β-benzamidothiopropionamide | 30761-30-9

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: β-benzamidothiopropionamide
• 英文别名: 3-(benzamido)thiopropionamide；3-benzamidothiopropionamide；N-benzoyl-thio-β-alanine amide；N-benzoyl-β-thioalanine amide；N-Benzoyl-β-thioalanin-amid；N-(3-amino-3-sulfanylidenepropyl)benzamide
• CAS: 30761-30-9
• 化学式: C₁₀H₁₂N₂OS
• 分子量: 208.284
• InChiKey: AXDMONXTMCNHMI-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.4
• 重原子数：
  14
• 可旋转键数：
  4
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.2
• 拓扑面积：
  87.2
• 氢给体数：
  2
• 氢受体数：
  2

安全信息

• 海关编码：
  2930909090

反应信息

• 作为反应物：
  描述：

  β-benzamidothiopropionamide 在 氨 作用下， 以 甲醇 为溶剂， 生成 2-(2-Benzamidoaethyl)-thiazol-4-carbonamid
  参考文献：
  名称：

  Zee-Cheng,K.Y.; Cheng,C.C., Journal of Heterocyclic Chemistry, 1970, vol. 7, p. 1439 - 1440

  摘要：

  DOI：
• 作为产物：
  描述：

  N-(2-氰乙基)苯甲酰胺 在 15-冠醚-5 、 sodium hydrosulfide hydrate 、 magnesium chloride 作用下， 以 N,N-二甲基甲酰胺 为溶剂， 以63%的产率得到β-benzamidothiopropionamide
  参考文献：
  名称：

  噻唑-2-乙胺的新型酰胺和脲衍生物的合成及其对布氏锥虫的活性

  摘要：

  2-（2-Benzamido）ethyl-4-phenylthiazole（1）是1035个分子（分为115个不同的支架）之一，被发现可抑制布氏锥虫（引起人类非洲锥虫病的病原体），浓度低于3.6μM，且非在由诺华研究基金会（GNF）的基因组学研究所进行的700,000种化合物库的表型高通量筛选中，对哺乳动物（Huh7）细胞具有毒性。在本实验室中，化合物1和72类似物是通过两种通用途径之一合成的。这些加10代市售的类似物进行了对所测试的T.布氏罗得西亚STIB900和体外大鼠L6成肌细胞（细胞毒性）。四十四个导数的强于一，其中八个IC 50值低于100 nM。对该寄生虫最有效和最具选择性的是尿素类似物2-（2-哌啶-1--1-基氨基）乙基-4-（3-氟苯基）噻唑（70，IC 50  = 9 nM，SI> 18,000）。测试的33种化合物中没有一种能够治愈被寄生虫感染的小鼠。但是，有7种化合

  DOI：

  10.1016/j.bmc.2016.04.006

文献信息

• 255. Synthesis of the 2-ω-aminoalkyl and 2-ω-sulphanilamidoalkyl derivatives of thiazole and pyrimidine
  作者：Alan A. Goldberg、William Kelly

  DOI：10.1039/jr9470001372

  日期：——
• Synthesis of tri- and tetrapeptide S: the extended C-terminus of bleomycin A2
  作者：Dale L. Boger、Royce F. Menezes

  DOI：10.1021/jo00042a003

  日期：1992.7

  Concise diastereocontrolled syntheses of tri- and tetrapeptide S, key subunits
• Total Synthesis of Bleomycin A2 and Related Agents. 1. Synthesis and DNA Binding Properties of the Extended C-Terminus: Tripeptide S, Tetrapeptide S, Pentapeptide S, and Related Agents
  作者：Dale L. Boger、Steven L. Colletti、Takeshi Honda、Royce F. Menezes

