1,3-bis-N-t-butyloxycarbonyl-2-cyanopropane | 159029-59-1

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 英文名称: 1,3-bis-N-t-butyloxycarbonyl-2-cyanopropane
• 英文别名: 3--2-<(N-(tert-butoxycarbonyl)amino)methyl>propionitrile；di-tert-butyl (2-cyano-1,3-propanediyl)biscarbamate；tert-butyl N-[3-(tert-butoxycarbonylamino)-2-cyano-propyl]carbamate；tert-butyl N-[2-cyano-3-[(2-methylpropan-2-yl)oxycarbonylamino]propyl]carbamate
• CAS: 159029-59-1
• 化学式: C₁₄H₂₅N₃O₄
• 分子量: 299.37
• InChiKey: NZGYKRZCFKSQDV-UHFFFAOYSA-N

物化性质

• 沸点：
  465.0±40.0 °C(Predicted)
• 密度：
  1.076±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  1.4
• 重原子数：
  21
• 可旋转键数：
  8
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.79
• 拓扑面积：
  100
• 氢给体数：
  2
• 氢受体数：
  5

反应信息

• 作为反应物：
  描述：

  1,3-bis-N-t-butyloxycarbonyl-2-cyanopropane 在 硫化氢 、 三乙胺 作用下， 以 乙醇 、 N,N-二甲基甲酰胺 为溶剂， 反应 74.0h， 生成 ethyl 2-<(1,3-bis(N-(tert-butoxycarbonyl)amino))-2-propyl>thiazole-4-carboxylate
  参考文献：
  名称：

  Guanosine-Specific DNA Damage by a Co(II).cntdot.Bithiazole Complex

  摘要：

  A bithiazole derivative structurally related to the bithiazole moiety of bleomycin (BLM) A(2) was prepared. This derivative contained a 2-(1,3-diaminopropyl) substituent, rather than the 2-(2-aminoethyl) substituent normally present in BLM, in order to facilitate metal coordination by the bithiazole moiety itself. In the presence of Co2+, th, modified bithiazole mediated the production of alkali labile lesions on double-stranded DNA. Following treatment with alkali, guanosine-specific DNA strand scission was observed. DNA degradation by this Co(II). bithiazole complex was not light dependent but did require molecular oxygen. DNA cleavage studies employing scavengers of activated oxygen species suggested that the observed DNA damage did not result from diffusible, activated forms of oxygen. Moreover, ESR spectroscopy utilizing a spin trapping reagent demonstrated conclusively that the Co(II). bithiazole complex did not produce diffusible oxygen radicals. Absorption spectroscopy with a thiazole analog of the modified bithiazole suggested that, in the presence of oxygen, a O-2 . Co . thiazole complex was formed. These mechanistic studies suggested that the (oxygenated) Co(II). bithiazole complex mediated the oxidative alteration or liberation of the guanine base, producing an alkali labile site. Further, the guanosine specificity appeared to derive from preferential reactivity at guanosine sites, as opposed to a guanosine binding selectivity of the bithiazole. The oxidative degradation of G residues in DNA appears to proceed by an inner sphere mechanism.

  DOI：

  10.1021/ja00141a001
• 作为产物：
  描述：

  1,3-二-(Boc-氨基)-2-羟基丙烷 在 吡啶 作用下， 以 二甲基亚砜 为溶剂， 反应 50.0h， 生成 1,3-bis-N-t-butyloxycarbonyl-2-cyanopropane
  参考文献：
  名称：

  Guanosine-Specific DNA Damage by a Co(II).cntdot.Bithiazole Complex

  摘要：

  A bithiazole derivative structurally related to the bithiazole moiety of bleomycin (BLM) A(2) was prepared. This derivative contained a 2-(1,3-diaminopropyl) substituent, rather than the 2-(2-aminoethyl) substituent normally present in BLM, in order to facilitate metal coordination by the bithiazole moiety itself. In the presence of Co2+, th, modified bithiazole mediated the production of alkali labile lesions on double-stranded DNA. Following treatment with alkali, guanosine-specific DNA strand scission was observed. DNA degradation by this Co(II). bithiazole complex was not light dependent but did require molecular oxygen. DNA cleavage studies employing scavengers of activated oxygen species suggested that the observed DNA damage did not result from diffusible, activated forms of oxygen. Moreover, ESR spectroscopy utilizing a spin trapping reagent demonstrated conclusively that the Co(II). bithiazole complex did not produce diffusible oxygen radicals. Absorption spectroscopy with a thiazole analog of the modified bithiazole suggested that, in the presence of oxygen, a O-2 . Co . thiazole complex was formed. These mechanistic studies suggested that the (oxygenated) Co(II). bithiazole complex mediated the oxidative alteration or liberation of the guanine base, producing an alkali labile site. Further, the guanosine specificity appeared to derive from preferential reactivity at guanosine sites, as opposed to a guanosine binding selectivity of the bithiazole. The oxidative degradation of G residues in DNA appears to proceed by an inner sphere mechanism.

  DOI：

  10.1021/ja00141a001

文献信息

• [EN] CEPHEM COMPOUNDS<br/>[FR] CEPHEMES
  申请人：FUJISAWA PHARMACEUTICAL CO

  公开号：WO2005027909A1

  公开（公告）日：2005-03-31

  The present invention relates to a compound of the formula [I]: wherein R1 is lower alkyl or hydroxy (lower) alkyl, and R2 is hydrogen or amino protecting group, or R1 and R2 are bonded together and form lower alkylene ; R3 is -A-R6 wherein A is bond, -NHCO-(CH2CO)n-, lower alkylene, -NH-CO-CO- or the like, and R6 is (a) ou (b) wherein R7, R8, R9 and R10 are independently amino, guanidino, amidino or the like ; R4 is carboxy or protected carboxy; and R5 is amino or protected amino, or a pharmaceutically acceptable salt thereof, a process for preparing a compound of the formula [I], and a pharmaceutical composition comprising a compound of the formula [I] in admixture with a pharmaceutically acceptable carrier.

