5,9,13-trimethyl-2-nitro-2,8,12-tetradecatriene | 834897-99-3

• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 异戊烯醇脂质
• 英文名称: 5,9,13-trimethyl-2-nitro-2,8,12-tetradecatriene
• 英文别名: 2,6,10-Trimethyl-13-nitrotetradeca-2,6,12-triene；2,6,10-trimethyl-13-nitrotetradeca-2,6,12-triene
• CAS: 834897-99-3
• 化学式: C₁₇H₂₉NO₂
• 分子量: 279.423
• InChiKey: YAVVCUPYAVQOJN-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  6.3
• 重原子数：
  20
• 可旋转键数：
  8
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.65
• 拓扑面积：
  45.8
• 氢给体数：
  0
• 氢受体数：
  2

反应信息

• 作为反应物：
  描述：

  5,9,13-trimethyl-2-nitro-2,8,12-tetradecatriene 在 双氧水 、 氢氧化钾 作用下， 以 1,4-二氧六环 、 甲醇 为溶剂， 反应 2.17h， 生成 2,3-epoxy-5,9,13-trimethyl-2-nitro-8,12-tetradecadiene
  参考文献：
  名称：

  Inactivation of Protein Farnesyltransferase by Active-Site-Targeted Dicarbonyl Compounds

  摘要：

  Upon farnesylation by protein farnesyltransferase (FTase), key proteins become compartmentalized in cells. For example, cell membrane localization is essential for the mitogenic role of mutant Ras protein, which acts as a switch for cancer cell proliferation. We repel? that alpha -dicarbonyl compounds derived from the isoprenoid skeleton or other hydrophobic groups potently obstruct farnesylation of a Ras model peptide by human recombinant FTase in vitro. A geranyl-derived isoprenoid diketone, 5.9-dimethyl-8-decene-2,3-dione, at 17 muM caused a 62% reduction in FTase activity after 30 minutes. A farnesyl-derived isoprenoid diketone, 5,9,13-trimethyl-8,12-tetradecadiene-2,3-dione, at 93 muM caused a 94% reduction after 30 minutes. Other dicarbonyl:compounds found to be effective against FTase in vitro were (+/-)-6-(camphorquinone-10-sulfonamido)-hexanoic acid, 4,4 ' -biphenyldiglyoxaldehyde, dehydroascorbic acid 6-palmitace, 2-oxododecanal, and phenylglyoxal. Higher concentrations of the alpha -dicarbonyl compound resulted in more rapid and more extensive inactivation. These findings demonstrate that ct-dicarbonyl compounds targeted to FTase interfere with protein farnesylation in vitro and may,lead to derivatives that have utility as chemotherapeutic agents.

  DOI：

  10.1002/1521-4184(200106)334:6<194::aid-ardp194>3.0.co;2-m
• 作为产物：
  描述：

  反式,反式-金合欢醇 在 Amberlyst A-21 ion exchange resin 、 potassium tert-butylate 、 pyridinium chlorochromate 、 氢化铝 、 nickel dichloride 作用下， 以 四氢呋喃 、 二氯甲烷 、 叔丁醇 为溶剂， 反应 61.17h， 生成 5,9,13-trimethyl-2-nitro-2,8,12-tetradecatriene
  参考文献：
  名称：

  Inactivation of Protein Farnesyltransferase by Active-Site-Targeted Dicarbonyl Compounds

  摘要：

  Upon farnesylation by protein farnesyltransferase (FTase), key proteins become compartmentalized in cells. For example, cell membrane localization is essential for the mitogenic role of mutant Ras protein, which acts as a switch for cancer cell proliferation. We repel? that alpha -dicarbonyl compounds derived from the isoprenoid skeleton or other hydrophobic groups potently obstruct farnesylation of a Ras model peptide by human recombinant FTase in vitro. A geranyl-derived isoprenoid diketone, 5.9-dimethyl-8-decene-2,3-dione, at 17 muM caused a 62% reduction in FTase activity after 30 minutes. A farnesyl-derived isoprenoid diketone, 5,9,13-trimethyl-8,12-tetradecadiene-2,3-dione, at 93 muM caused a 94% reduction after 30 minutes. Other dicarbonyl:compounds found to be effective against FTase in vitro were (+/-)-6-(camphorquinone-10-sulfonamido)-hexanoic acid, 4,4 ' -biphenyldiglyoxaldehyde, dehydroascorbic acid 6-palmitace, 2-oxododecanal, and phenylglyoxal. Higher concentrations of the alpha -dicarbonyl compound resulted in more rapid and more extensive inactivation. These findings demonstrate that ct-dicarbonyl compounds targeted to FTase interfere with protein farnesylation in vitro and may,lead to derivatives that have utility as chemotherapeutic agents.

