Discovery and Development of First-in-Class ACKR3/CXCR7 Superagonists for Platelet Degranulation Modulation

J Med Chem. 2022 Oct 13;65(19):13365-13384. doi: 10.1021/acs.jmedchem.2c01198. Epub 2022 Sep 23.

Abstract

The atypical chemokine receptor 3 (ACKR3), formerly known as CXC-chemokine receptor 7 (CXCR7), has been postulated to regulate platelet function and thrombus formation. Herein, we report the discovery and development of first-in-class ACKR3 agonists, which demonstrated superagonistic properties with Emax values of up to 160% compared to the endogenous reference ligand CXCL12 in a β-arrestin recruitment assay. Initial in silico screening using an ACKR3 homology model identified two hits, C10 (EC50 19.1 μM) and C11 (EC50 = 11.4 μM). Based on these hits, extensive structure-activity relationship studies were conducted by synthesis and testing of derivatives. It resulted in the identification of the novel thiadiazolopyrimidinone-based compounds 26 (LN5972, EC50 = 3.4 μM) and 27 (LN6023, EC50 = 3.5 μM). These compounds are selective for ACKR3 versus CXCR4 and show metabolic stability. In a platelet degranulation assay, these agonists effectively reduced P-selectin expression by up to 97%, suggesting potential candidates for the treatment of platelet-mediated thrombosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Arrestin / metabolism
  • Chemokine CXCL12 / metabolism
  • Ligands
  • P-Selectin* / metabolism
  • Receptors, CXCR* / metabolism
  • Receptors, CXCR4 / metabolism
  • Signal Transduction / physiology
  • beta-Arrestins / metabolism

Substances

  • ACKR3 protein, human
  • Arrestin
  • Chemokine CXCL12
  • Ligands
  • P-Selectin
  • Receptors, CXCR
  • Receptors, CXCR4
  • beta-Arrestins