5-hydroxy-3,7,2',4'-tetramethoxyflavone | 19056-75-8

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 黄酮类化合物
• 英文名称: 5-hydroxy-3,7,2',4'-tetramethoxyflavone
• 英文别名: 2-(2,4-dimethoxyphenyl)-5-hydroxy-3,7-dimethoxy-4H-chromen-4-one；3,7,2',4'-Tetramethoxy-5-hydroxyflavone；2-(2,4-dimethoxyphenyl)-5-hydroxy-3,7-dimethoxychromen-4-one
• CAS: 19056-75-8
• 化学式: C₁₉H₁₈O₇
• 分子量: 358.348
• InChiKey: VHQCDGLXBNYODC-UHFFFAOYSA-N

物化性质

• 熔点：
  132-133 °C
• 沸点：
  587.4±50.0 °C(Predicted)
• 密度：
  1.36±0.1 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.8
• 重原子数：
  26
• 可旋转键数：
  5
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.21
• 拓扑面积：
  83.4
• 氢给体数：
  1
• 氢受体数：
  7

安全信息

• 储存条件：
  存储条件：2-8°C，密封保存，置于干燥处。

制备方法与用途

BCRP/ABCG2-IN-1 是一种针对乳腺癌耐药蛋白（BCRP/ABCG2）的抑制剂，其 IC50 值为 5.98 μM，可应用于乳腺癌的多药耐药性研究。

反应信息

• 作为反应物：
  描述：

  5-hydroxy-3,7,2',4'-tetramethoxyflavone 在 氢氧化钾 、 potassium peroxomonosulphate 、 potassium carbonate 作用下， 以 吡啶 、 丙酮 为溶剂， 反应 7.0h， 生成 5-hydroxy-3,7,8,2',4'-pentamethoxyflavone
  参考文献：
  名称：

  Pathak, V. P.; Khanna, R. N., Indian Journal of Chemistry - Section B Organic and Medicinal Chemistry, 1982, vol. 21, # 9, p. 891 - 892

  摘要：

  DOI：
• 作为产物：
  描述：

  2'-hydroxy-2,4,4',6'-tetramethoxychalkone 在 sodium hydroxide 、 三氯化铝 、 双氧水 、 potassium carbonate 作用下， 以 甲醇 、 乙醚 、 丙酮 为溶剂， 反应 16.5h， 生成 5-hydroxy-3,7,2',4'-tetramethoxyflavone
  参考文献：
  名称：

  Pathak, V. P.; Khanna, R. N., Indian Journal of Chemistry - Section B Organic and Medicinal Chemistry, 1982, vol. 21, # 9, p. 891 - 892

  摘要：

  DOI：

文献信息

• NMR of a series of novel hydroxyflavothiones
  作者：Tuyen Kim Pham Nguyen、Kim Phi Phung Nguyen、Fadhil S. Kamounah、Wei Zhang、Poul Erik Hansen

  DOI：10.1002/mrc.2510

  日期：2009.12

  Alkylated hydroxyflavothiones, namely flavothione, 5-hydroxyflavothione, 5,7-dihydroxyflavothione (chrysinthione), 7-dodecyloxy-5-hydroxyflavothione, 7-butyloxy-5-hydroxyflavothione, 2',3,4',7-tetramethoxy-5-hydroxyflavothione, 3,3',4',7-tetramethoxy-5-hydroxyflavothione, 7-butyloxy-4',5-dihydroxyflavothione and 7-butyloxy-4',5-hydroxyflavanonethione have been synthesized from the corresponding hydroxyflavones

  烷基化的羟基黄酮硫酮，即黄酮硫酮，5-羟基黄酮硫酮，5,7-二羟基黄酮硫酮（chrysinthione），7-十二烷氧基-5-羟基黄酮硫酮，7-丁氧基-5-羟基黄酮硫酮，2'，3,4'，7-四甲氧基-5-羟基黄酮硫酮在两个步骤中，由烷基化的羟基黄酮合成了3,3'，4'，7-四甲氧基-5-羟基黄酮硫酮，7-丁氧基-4'，5-二羟基黄酮硫酮和7-丁氧基-4'，5-羟基黄酮硫酮溴代烷烃或硫酸二甲酯对非氢键合的羟基进行分析，然后在微波辐射和无溶剂条件下使用Lawesson试剂将羰基转化为硫酮。在用Lawesson'处理的过程中，部分烷基化的黄烷酮7-丁氧基-4'，5-二羟基黄烷酮被氧化 除了目标产物丁氧基-4'，5-羟基黄烷硫酮以外，还可以得到第二种产物7-丁氧基-4'，5-二羟基黄烷硫酮。氘同位素对13C化学位移的影响已在羟基黄酮，异黄酮，黄烷酮和硫代类似物中进行了测量。正式的四键氘同位素对13C化学位移的影响，nDeltaC
• Synthesis and biological evaluation of flavones and benzoflavones as inhibitors of BCRP/ABCG2
  作者：Kapil Juvale、Katja Stefan、Michael Wiese

