2,4-二甲基-5-甲氧基硝基苯 | 188017-09-6

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 中文名称: 2,4-二甲基-5-甲氧基硝基苯
• 英文名称: 2,4-dimethyl-5-methoxynitrobenzene
• 英文别名: 2,4-dimethyl-5-nitro-anisole；2,4-Dimethyl-5-nitro-anisol；1-Methoxy-2,4-dimethyl-5-nitrobenzene
• CAS: 188017-09-6
• 化学式: C₉H₁₁NO₃
• 分子量: 181.191
• InChiKey: FOXLHMCGWDQLAW-UHFFFAOYSA-N

物化性质

• 沸点：
  293.4±35.0 °C(Predicted)
• 密度：
  1.148±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.5
• 重原子数：
  13
• 可旋转键数：
  1
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.33
• 拓扑面积：
  55
• 氢给体数：
  0
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  2,4-二甲基-5-甲氧基硝基苯 在 盐酸 、 硫酸 、 铁粉 作用下， 生成 Methyl-(5-hydroxy-2.4-dimethyl-phenyl)-aether
  参考文献：
  名称：

  Tea as a Potential Chemopreventive Agent in PhIP Carcinogenesis: Effects of Green Tea and Black Tea on PhIP-DNA Adduct Formation in Female F-344 Rats

  摘要：

  The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is formed during the cooking of proteinaceous animal foods (meat, chicken, and fish). PhIP is a carcinogen in the Fischer 344 (F-344) rat; it induces mammary tumors in female rats and lymphomas and colon and prostate rumors in male rats. In F-344 rats, PhIP forms DNA adducts in various organs, including the target organs. Inhibition of PhIP-DNA adduct formation is likely to lead to inhibition of PhIP tumorigenicity. We have examined the chemopreventive properties of green tea and black tea in PhIP carcinogenesis by evaluating their effects on PhIP-DNA adduct formation in the female F-344 rat. Young adult animals were maintained on powdered AIN-76A diet while receiving regular drinking water or 2% (wt/vol) infusions of green tea or black tea for a total of six weeks. During Weeks 3, 4, and 5, all animals received PhIP by gavage (1 mg/kg/day). Three rats per group were euthanized on Days 1 and 8 after termination of PhIP exposure. DNA was isolated from a number of organs and analyzed for PhIP-DNA adducts by P-32-postlabeling assays. Compared with animals on regular drinking wafer, PhIP-DMA adduct formation was inhibited in small intestine, colon, liver, and mammary epithelial cells (MECS) of animals receiving green tea or black tea as the sole source of drinking fluid. Green tea inhibited adduct formation in colon, liver, and MECs (33.3-80.0%) on both days, but only on Day 8 (54.4%) in small intestine. Black tea inhibited adduct formation on both days in liver (71.4-80.0%), on Day 1 in colon (40.0%), and on Day 8 in small intestine (81.8%); it had no effect on MEC adducts. Neither green tea nor black tea had an effect on adduct levels in pancreas: lungs, white blood cells, heart, kidneys, spleen, cecum, or stomach. Similarly, these teas did not affect the rate of adduct removal (percent change from Day 1 to Day 8) in any organ. It is concluded that green tea and black tea are potential chemopreventive agents in PhIP-induced tumorigenesis in the F-344 rat.

  DOI：

  10.1207/s15327914nc3601_8
• 作为产物：
  描述：

  2,4-二甲基-5-硝基-苯酚 、 碘甲烷 在 potassium carbonate 作用下， 生成 2,4-二甲基-5-甲氧基硝基苯
  参考文献：
  名称：

