1. Academic Validation
  2. Optimization of cellular activity of G9a inhibitors 7-aminoalkoxy-quinazolines

Optimization of cellular activity of G9a inhibitors 7-aminoalkoxy-quinazolines

  • J Med Chem. 2011 Sep 8;54(17):6139-50. doi: 10.1021/jm200903z.
Feng Liu 1 Dalia Barsyte-Lovejoy Abdellah Allali-Hassani Yunlong He J Martin Herold Xin Chen Christopher M Yates Stephen V Frye Peter J Brown Jing Huang Masoud Vedadi Cheryl H Arrowsmith Jian Jin
Affiliations

Affiliation

  • 1 Center for Integrative Chemical Biology and Drug Discovery, Division of Medicinal Chemistry and Natural Products, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
Abstract

Protein lysine methyltransferase G9a plays key roles in the transcriptional repression of a variety of genes via dimethylation of lysine 9 on histone H3 (H3K9me2) of chromatin as well as dimethylation of nonhistone proteins including tumor suppressor p53. We previously reported the discovery of UNC0321 (3), the most potent G9a inhibitor to date, via structure-based design and structure-activity relationship (SAR) exploration of the quinazoline scaffold represented by BIX01294 (1). Despite its very high in vitro potency, compound 3 lacks sufficient cellular potency. The design and synthesis of several generations of new analogues aimed at improving cell membrane permeability while maintaining high in vitro potency resulted in the discovery of a number of novel G9a inhibitors such as UNC0646 (6) and UNC0631 (7) with excellent potency in a variety of cell lines and excellent separation of functional potency versus cell toxicity. The design, synthesis, and cellular SAR of these potent G9a inhibitors are described.

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