Identification of 5-Substituted 2-Acylaminothiazoles That Activate Tat-Mediated Transcription in HIV-1 Latency Models

J Med Chem. 2019 May 23;62(10):5148-5175. doi: 10.1021/acs.jmedchem.9b00462. Epub 2019 Apr 29.

Abstract

The persistent reservoir of cells latently infected with human immunodeficiency virus (HIV)-integrated proviral DNA necessitates lifelong suppressive antiretroviral therapy (ART). Epigenetic targeted compounds have shown promise as potential latency-reversing agents; however, these drugs have undesirable toxicity and lack specificity for HIV. We utilized a novel HEK293-derived FlpIn dual-reporter cell line, which quantifies specific HIV provirus reactivation (LTR promoter) relative to nonspecific host cell gene expression (CMV promoter), to identify the 5-substituted 2-acylaminothiazole hit class. Here, we describe the optimization of the hit class, defining the functionality necessary for HIV gene activation and for improving in vitro metabolism and solubility. The optimized compounds displayed enhanced HIV gene expression in HEK293 and Jurkat 10.6 latency cellular models and increased unspliced HIV RNA in resting CD4+ T cells isolated from HIV-infected individuals on ART, demonstrating the potential of the 2-acylaminothiazole class as latency-reversing agents.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-HIV Agents / chemical synthesis*
  • Anti-HIV Agents / pharmacokinetics
  • Anti-HIV Agents / pharmacology*
  • Antiretroviral Therapy, Highly Active / methods
  • CD4-Positive T-Lymphocytes / drug effects
  • CD4-Positive T-Lymphocytes / virology
  • Drug Design
  • Gene Expression Regulation, Viral / drug effects
  • HEK293 Cells
  • HIV-1 / drug effects*
  • Humans
  • Jurkat Cells
  • Mice
  • Microsomes, Liver
  • RNA, Viral / biosynthesis
  • RNA, Viral / drug effects
  • RNA, Viral / genetics
  • Structure-Activity Relationship
  • Thiazoles / chemical synthesis*
  • Thiazoles / pharmacokinetics
  • Thiazoles / pharmacology*
  • Transcription, Genetic
  • Virus Latency / drug effects*
  • tat Gene Products, Human Immunodeficiency Virus / biosynthesis*
  • tat Gene Products, Human Immunodeficiency Virus / drug effects*

Substances

  • Anti-HIV Agents
  • RNA, Viral
  • Thiazoles
  • tat Gene Products, Human Immunodeficiency Virus