Synthetic Indolactam V Analogues as Inhibitors of PAR2-Induced Calcium Mobilization in Triple-Negative Breast Cancer Cells

ChemMedChem. 2018 Jan 22;13(2):147-154. doi: 10.1002/cmdc.201700640. Epub 2018 Jan 4.

Abstract

Human proteinase-activated receptor 2 (PAR2), a transmembrane G-protein-coupled receptor (GPCR), is an attractive target for a novel anticancer therapy, as it plays a critical role in cell migration and invasion. Selective PAR2 inhibitors therefore have potential as anti-metastatic drugs. Knowing that the natural product teleocidin A2 is able to inhibit PAR2 in tumor cells, the goal of the present study was to elaborate structure-activity relationships and to identify potent PAR2 inhibitors with lower activity against the adverse target, protein kinase C (PKC). For this purpose, an efficient gram-scale total synthesis of indolactam V (i.e., the parent structure of all teleocidins) was developed, and a library of derivatives was prepared. Some compounds were indeed found to exhibit high potency as PAR2 inhibitors at low nanomolar concentrations with improved selectivity (relative to teleocidin A2). The pseudopeptidic fragment bridging the C3 and C4 positions of the indole core proved to be essential for target binding, whereas activity and target selectivity depends on the substituents at N1 or C7. This study revealed novel derivatives that show high efficacy in PAR2 antagonism combined with increased selectivity.

Keywords: breast cancer; indole alkaloids; proteinase-activated receptor 2; teleocidins; total synthesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / chemical synthesis*
  • Antineoplastic Agents / pharmacology
  • Calcium / metabolism*
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Survival / drug effects
  • Humans
  • Indoles / chemical synthesis*
  • Indoles / pharmacology
  • Lactams / chemical synthesis*
  • Lactams / pharmacology
  • Lyngbya Toxins / chemistry
  • Molecular Structure
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • Receptor, PAR-2 / antagonists & inhibitors*
  • Structure-Activity Relationship
  • Triple Negative Breast Neoplasms / metabolism*

Substances

  • Antineoplastic Agents
  • Indoles
  • Lactams
  • Lyngbya Toxins
  • Receptor, PAR-2
  • teleocidins
  • indolactam V
  • Protein Kinase C
  • Calcium