2-chloro-9-isopropyl-N-(3-(trifluoromethyl)benzyl)-9H-purin-6-amine | 1240046-58-5

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 咪唑并嘧啶类
• 英文名称: 2-chloro-9-isopropyl-N-(3-(trifluoromethyl)benzyl)-9H-purin-6-amine
• 英文别名: 2-chloro-9-propan-2-yl-N-[[3-(trifluoromethyl)phenyl]methyl]purin-6-amine
• CAS: 1240046-58-5
• 化学式: C₁₆H₁₅ClF₃N₅
• 分子量: 369.777
• InChiKey: ATGRMMWUOLAENA-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.4
• 重原子数：
  25
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.31
• 拓扑面积：
  55.6
• 氢给体数：
  1
• 氢受体数：
  7

反应信息

• 作为反应物：
  描述：

  2-氨基丁醇 、 2-chloro-9-isopropyl-N-(3-(trifluoromethyl)benzyl)-9H-purin-6-amine 反应 8.0h， 以74%的产率得到(R)-2-(9-isopropyl-6-(3-(trifluoromethyl)benzylamino)-9H-purin-2-ylamino)butan-1-ol
  参考文献：
  名称：

  作为Trk激酶抑制剂的嘌呤类化合物

  摘要：

  本发明公开了作为Trk激酶抑制剂的嘌呤类化合物，属于化学医药领域。本发明嘌呤类化合物如通式(I)所示，具有良好Trk家族蛋白酪氨酸激酶抑制活性，可用于治疗哺乳动物的癌症、疼痛、炎症、神经变性疾病、克氏锥虫感染或溶骨性疾病，应用前景广阔。

  公开号：

  CN110256436B
• 作为产物：
  描述：

  2,6-二氯嘌呤 在 potassium carbonate 、 三乙胺 作用下， 以 二甲基亚砜 、 正丁醇 为溶剂， 反应 0.5h， 生成 2-chloro-9-isopropyl-N-(3-(trifluoromethyl)benzyl)-9H-purin-6-amine
  参考文献：
  名称：

  [EN] CALCIUM CHANNEL AGONISTS
  [FR] AGONISTES DE CANAUX CALCIQUES

  摘要：

  披露了钙通道激动剂的实施方式，以及制备和使用钙通道激动剂的方法。披露的钙通道激动剂及其相应的盐形式具有如下通用式I所示的结构，其中每个表示为“ ”的键是为了满足化合价要求而需要的单键或双键；Z1、Z2、Z3、Z4和Z5独立地是氮或碳；R1和R3是烷基；R2是烷基、芳基、杂环芳基、芳基烷基或杂环芳基烷基；而R4是烷基或羟基烷基。

  公开号：

  WO2014189830A1

文献信息

• In Vitro Cytotoxic‐Active Platinum(II) Complexes Derived from Carboplatin and Involving Purine Derivatives
  作者：Lukáš Dvořák、Igor Popa、Pavel Štarha、Zdeněk Trávníček

  DOI：10.1002/ejic.201000322

  日期：2010.8

  C, 15 N and 195 Pt) spectroscopy. Based on the results of these techniques, it can be concluded that the central Pt II atom of the complexes 1-6 is coordinated to two oxygen atoms originating from the cyclobutane-1,1-dicarboxylate group and to two nitrogen atoms from two HL n molecules, that is, having a PtN 2 O 2 donor set. Detailed multinuclear and two-dimensional NMR studies indicated the N-7 atom

  六种铂 (II) 配合物的通式为 [Pt(cbdc)-(HL n ) 2 ] (1-6; cbdc = 环丁烷-1,1-二羧酸酯和 HL 1 -HL 6 = 苄基取代的 6-苄氨基-已经通过 [Pt(cbdc)(dmso) 2 ] 与相应的 HL n 化合物反应合成了 2-氯-9-异丙基嘌呤衍生物。制备的配合物通过元素分析和 FTIR、拉曼和 NMR（ 1 H、 13 C、 15 N 和 195 Pt）光谱表征。基于这些技术的结果，可以得出结论，配合物 1-6 的中心 Pt II 原子与来自 1,1-二羧酸环丁烷基团的两个氧原子和来自两个 HL n 的两个氮原子配位分子，即具有 PtN 2 O 2 供体组。详细的多核和二维 NMR 研究表明 N-7 原子是嘌呤衍生物的配位位点。[Pt(cbdc)(dmso)-(HL 7 )]·H 2 O (7a·H 2 O) 中间体 [HL 7 = 2-氯-
• CALCIUM CHANNEL AGONISTS
  申请人：WIPF Peter

  公开号：US20160090387A1

  公开（公告）日：2016-03-31

  Embodiments of calcium channel agonists, as well as methods of making and using the calcium channel agonists, are disclosed. The disclosed calcium channel agonists and corresponding salt forms have a structure according to general formula I: wherein each bond depicted as “ ” is a single bond or a double bond as needed to satisfy valence requirements; Z 1 , Z 2 , Z 3 , Z 4 , and Z 5 independently are nitrogen or carbon; R 1 and R 3 are alkyl; R 2 is alkyl, aryl, heteroaryl, arylalkyl, or heteroarylalkyl; and R 4 is alkyl or hydroxyalkyl.