  本发明涉及一种公式的化合物[I]：其中R1是低级烷基或羟基（低级）烷基，R2是氢或氨基保护基团，或者R1和R2连接并形成低级亚烷基；R3是-A-R6，其中A是键，-NHCO-(CH2CO)n-，低级亚烷基，-NH-CO-CO-或类似物质，R6是(a)或(b)其中R7，R8，R9和R10是独立的氨基，胍基，脒基或类似物质；R4是羧基或受保护的羧基；R5是氨基或受保护的氨基，或药用可接受的盐，一种制备公式化合物[I]的方法，以及一种包括与药用可接受载体混合的公式化合物[I]的药物组合物。
• Cephem compounds
  申请人：Yamanaka Toshio

  公开号：US20050096306A1

  公开（公告）日：2005-05-05

  The present invention relates to a compound of the formula [I]: wherein R 1 is lower alkyl or hydroxy(lower)alkyl, and R 2 is hydrogen or amino protecting group, or R 1 and R 2 are bonded together and form lower alkylene; R is -A-R 6 wherein A is bond, —NHCO—(CH 2 CO) n —, lower alkylene, —NH—CO—CO— or the like, and R 6 is wherein R 7 , R 8 , R 9 and R 10 are independently amino, guanidino, amidino or the like; R 4 is carboxy or protected carboxy; and R 5 is amino or protected amino, or a pharmaceutically acceptable salt thereof, a process for preparing a compound of the formula [I], and a pharmaceutical composition comprising a compound of the formula [I] in admixture with a pharmaceutically acceptable carrier.

  本发明涉及一种式[I]的化合物：其中R1是较低的烷基或羟基（较低）烷基，而R2是氢或氨基保护基，或者R1和R2结合在一起形成较低的烷基；R是-A-R6，其中A是键，—NHCO—（CH2CO）n—，较低的烷基，—NH—CO—CO—或类似物，而R6是其中R7，R8，R9和R10独立地是氨基，鸟氨酸基，酰胺基或类似物；R4是羧基或保护羧基；而R5是氨基或保护氨基，或其药学上可接受的盐，以及制备式[I]的化合物的方法，以及包含式[I]的化合物与药学上可接受的载体混合的药物组合物。
• An efficient synthesis of some 6-substituted 4,8-diaza-3,3,9,9- tetramethylundeca-2,10-dione dioximes (propylene amine oximes, PnAOs): Ligands for 99mTc complexes used in structure distribution relationship (SDR) studies
  作者：Palaniappa Nanjappan、Natarajan Raju、Kondareddiar Ramalingam、David P. Nowotnik

  DOI：10.1016/s0040-4020(01)85336-9

  日期：1994.1

  Technetium complexes of the ligand PnAO [4,8-diaza-3,3,9,9-fetramethylundeca-2,10-dione dioximes (3)] are of interest as commercial radiopharmaceuticals. In general, PnAOs are synthesized by alkylation of a propylenediamine derivative with 3-chloro-3-methyl-2-nitrosobutane (2). This alkylation reaction proved to be low yielding. With modestly bulky substituents at the 2-position of 1,3-diaminopropane, little or none of the required PnAO was obtained. As a result, an alternative approach of the synthesis of PnAO was developed. This method involved the alkylation of the propylenediamine with 3-bromo-3-methylbutan-2-one (18) followed by oximation of the resulting diamine-diketone (19). By this method, PnAOs were prepared in goad yield, even with bulky C-2 substituents. Fourteen PnAO derivatives were prepared by this method. We also describe the syntheses of several new propylenediamine derivatives.
• Guanosine-Specific DNA Damage by a Co(II).cntdot.Bithiazole Complex
  作者：Stefanie A. Kane、Hideaki Sasaki、Sidney M. Hecht

  DOI：10.1021/ja00141a001

  日期：1995.9

  A bithiazole derivative structurally related to the bithiazole moiety of bleomycin (BLM) A(2) was prepared. This derivative contained a 2-(1,3-diaminopropyl) substituent, rather than the 2-(2-aminoethyl) substituent normally present in BLM, in order to facilitate metal coordination by the bithiazole moiety itself. In the presence of Co2+, th, modified bithiazole mediated the production of alkali labile lesions on double-stranded DNA. Following treatment with alkali, guanosine-specific DNA strand scission was observed. DNA degradation by this Co(II). bithiazole complex was not light dependent but did require molecular oxygen. DNA cleavage studies employing scavengers of activated oxygen species suggested that the observed DNA damage did not result from diffusible, activated forms of oxygen. Moreover, ESR spectroscopy utilizing a spin trapping reagent demonstrated conclusively that the Co(II). bithiazole complex did not produce diffusible oxygen radicals. Absorption spectroscopy with a thiazole analog of the modified bithiazole suggested that, in the presence of oxygen, a O-2 . Co . thiazole complex was formed. These mechanistic studies suggested that the (oxygenated) Co(II). bithiazole complex mediated the oxidative alteration or liberation of the guanine base, producing an alkali labile site. Further, the guanosine specificity appeared to derive from preferential reactivity at guanosine sites, as opposed to a guanosine binding selectivity of the bithiazole. The oxidative degradation of G residues in DNA appears to proceed by an inner sphere mechanism.