  Pfaff, Chemische Berichte, 1883, vol. 16, p. 1137

  摘要：

  DOI：

文献信息

• Optimization of 4-Phenylamino-3-quinolinecarbonitriles as Potent Inhibitors of Src Kinase Activity
  作者：Diane H. Boschelli、Fei Ye、Yanong D. Wang、Minu Dutia、Steve L. Johnson、Biqi Wu、Karen Miller、Dennis W. Powell、Deanna Yaczko、Mairead Young、Mark Tischler、Kim Arndt、Carolyn Discafani、Carlo Etienne、Jay Gibbons、Janet Grod、Judy Lucas、Jennifer M. Weber、Frank Boschelli

  DOI：10.1021/jm0102250

  日期：2001.11.1

  Subsequent to the discovery of 4-[(2,4-dichlorophenyl)amino]-6,7-dimethoxy-3-quinolinecarbonitrile (1a) as an inhibitor of Src kinase activity (IC50 = 30 nM), several additional analogues were prepared. Optimization of the C-4 anilino group of la led to le, which contains a 2,4-dichloro-5-methoxy-substituted aniline. Replacement of the methoxy group at C-7 of le with a 3-(morpholin-4-yl)propoxy group provided 2c, resulting in increased inhibition of both Src kinase activity and Src-mediated cell proliferation. Analogues of 2c, with other trisubstituted anilines at C-4 were also potent Src inhibitors, and the propoxy group of 2c was preferred over ethoxy, butoxy, or pentoxy. Replacement of the morpholine group of 2c with a 4-methylpiperazine group provided 31a, which had an IC50 of 1.2 nM in the Src enzymatic assay, an IC50 of 100 nM for the inhibition of Src-dependent cell proliferation and was selective for Src over non-Src family kinases. Compound 31a, which had higher 1 and 4 h plasma levels than 2c, effectively inhibited tumor growth in xenograft models.
• Photochemical Nitration by Tetranitromethane. Part XXXVII. Adduct Formation and the Regiochemistry of Attack of Trinitromethanide Ion on Radical Cations in the Photochemical Reactions of 2-Methyl-, 2,3-Dimethyl- and 2,4-Dimethylanisoles.
  作者：Craig P. Butts、Lennart Eberson、Michael P. Hartshorn、Ward T. Robinson、David J. Timmerman-Vaughan、Lauri Niinistö、Stenbjörn Styring、Cecilia Tommos、Kurt Warncke、Bryan R. Wood

  DOI：10.3891/acta.chem.scand.51-0073

  日期：——

  The photolysis of the charge transfer (CT) complex of tetranitromethane and 2-methylanisole 2 in dichloromethane at 20 degrees C gives the epimeric 1-methoxy-6-methyl-6-nitro-3-trinitromethylcyclohexa-1,4-dienes 8 and 9 in addition to 2-methyl-4-trinitromethylanisole (3) and 2-methyl-4-nitroanisole (4). In acetonitrile the yields of compound 4 and adducts 8 and 9 are significantly higher. Similar reaction of 2,3-dimethylanisole (6) in dichloromethane gave nitrotrinitromethyl adducts 10 and 11, hydroxy-trinitromethyl adducts 12 and 13, 2,3-dimethyl-5-trinitromethylanisole (14), 4-methoxy-2,3-dimethylbenzonitrile N-oxide (15), 2,3-dimethyl-4-trinitromethylanisole (16), 2,3-dimethyl-4-nitroanisole (17), 2,3-dimethyl-4,6-dinitrophenol (18), 3-methoxy-4,5-dimethyl-benzoic acid (19) and the hydroxy dinitro compound (20).The photolysis of the CT complex of 2,4-dimethylanisole (7) with tetranitromethane in dichloromethane gave the epimeric 1-methoxy-4,6-dimethyl-6-nitro-3-trinitromethylcyclohexa-1,4-dienes 21 and 22, together with 4,6-dimethyl-3-trinitromethylanisole (23), 4,6-dimethyl-2-nitrophenol (24), 4,6-dimethyl-2-trinitromethylanisole (25), 4,6-dimethyl-3-nitroanisole (26), 4,6-dimethyl-2-nitroanisole (27) and 4,6-dimethyl-4-nitrocyclohexa-2,5-dienone (28).The modes of formation of the above products are discussed, including the effects of the reaction solvent on those processes. The X-ray crystal structure of 1-methoxy-2-methyl-c-6-nitro-r-3-trinitromethylcyclohexa-1,4-diene (9) is reported.
• Maltese, Gazzetta Chimica Italiana, 1907, vol. 37 II, p. 284
  作者：Maltese