  DOI：10.1016/j.ejmech.2013.06.035

  日期：2013.9

  Multidrug resistance (MDR) often leads to a failure of cancer chemotherapy. Breast Cancer Resistance Protein (BCRP/ABCG2), a member of the superfamily of ATP binding cassette proteins has been found to confer MDR in cancer cells by transporting molecules with amphiphilic character out of the cells using energy from ATP hydrolysis. Inhibiting BCRP can be a solution to overcome MDR. We synthesized a series of flavones, 7,8-benzoflavones and 5,6-benzoflavones with varying substituents at positions 3, 3' and 4' of the (benzo)flavone structure. All synthesized compounds were tested for BCRP inhibition in Hoechst 33342 and pheophorbide A accumulation assays using MDCK cells expressing BCRP. All the compounds were further screened for their P-glycoprotein (P-gp) and Multidrug resistance-associated protein 1 (MRP1) inhibitory activity by calcein AM accumulation assay to check the selectivity towards BCRP. In addition most active compounds were investigated for their cytotoxicity. It was observed that in most cases 7,8-benzoflavones are more potent in comparison to the 5,6-benzoflavones. In general it was found that presence of a 3-OCH3 substituent leads to increase in activity in comparison to presence of OH or no substitution at position 3. Also, it was found that presence of 3',4'-OCH3 on phenyl ring lead to increase in activity as compared to other substituents. Compound 24, a 7,8-benzoflavone derivative was found to be most potent being 50 times selective for BCRP and showing very low cytotoxicity at higher concentrations. (C) 2013 Elsevier Masson SAS. All rights reserved.
• Pharmacokinetics and Metabolites of 12 Bioactive Polymethoxyflavones in Rat Plasma
  作者：Qiang You、Dan Li、Haiyan Ding、Hongping Chen、Yuan Hu、Youping Liu

  DOI：10.1021/acs.jafc.1c05004

  日期：2021.11.3
• Jain et al., Proceedings - Indian Academy of Sciences, Section A, 1952, # 36, p. 217,227
  作者：Jain et al.

  DOI：——

  日期：——
• Neural Glyoxalase Pathway Enhancement by Morin Derivatives in an Alzheimer’s Disease Model
  作者：Joel Frandsen、Seoung-ryoung Choi、Prabagaran Narayanasamy

  DOI：10.1021/acschemneuro.9b00566

  日期：2020.2.5

  The glyoxalase pathway (GP) is an antioxidant defense system that detoxifies metabolic byproduct methylglyoxal (MG). Through sequential reactions, reduced glutathione (GSH), glyoxalase I (glo-I), and glyoxalase II (glo-2) convert MG into D-lactate. Spontaneous reactions involving MG alter the structure and function of cellular macromolecules through the formation of inflammatory advanced glycation endproducts (AGEs). Accumulation of MG and AGEs in neural cells contributes to oxidative stress (OS), a state of elevated inflammation commonly found in neurodegenerative diseases including Alzheimer's disease (AD). Morin is a common plant-produced flavonoid polyphenol that exhibits the ability to enhance the GP-mediated detoxification of MG. We hypothesize that structural modifications to morin will improve its inherent GP enhancing ability. Here we synthesized a morin derivative, dibromo-morin (DBM), formulated a morin encapsulated nanoparticle (MNP), and examined their efficacy in enhancing neural GP activity. Cultured mouse primary cerebellar neurons and Caenorhabditis elegans were induced to a state of OS with MG and treated with morin, DBM, and MNP. Results indicated the morin derivatives were more effective compared to the parent compound in neural GP enhancement and preventing MG-mediated OS in an AD model.