Discovery and Evaluation of TLR-Targeted Immune Agonists

J Med Chem. 2024 Sep 26;67(18):16222-16234. doi: 10.1021/acs.jmedchem.4c00804. Epub 2024 Sep 5.

Abstract

Toll-like receptor (TLR) activation converts immunologically inactive tumors into immunologically active tumors by activating tumor residing antigen-presenting cells and recruitment of cytotoxic T lymphocytes. Targeted immune agonists (TIAs) are antibody drug conjugates with small-molecule TLR agonist payloads. The mechanism of action of TIAs involves tumor antigen recognition, Fcγ-receptor-dependent phagocytosis, and TLR-mediated activation to drive tumor killing by myeloid cells. Several new low DAR anti-HER2 TIAs conjugated with novel TLR7 or dual-TLR7/8 agonists with cleavable and noncleavable linkers were synthesized and profiled. In vitro studies demonstrated that these TIAs activate myeloid cells only in the presence of antigen-expressing cancer cells. Evaluation in ELISpot-based assays confirmed the low immunogenicity of these constructs. Systemic administration of the novel TIAs in tumor-bearing mice resulted in tumor reduction at low doses. These results provide a strong rationale for further development of the TIAs as a novel class of immunotherapeutics.

MeSH terms

  • Animals
  • Antibodies / chemistry
  • Antibodies / pharmacology
  • Antineoplastic Agents / chemical synthesis
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Cell Line, Tumor
  • Drug Discovery
  • Female
  • Humans
  • Immunoconjugates / chemistry
  • Immunoconjugates / pharmacology
  • Mice
  • Receptor, ErbB-2 / immunology
  • Receptor, ErbB-2 / metabolism
  • Toll-Like Receptor 7* / agonists
  • Toll-Like Receptor 8 / agonists
  • Toll-Like Receptors / agonists

Substances

  • Antibodies
  • Antineoplastic Agents
  • Immunoconjugates
  • Receptor, ErbB-2
  • Toll-Like Receptor 7
  • Toll-Like Receptor 8
  • Toll-Like Receptors