ARN25068, a versatile starting point towards triple GSK-3β/FYN/DYRK1A inhibitors to tackle tau-related neurological disorders

Eur J Med Chem. 2022 Feb 5:229:114054. doi: 10.1016/j.ejmech.2021.114054. Epub 2021 Dec 16.

Abstract

The human kinome plays a crucial role in several pathways. Its dysregulation has been linked to diverse central nervous system (CNS)-related disorders with a drastic impact on the aging population. Among them, tauopathies, such as Alzheimer's Disease (AD) and Frontotemporal Lobar degeneration (FTLD-tau), are neurodegenerative disorders pathologically defined by the presence of hyperphosphorylated tau-positive intracellular inclusions known as neurofibrillary tangles (NFTs). Compelling evidence has reported the great potential of the simultaneous modulation of multiple protein kinases (PKs) involved in abnormal tau phosphorylation through a concerted pharmacological approach to achieve a superior therapeutic effect relative to classic "one target, one drug" approaches. Here, we report on the identification and characterization of ARN25068 (4), a low nanomolar and well-balanced dual GSK-3β and FYN inhibitor, which also shows inhibitory activity against DYRK1A, an emerging target in AD and tauopathies. Computational and X-Ray studies highlight compound 4's typical H-bonding pattern of ATP-competitive inhibitors at the binding sites of all three PKs. In a tau phosphorylation assay on Tau0N4R-TM-tGFP U2OS cell line, 4 reduces the extent of tau phosphorylation, promoting tau-stabilized microtubule bundles. In conclusion, this compound emerges as a promising prototype for further SAR explorations to develop potent and well-balanced triple GSK-3β/FYN/DYRK1A inhibitors to tackle tau hyperphosphorylation.

Keywords: Central nervous system; Docking studies; Enzymatic and cell-based assays; Kinase inhibitors; Multitarget compounds; Selectivity; Tau phosphorylation assay; Tauopathies; X-ray studies.

MeSH terms

  • Binding Sites
  • Drug Evaluation, Preclinical
  • Dyrk Kinases
  • Glycogen Synthase Kinase 3 beta / metabolism*
  • Humans
  • Microtubules / metabolism
  • Models, Molecular
  • Neurofibrillary Tangles / metabolism
  • Neuroprotective Agents / chemical synthesis*
  • Neuroprotective Agents / pharmacology
  • Phosphorylation
  • Protein Binding
  • Protein Conformation
  • Protein Kinase Inhibitors / chemical synthesis*
  • Protein Kinase Inhibitors / pharmacology
  • Protein Serine-Threonine Kinases / antagonists & inhibitors*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-fyn / antagonists & inhibitors*
  • Structure-Activity Relationship
  • Tauopathies / drug therapy*
  • tau Proteins / metabolism

Substances

  • Neuroprotective Agents
  • Protein Kinase Inhibitors
  • tau Proteins
  • Protein-Tyrosine Kinases
  • FYN protein, human
  • Proto-Oncogene Proteins c-fyn
  • Glycogen Synthase Kinase 3 beta
  • Protein Serine-Threonine Kinases