及用于此类治疗的化合物。本发明还涉及预测治疗中枢神经系统疾病的候选药物的疗效的方法。该技术还适用于药物发现，以在神经退行性疾病动物模型中进行评估。
• Compounds and matrices for use in bone growth and repair
  申请人：HUMAN BIOMOLECULAR RESEARCH INSTITUTE

  公开号：US10874766B2

  公开（公告）日：2020-12-29

  Compositions of small molecules, matrices, and isolated cells including methods of preparation, and methods for differentiation, trans-differentiation, and proliferation of animal cells into the osteoblast blast cell lineage were described. Examples of osteogenic materials that were administered to cells or co-cultured with cells are represented by compounds of Formula II, IV, and VI independently or preferably in combination with a matrix to afford bone cells. Small molecule-stimulated cells were also combined with a matrix, placed with a cellular adhesive or material carrier and implanted to a site in an animal for bone repair. Matrix pretreated with compounds of Formula II, IV, and VI were also used to cause cells to migrate to the matrix that is of use for therapeutic purposes.

  描述了小分子、基质和分离细胞的组合物，包括制备方法，以及将动物细胞分化、转分化和增殖为成骨细胞的方法。向细胞施用或与细胞共培养的成骨材料的例子以式 II、IV 和 VI 的化合物为代表，这些化合物可独立使用，或最好与基质结合使用，以产生骨细胞。小分子刺激的细胞也与基质结合，与细胞粘合剂或材料载体一起放置，并植入动物的骨修复部位。用式 II、IV 和 VI 的化合物预处理的基质也用于使细胞迁移到用于治疗目的的基质上。
• New MD2 inhibitors derived from curcumin with improved anti-inflammatory activity
  作者：Yali Zhang、Zhiguo Liu、Jianzhang Wu、Bin Bai、Hongjin Chen、Zhongxiang Xiao、Lingfeng Chen、Yunjie Zhao、Hazel Lum、Yi Wang、Hong Zhang、Guang Liang

  DOI：10.1016/j.ejmech.2018.02.008

  日期：2018.3

  An overactive Toll-like receptor (TLR) signaling complex is a significant pathogenic factor of acute and chronic inflammatory diseases. The natural product curcumin is reported to inhibit the TLR4 co-receptor, MD2 (myeloid differentiation protein 2), but its low in vivo bioavailability limits its therapeutic potential. We developed new curcumin analogs (MACs) with removal of the beta-diketone moiety and substituted residues in benzene rings, and identify these as potential MD2 inhibitors with improved inhibition potency and stability over that of curcumin. Specifically, MAC 17 and 28 showed the highest anti-inflammatory activity, with >90% inhibition of LPS-stimulated cytokine secretion from macrophages, and protected against LPS-induced acute lung injury and sepsis. The MACs inhibited the TLR4-MD2 signaling complex through competition with LPS for binding on MD2, likely at Arg(90). Our findings indicated that MAC 17 and 28 are promising candidates for future development as therapeutic drugs for inflammatory diseases with an endotoxin etiology. (C) 2018 Elsevier Masson SAS. All rights reserved.
• Synthesis and anti-tumor activity of EF24 analogues as IKKβ inhibitors
  作者：Rong Jin、Qiuxiang Chen、Song Yao、Encheng Bai、Weitao Fu、Ledan Wang、Jiabing Wang、Xiaojing Du、Tao Wei、Haineng Xu、Chengxi Jiang、Peihong Qiu、Jianzhang Wu、Wulan Li、Guang Liang

  DOI：10.1016/j.ejmech.2017.11.077

  日期：2018.1

  EF24 is an IKK beta inhibitor (IC50: 72 mu M) containing various anti-tumor activities. In this study, a series of EF24 analogs targeting IKK beta were designed and synthesized. Several IKK beta inhibitors with better activities than EF24 were screened out and B3 showed best IKK beta inhibitory (IC50: 6.6 mu M). Molecular docking and dynamic simulation experiments further confirmed this inhibitory effect. B3 obviously suppressed the viability of Hela229, A549, SGC-7901 and MGC-803 cells. Then, in SGC-7901 and MGC-803 cells, B3 blocked the NF-kappa B signal pathway by inhibiting IKK beta phosphorylation, and followed arrested the cell cycle at G2/M phase by suppressing the Cyclin B1 and Cdc2 p34 expression, induced the cell apoptosis by down-regulating Bcl-2 protein and up-regulating cleaved-caspase3. Moreover, B3 significantly reduced tumor growth and suppressed the IKK beta-NF-kappa B signal pathway in SGC-7901 xenograft model. In total, this study present a potential IKK beta inhibitor as anti-tumor precursor. (C) 2017 Published by Elsevier Masson SAS.