N⁴-butyl-5-ethyl-6-methylpyrimidine-2,4-diamine

• 分子结构分类: 有机化合物 - 有机氮化合物
• 英文名称: N⁴-butyl-5-ethyl-6-methylpyrimidine-2,4-diamine
• 英文别名: 4-N-butyl-5-ethyl-6-methylpyrimidine-2,4-diamine
• 化学式: C₁₁H₂₀N₄
• 分子量: 208.307
• InChiKey: YPMSRSWJBFPGSV-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.6
• 重原子数：
  15
• 可旋转键数：
  5
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.64
• 拓扑面积：
  63.8
• 氢给体数：
  2
• 氢受体数：
  4

反应信息

• 作为产物：
  描述：

  2-氨基-5-乙基-6-甲基嘧啶-4-醇 在 三乙胺 、 三氯氧磷 作用下， 以 甲醇 为溶剂， 反应 15.0h， 生成 N⁴-butyl-5-ethyl-6-methylpyrimidine-2,4-diamine
  参考文献：
  名称：

  PYRIMIDINES AND USES THEREOF

  摘要：

  本文提供的各种示例是针对下述公式的化合物的：其中R1-R5在此处被定义，并且这些化合物的用途包括在其他方面抑制受试者的免疫反应。

  公开号：

  US20180215720A1

文献信息

• Pyrimidines and uses thereof
  申请人：Regents of the University of Minnesota

  公开号：US10662161B2

  公开（公告）日：2020-05-26

  The various examples presented herein are directed to compounds of the Formula: wherein R1-R5 are defined herein, and uses of such compounds to, among other things, inhibit an immune response in a subject.

  本文介绍的各种示例均针对式化合物： 其中 R1-R5 在本文中定义，以及此类化合物在抑制受试者免疫反应等方面的用途。
• Identification of High-Potency Human TLR8 and Dual TLR7/TLR8 Agonists in Pyrimidine-2,4-diamines
  作者：Mallesh Beesu、Alex C. D. Salyer、Michael J. H. Brush、Kathryn L. Trautman、Justin K. Hill、Sunil A. David

  DOI：10.1021/acs.jmedchem.6b01860

  日期：2017.3.9

  The induction of toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid dendritic cells as well as the production of TLR8-dependent type II interferon (IFN-y), TNF-alpha, and IL-12 in myeloid dendritic cells are of importance in generating T helper-1 biased adaptive immune responses. In an effort to identify novel dual TLR7/TLR8-active compounds, we undertook structure activity relationship studies in pyrimidine 2,4-diamines, focusing on substituents at CS. Several analogues substituted with aminopropyl appendages at CS displayed dominant TLR8-agonistic activity. N4-Butyl-6-methyl-S-(3morpholinopropyl)pyrimidine-2,4-diamine was found to be a very potent dual TLR7/TLR8 agonist. Employing novel cytokine reporter cell assays, we verified that potency at TLR7 correlates with IFN-alpha/beta production in human blood, whereas IFN-y and TNF-a induction is largely TLR8dependent. Dual TLR7/TLR8 agonists markedly upregulate CD80 expression in multiple dendritic cell subsets, providing insight into the immunological basis for the superior adjuvantic properties of such innate immune stimuli.