  DOI：10.1021/ja00092a011

  日期：1994.6

  Full details of concise, diastereocontrolled syntheses of 2-5 and their incorporation into tri-, tetra-, and pentapeptide S, the C-terminus of bleomycin Alt are described. The extension of the studies to the synthesis of a complete set of tri- and tetrapeptide S structural analogs 29a,b and 43b-j is detailed, and their DNA binding constants (apparent K-B, calf thymus DNA) and apparent binding site sizes were determined. Consistent with past observations, the studies highlight the fact that the majority of the DNA binding affinity for bleomycin A(2) (1.0 X 10(5) M(-1)) and deglycobleomycin Aa (1.1 x 10(5) M(-1)) is embodied within N-BOC-tripeptide S (0.26 X 10(5) M(-1)). The additional comparisons of 29a (O.18 x 10(5) M(-1)), N-BOC-tetrapeptide S (0.21 x 10(5) M(-1)), 43h (0.20 x 10(5) M(-1)), and N-BOC-pentapeptide S (0.23 X 10(5) M(-1)) versus N-BOC-dipeptide S (0.10 x 10(5) M(-1)) indicate productive stabilizing binding interactions for the tripeptide S L-threonine subunit and substituent, illustrate that the entire pentanoic acid subunit of tetrapeptide S and its substituents do not significantly contribute to DNA binding affinity, and indicate that the entire beta-hydroxy-L-histidine subunit of pentapeptide S does not contribute to DNA binding affinity. With the exception of the L-threonine side chain substituent, the observations suggest that the tri- and tetrapeptide S substituent effects on the bleomycin A(2) DNA cleavage reaction are not due to substantial stabilizing binding interactions with duplex DNA. In addition, the measured apparent binding site sizes for bleomycin A(2)(3.8 base pairs), deglycobleomycin A(2) (3.9 base pairs), N-BOC-tripeptide S (3.6 base pairs), N-BOC-tetrapeptide S (3.7 base pairs), 43h (3.5 base pairs), and N-BOC-pentapeptide S (4.2 base pairs) versus N-BOC-dipeptide S (2.2 base pairs) and 29a (2.7 base pairs) suggest that it is the tripeptide S subunit of bleomycin A(2) that is fully bound to duplex DNA, that the tripeptide S L-threonine hydroxyethyl substituent detectably affects the agent interaction with duplex DNA, but that the presence or absence of the other tetrapeptide S and pentapeptide S backbone substituents do not substantially alter the binding site size or tripeptide S binding mode.
• An approach to the design of brain-penetrating histaminergic agonists
  作者：RC Young、CR Ganellin、R Griffiths、RC Mitchell、ME Parsons、D Saunders、NE Sore

  DOI：10.1016/0223-5234(93)90135-2

  日期：1993.1

  Known and novel histaminergic H-1- and H-2-receptor agonists were investigated as potentially potent and selective brain-penetrating compounds. Structural modifications were introduced in an attempt to favour passive diffusion across the blood-brain barrier by reducing hydrogen-bonding ability according to a previously developed model. While no novel compound was identified which satisfied our requirements for a brain-penetrating agonist, betahistine 14 and 2-(thiazol-2-yl)ethylamine 16 can be regarded as H-1-receptor agonists with moderate brain-penetrating ability, of potential value as pharmacological tools. A novel histamine analogue, N,N-bis-2-[4(5)-imidazolyl]ethyl)amine 25 is reported which. although unlikely to be brain penetrant, was found to be equipotent with histamine at H-1- and H-1-receptors.
• Synthesis and DNA binding of [3-[2'-(2-acetamidoethyl)-2,4'-bithiazole-4-carboxamido]propyl]dimethylsulfonium chloride, a fragment of bleomycin A2
  作者：Ted T. Sakai、James M. Riordan、Thomas E. Booth、Jerry D. Glickson

  DOI：10.1021/jm00135a008

  日期：1981.3

  [3-[2'-(2-Acetamidoethyl)-2,4'-bithiazole-4-carboxamido]propyl]dimethylsulfonium chloride (1), the acetyl derivative of the cationic terminal dipeptide of bleomycin A2, has been synthesized and its binding to DNA and poly(dA-dT) has been studied by proton NMR and fluorescence spectroscopy. The spectral perturbations which occur upon binding of the compound to either nucleic acid indicate that that portion of bleomycin which binds to the nucleic acid can, for the most part, be mimicked by the fragment. The data are discussed in terms of the structure of the drug and the drug-nucleic acid complex.