  DOI：——

  日期：——
• A-Ring Ortho-Disubstituted Aporphine Derivatives as Potential Agonists or Antagonists at Serotonergic 5-HT1A Receptors
  作者：Joseph G. Cannon、Patrick T. Flaherty、Ugur Ozkutlu、John Paul Long

  DOI：10.1021/jm00011a002

  日期：1995.5

  (R)- And (S)-11-hydroxy-10-methylaporphine 1 and 2 are, respectively, a potent, highly specific serotonergic (5-HT1A) agonist and antagonist. In an ongoing structure-activity study, racemates of the positional isomers 8-hydroxy-9-methyl- and 8-methyl-9-hydroxyaporphine were prepared by modifications of literature methods and were resolved. The methyl ethers of the target compounds were also evaluated pharmacologically. All of the free phenolic derivatives [(+)- and (-)-8 and 10] were inert in an assay for 5-HT1A receptor activity. All of the methyl ethers [(+)- and (-)-9 and 11] demonstrated quantitatively similar low potency stimulant effect at 5-HT1A receptors. The agonist or antagonist activity exhibited by 1 and 2 reflects the high degree of structural specificity required of aporphine derivatives for action at 5-HT1A receptors.
• Tea as a Potential Chemopreventive Agent in PhIP Carcinogenesis: Effects of Green Tea and Black Tea on PhIP-DNA Adduct Formation in Female F-344 Rats
  作者：Herman A. J. Schut、Ruisheng Yao

  DOI：10.1207/s15327914nc3601_8

  日期：2000.1

  The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is formed during the cooking of proteinaceous animal foods (meat, chicken, and fish). PhIP is a carcinogen in the Fischer 344 (F-344) rat; it induces mammary tumors in female rats and lymphomas and colon and prostate rumors in male rats. In F-344 rats, PhIP forms DNA adducts in various organs, including the target organs. Inhibition of PhIP-DNA adduct formation is likely to lead to inhibition of PhIP tumorigenicity. We have examined the chemopreventive properties of green tea and black tea in PhIP carcinogenesis by evaluating their effects on PhIP-DNA adduct formation in the female F-344 rat. Young adult animals were maintained on powdered AIN-76A diet while receiving regular drinking water or 2% (wt/vol) infusions of green tea or black tea for a total of six weeks. During Weeks 3, 4, and 5, all animals received PhIP by gavage (1 mg/kg/day). Three rats per group were euthanized on Days 1 and 8 after termination of PhIP exposure. DNA was isolated from a number of organs and analyzed for PhIP-DNA adducts by P-32-postlabeling assays. Compared with animals on regular drinking wafer, PhIP-DMA adduct formation was inhibited in small intestine, colon, liver, and mammary epithelial cells (MECS) of animals receiving green tea or black tea as the sole source of drinking fluid. Green tea inhibited adduct formation in colon, liver, and MECs (33.3-80.0%) on both days, but only on Day 8 (54.4%) in small intestine. Black tea inhibited adduct formation on both days in liver (71.4-80.0%), on Day 1 in colon (40.0%), and on Day 8 in small intestine (81.8%); it had no effect on MEC adducts. Neither green tea nor black tea had an effect on adduct levels in pancreas: lungs, white blood cells, heart, kidneys, spleen, cecum, or stomach. Similarly, these teas did not affect the rate of adduct removal (percent change from Day 1 to Day 8) in any organ. It is concluded that green tea and black tea are potential chemopreventive agents in PhIP-induced tumorigenesis in the F-344 rat.