  DOI：

  10.1002/1521-4184(200106)334:6<194::aid-ardp194>3.0.co;2-m

文献信息

• Conjugated nitro alkene anticancer agents based on isoprenoid metabolism
  申请人：Rose D. Seth

  公开号：US20050026812A1

  公开（公告）日：2005-02-03

  Conjugated nitro alkene compounds hamper or prevent proliferation of cancer cells in cell culture and in cancer patients, which can result in a decrease in tumor size and/or disappearance of the cancer. The compounds may act by interference with cancer cell biochemistry, in which isoprenoid groups such as farnesyl and geranylgeranyl become bonded to various oncogenic proteins such as Ras, RhoA, RhoB, or some other growth-related cellular protein(s).

  共轭硝基烯烃化合物可以阻碍或预防癌细胞在细胞培养和癌症患者中的增殖，从而导致肿瘤大小减小和/或癌症消失。这些化合物可能通过干扰癌细胞生物化学作用发挥作用，其中类似异戊二烯基和戊二烯基的异戊二烯基类物质与各种致癌蛋白质（如Ras、RhoA、RhoB或其他与生长有关的细胞蛋白质）结合。
• Conjugated Nitro Alkene Anticancer Agents Based on Isoprenoid Metabolism
  申请人：ROSE Seth D.

  公开号：US20080113919A1

  公开（公告）日：2008-05-15

  Conjugated nitro alkene compounds hamper or prevent proliferation of cancer cells in cell culture and in cancer patients, which can result in a decrease in tumor size and/or disappearance of the cancer. The compounds may act by interference with cancer cell biochemistry, in which isoprenoid groups such as farnesyl and geranylgeranyl become bonded to various oncogenic proteins such as Ras, RhoA, RhoB, or some other growth-related cellular protein(s).

  硝基烯烃化合物在细胞培养和癌症患者中阻碍或预防癌细胞增殖，这可能导致肿瘤大小的减小和/或癌症的消失。这些化合物可能通过干扰癌细胞的生物化学作用来发挥作用，其中异戊二烯基和戊二烯基等异戊二烯基类似物与各种致癌蛋白质（如Ras、RhoA、RhoB或其他与生长相关的细胞蛋白质）结合。
• Inactivation of Protein Farnesyltransferase by Active-Site-Targeted Dicarbonyl Compounds
  作者：Karl J. Okolotowicz、Wei-Jen Lee、Rosemarie F. Hartman、Ann Y. Kim、Steven R. Ottersberg、Dale E. Robinson, Jr.、Scott R. Lefler、Seth D. Rose

  DOI：10.1002/1521-4184(200106)334:6<194::aid-ardp194>3.0.co;2-m

  日期：2001.6

  Upon farnesylation by protein farnesyltransferase (FTase), key proteins become compartmentalized in cells. For example, cell membrane localization is essential for the mitogenic role of mutant Ras protein, which acts as a switch for cancer cell proliferation. We repel? that alpha -dicarbonyl compounds derived from the isoprenoid skeleton or other hydrophobic groups potently obstruct farnesylation of a Ras model peptide by human recombinant FTase in vitro. A geranyl-derived isoprenoid diketone, 5.9-dimethyl-8-decene-2,3-dione, at 17 muM caused a 62% reduction in FTase activity after 30 minutes. A farnesyl-derived isoprenoid diketone, 5,9,13-trimethyl-8,12-tetradecadiene-2,3-dione, at 93 muM caused a 94% reduction after 30 minutes. Other dicarbonyl:compounds found to be effective against FTase in vitro were (+/-)-6-(camphorquinone-10-sulfonamido)-hexanoic acid, 4,4 ' -biphenyldiglyoxaldehyde, dehydroascorbic acid 6-palmitace, 2-oxododecanal, and phenylglyoxal. Higher concentrations of the alpha -dicarbonyl compound resulted in more rapid and more extensive inactivation. These findings demonstrate that ct-dicarbonyl compounds targeted to FTase interfere with protein farnesylation in vitro and may,lead to derivatives that have utility as chemotherapeutic agents.