3-Methyl-5-(p-aminophenyl)-isoxazol | 64656-94-6

• 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: 3-Methyl-5-(p-aminophenyl)-isoxazol
• 英文别名: 4-(3-methyl-isoxazol-5-yl)-aniline；4-(3-Methyl-isoxazol-5-yl)-anilin；3-Methyl-5-(4-aminophenyl)isoxazole；4-(3-methyl-1,2-oxazol-5-yl)aniline
• CAS: 64656-94-6
• 化学式: C₁₀H₁₀N₂O
• 分子量: 174.202
• InChiKey: CFOHIFUPLRXIGT-UHFFFAOYSA-N

物化性质

• 熔点：
  151-152 °C
• 沸点：
  333.1±27.0 °C(Predicted)
• 密度：
  1.166±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  1.7
• 重原子数：
  13
• 可旋转键数：
  1
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.1
• 拓扑面积：
  52
• 氢给体数：
  1
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  Lactose 、 3-Methyl-5-(p-aminophenyl)-isoxazol 以 乙醇 为溶剂， 生成 O4-β-D-galactopyranosyl-N-[4-(3-methyl-isoxazol-5-yl)-phenyl]-β-D-glucopyranosylamine
  参考文献：
  名称：

  Sykulski,J.; Rokita,T., Roczniki Chemii, 1977, vol. 51, p. 345 - 349

  摘要：

  DOI：
• 作为产物：
  描述：

  1-[4-(N-acetylamino)phenyl]-1,3-butanedione 在 盐酸 、 盐酸羟胺 作用下， 生成 3-Methyl-5-(p-aminophenyl)-isoxazol
  参考文献：
  名称：

  Sykulski,J.; Rokita,T., Roczniki Chemii, 1977, vol. 51, p. 345 - 349

  摘要：

  DOI：

文献信息

• Pyrrolinone derivatives as a new class of P2X3 receptor antagonists. Part 3: Structure-activity relationships of pyrropyrazolone derivatives
  作者：Hiroyuki Tobinaga、Takayuki Kameyama、Kentarou Asahi、Tohru Horiguchi、Miho Oohara、Yoshiyuki Taoda、Kayoko Hata、Tsuyoshi Hasegawa、Yukio Tada、Naoko Kurihara、Yasuhiko Kanda、Shigenori Yagi、Maki Tomari、Yoshikazu Tanaka、Fumiyo Takahashi、Emiko Taniguchi、Yukio Takahara、Shinji Shimada、Chie Takeyama、Shoichi Yamamoto、Shunji Shinohara、Hiroyuki Kai

  DOI：10.1016/j.bmcl.2020.127636

  日期：2020.12

  The P2X3 receptor is an attractive target for the treatment of pain and chronic coughing, and thus P2X3 antagonists have been developed as new therapeutic drugs. We previously reported selective P2X3 receptor antagonists by derivatization of hit compound 1. As a result, we identified hit compound 3, the structure of which was similar to hit compound 1. On the basis of SAR studies of hit compound 1

  P2X3受体是治疗疼痛和慢性咳嗽的有吸引力的靶标，因此，P2X3拮抗剂已被开发为新的治疗药物。我们先前报道了命中化合物1衍生化的选择性P2X3受体拮抗剂。结果，我们确定了命中化合物3，其结构类似于命中化合物1。在对命中化合物1进行SAR研究的基础上，我们对命中化合物3进行了修饰，化合物42通过口服给药被确认具有镇痛作用。
• Repair of sulfur mustard-induced DNA damage in mammalian cells measured by a host cell reactivation assay
  作者：Z. Matijasevic、M.L. Precopio、J.E. Snyder、D.B. Ludlum

  DOI：10.1093/carcin/22.4.661

  日期：2001.4

  DNA damage is thought to be the initial event that causes sulfur mustard (SM) toxicity, while the ability of cells to repair this damage is thought to provide a degree of natural protection. To investigate the repair process, we have damaged plasmids containing the firefly luciferase gene with either SM or its monofunctional analog, 2-chloroethyl ethyl sulfide (CEES). Damaged plasmids were transfected into wild-type and nucleotide excision repair (NER) deficient Chinese hamster ovary cells; these cells were also transfected with a second reporter plasmid containing Renilla luciferase as an internal control on the efficiency of transfection. Transfected cells were incubated at 37°C for 27 h and then both firefly and Renilla luciferase intensities were measured on the same samples with the dual luciferase reporter assay. Bioluminescence in lysates from cells transfected with damaged plasmid, expressed as a percentage of the bioluminescence from cells transfected with undamaged plasmid, is increased by host cell repair activity. The results show that NER-competent cells have a higher reactivation capacity than NER-deficient cells for plasmids damaged by either SM or CEES. Significantly, NER-competent cells are also more resistant to the toxic effects of SM and CEES, indicating that NER is not only proficient in repairing DNA damage caused by either agent but also in decreasing their toxicity. This host cell repair assay can now be used to determine what other cellular mechanisms protect cells from mustard toxicity and under what conditions these mechanisms are most effective.

  DNA损伤被认为是引起硫芥(SM)毒性的起始事件，而细胞修复这种损伤的能力则被认为提供了一定程度的自然保护。为了研究修复过程，我们使用SM或其单功能类似物2-氯乙基乙基硫化物(CEES)对含有萤火虫荧光素酶基因的质粒进行了损伤。损伤后的质粒被转染到野生型和核苷酸切除修复(NER)缺陷的中国仓鼠卵巢细胞中；这些细胞还转染了第二个报告质粒，其中包含海肾荧光素酶作为转染效率的内部对照。转染后的细胞在37°C下孵育27小时，然后用双荧光素酶报告分析法在同一样本上测量萤火虫和海肾荧光素酶的强度。细胞裂解液中转染了损伤质粒的生物发光，以转染了未损伤质粒的细胞的生物发光的百分比表示，随宿主细胞修复活性而增加。结果显示，对于被SM或CEES损伤的质粒，具有NER能力的细胞比NER缺陷的细胞具有更高的再激活容量。值得注意的是，具有NER能力的细胞对SM和CEES的毒性影响也更具抵抗力，表明NER不仅擅长修复这两种试剂引起的DNA损伤，还能降低它们的毒性。现在，这种宿主细胞修复分析可以用来确定其他哪些细胞机制保护细胞免受芥子气毒性影响及其在这些机制最有效时的条件。
• Sykulski,J.; Rokita,T., Roczniki Chemii, 1977, vol. 51, p. 345 - 349
  作者：Sykulski,J.、Rokita,T.

  DOI：——

  日期：——