  本发明揭示了钙通道激动剂的实施方式，以及制备和使用钙通道激动剂的方法。所述的钙通道激动剂和相应的盐形式具有通式I的结构：其中，每个表示为“”的键是单键或双键，以满足价键要求；Z1、Z2、Z3、Z4和Z5独立地为氮或碳；R1和R3为烷基；R2为烷基、芳基、杂芳基、芳基烷基或杂芳基烷基；R4为烷基或羟基烷基。
• Calcium channel agonists
  申请人：University of Pittsburgh—Of the Commonwealth System of Higher Education

  公开号：US10174031B2

  公开（公告）日：2019-01-08

  Embodiments of calcium channel agonists, as well as methods of making and using the calcium channel agonists, are disclosed. The disclosed calcium channel agonists and corresponding salt forms have a structure according to general formula I: wherein each bond depicted as “” is a single bond or a double bond as needed to satisfy valence requirements; Z1, Z2, Z3, Z4, and Z5 independently are nitrogen or carbon; R1 and R3 are alkyl; R2 is alkyl, aryl, heteroaryl, arylalkyl, or heteroarylalkyl; and R4 is alkyl or hydroxyalkyl.

  本发明公开了钙通道激动剂的实施方案以及钙通道激动剂的制造和使用方法。所公开的钙通道激动剂和相应的盐形式具有通式 I 的结构： 其中描述为""的每个键是单键或双键，以满足化合价要求；Z1、Z2、Z3、Z4 和 Z5 独立地为氮或碳；R1 和 R3 为烷基；R2 为烷基、芳基、杂芳基、芳烷基或杂芳基烷基；R4 为烷基或羟烷基。
• Synthesis and Biological Evaluation of a Selective N- and P/Q-Type Calcium Channel Agonist
  作者：Mary Liang、Tyler B. Tarr、Karla Bravo-Altamirano、Guillermo Valdomir、Gabriel Rensch、Lauren Swanson、Nicholas R. DeStefino、Cara M. Mazzarisi、Rachel A. Olszewski、Gabriela Mustata Wilson、Stephen D. Meriney、Peter Wipf

  DOI：10.1021/ml3002083

  日期：2012.12.13

  The acute effect of the potent cyclin-dependent kinase (cdk) inhibitor (R)-roscovitine on Ca2+ channels inspired the development of structural analogues as a potential treatment for motor nerve terminal dysfunction. On the basis of a versatile chlorinated purine scaffold, we have synthesized ca. 20 derivatives and characterized their N-type Ca2+ channel agonist action. Agents that showed strong agonist effects were also characterized in a kinase panel for their off-target effects. Among several novel compounds with diminished cdk activity, we identified a new lead structure with a 4-fold improved N-type Ca2+ channel agonist effect and a 22-fold decreased cdk2 activity as compared to (R)-roscovitine. This compound was selective for agonist activity on N- and P/Q-type over L-type calcium channels.
• Chemical Control of Mammalian Circadian Behavior through Dual Inhibition of Casein Kinase Iα and δ
  作者：Jae Wook Lee、Tsuyoshi Hirota、Daisuke Ono、Sato Honma、Ken-ichi Honma、Keunwan Park、Steve A. Kay

  DOI：10.1021/acs.jmedchem.8b01541

  日期：2019.2.28

  Circadian rhythms are controlled by transcriptional feedback loops of clock genes and proteins. The stability of clock proteins is regulated by post-translational modification, such as phosphorylation by kinases. In particular, casein kinase I (CKI) phosphorylates the PER protein to regulate proteasomal degradation and nuclear localization. Therefore, CKI inhibition can modulate mammalian circadian rhythms. In the present study, we have developed novel CKI alpha and CKI delta dual inhibitors by extensive structural modification of N9 and C2 position of longdaysin. We identified NCC007 that showed stronger period effects (0.32 mu M for 5 h period lengthening) in a cell-based circadian assay. The following in vitro kinase assay showed that NCC007 inhibited CKI alpha and CKI delta with an IC50 of 1.8 and 3.6 mu M. We further demonstrated that NCC007 lengthened the period of mouse behavioral rhythms in vivo. Thus, NCC007 is a valuable tool compound to control circadian rhythms through CKI inhibition.