vertex-AT | 1611444-06-4

• 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: vertex-AT
• 英文别名: N-(4-chlorophenyl)-1H-1,2,3-triazol-5-amine；N-(4-chlorophenyl)-2H-triazol-4-amine
• CAS: 1611444-06-4
• 化学式: C₈H₇ClN₄
• 分子量: 194.623
• InChiKey: IUTZKZLVPUPHDA-UHFFFAOYSA-N

物化性质

• 沸点：
  409.4±25.0 °C(Predicted)
• 密度：
  1.472±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.1
• 重原子数：
  13
• 可旋转键数：
  2
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  53.6
• 氢给体数：
  2
• 氢受体数：
  3

反应信息

• 作为产物：
  描述：

  2-[2-(4-chlorophenyl)iminohydrazino]acetonitrile 以 乙醇 为溶剂， 以5.6 g的产率得到vertex-AT
  参考文献：
  名称：

  吲哚胺 2,3-双加氧酶的新型 4-氨基-1,2,3-三唑抑制剂与酶形成长寿复合物并显示出精致的细胞效力

  摘要：

  袖珍型：吲哚胺 2,3-双加氧酶 1 (IDO1) 是一种被癌症用来逃避免疫系统反应的免疫抑制酶，因此是药物发现的一个令人兴奋的目标。动力学、生化和结构研究揭示了一系列 IDO1 抑制剂在细胞中发挥效力的惊人机制。

  DOI：

  10.1002/cbic.201700560

文献信息

• COMPOUNDS USEFUL AS INHIBITORS OF INDOLEAMINE 2,3-DIOXYGENASE
  申请人：VERTEX PHARMACEUTICALS INCORPORATED

  公开号：US20140179699A1

  公开（公告）日：2014-06-26

  The present invention relates to compounds useful as inhibitors of indoleamine 2,3-dioxygenase (IDO). The invention also relates to pharmaceutically acceptable compositions comprising the compounds of this invention; methods of treating of various diseases, disorders, and conditions using the compounds of this invention; processes for preparing the compounds of this invention; intermediates for the preparation of the compounds of this invention; and methods of using the compounds in in vitro applications. The compounds of this invention have formula I-A: wherein the variables are as defined herein.

  本发明涉及用作吲哚胺2,3-二氧化酶(IDO)抑制剂的化合物。本发明还涉及包含本发明化合物的药学上可接受的组合物；使用本发明化合物治疗各种疾病、疾病和病况的方法；制备本发明化合物的过程；用于制备本发明化合物的中间体；以及在体外应用中使用化合物的方法。本发明化合物具有式I-A：其中变量如本文所定义。
• Treatment of aneurysms
  申请人：Georgia State University Research Foundation, Inc.

  公开号：US11376248B2

  公开（公告）日：2022-07-05

  The present invention provides methods for detecting and/or treating a subject having an aneurysm or at risk for developing an aneurysm. It has been discovered that a key metabolite of the kynurenine (Kyn) pathway, a major route for the metabolism of essential amino acid tryptophan (Trp) into nicotinamide adenine dinucleotide (NAD+), plays a critical role in the formation of aneurysms, for example abdominal aortic aneurysms. In particular, it has been discovered that 3-Hydroxyanthranilic acid (3-HAA), a product of kynureninase (KYNU), plays a causative role in the formation of aneurysms by, for example exerting pro-inflammatory effects on vascular smooth muscle cells. It has further been discovered that elevated levels of 3-HAA are indicative of the presence and/or progression of an aneurysm, and 3-HAA levels correlate with the size (aortic diameter) of the aneurysm.

  本发明提供了检测和/或治疗患有动脉瘤或有罹患动脉瘤风险的受试者的方法。现已发现，犬尿氨酸（Kyn）途径的一种关键代谢物--将必需氨基酸色氨酸（Trp）代谢为烟酰胺腺嘌呤二核苷酸（NAD+）的主要途径--在动脉瘤（例如腹主动脉瘤）的形成中起着关键作用。特别是，研究发现，3-羟基氨基苯甲酸（3-HAA）是犬尿苷酶（KYNU）的产物，通过对血管平滑肌细胞产生促炎作用等方式，在动脉瘤的形成过程中起着致病作用。研究进一步发现，3-HAA 水平的升高表明动脉瘤的存在和/或发展，3-HAA 水平与动脉瘤的大小（主动脉直径）相关。
• TREATMENT OF ANEURYSMS
  申请人：Georgia State University Research Foundation, Inc.

  公开号：US20200138810A1

  公开（公告）日：2020-05-07

  The present invention provides methods for detecting and/or treating a subject having an aneurysm or at risk for developing an aneurysm. It has been discovered that a key metabolite of the kynurenine (Kyn) pathway, a major route for the metabolism of essential amino acid tryptophan (Trp) into nicotinamide adenine dinucleotide (NAD+), plays a critical role in the formation of aneurysms, for example abdominal aortic aneurysms. In particular, it has been discovered that 3-Hydroxyanthranilic acid (3-HAA), a product of kynureninase (KYNU), plays a causative role in the formation of aneurysms by, for example exerting pro-inflammatory effects on vascular smooth muscle cells. It has further been discovered that elevated levels of 3-HAA are indicative of the presence and/or progression of an aneurysm, and 3-HAA levels correlate with the size (aortic diameter) of the aneurysm.
• US9073875B2
  申请人：——

  公开号：US9073875B2

  公开（公告）日：2015-07-07
• US9499497B2
  申请人：——

  公开号：US9499497B2

  公开（公告）日：2016-11-22