Diseases driven by chronic inflammation are major health burdens and controlling inflammation is an important preventative and therapeutic goal. A network of over 40 ‘Complement’ proteins is produced in blood and on cell surfaces in response to infection/injury. Complement protein C3 is a central mediator of all avenues of complement activation leading to pathogen destruction and elimination. However, blocking C3 also blocks beneficial roles of complement cascade in fighting infection.

University of Queensland (UQ) researchers have developed multiple series of novel, potent and selective, small organic molecules that mimic C3a (agonists) or inhibit its action (antagonists).

Key Features

  • Novel small molecule modulators of C3aR
  • Potent and selective for human/mouse C3aR
  • Orally active in inflammatory disease models
  • Distinct ‘Complement’ target and mechanism of action.

Potential applications

The C3aR antagonists have potential as treatments for inflammation-related diseases where C3aR has been implicated as important, including but not limited to:

  • Asthma, allergies, respiratory diseases
  • Arthritis, diseases of musculoskeletal system
  • Metabolic Syndrome (including obesity, diabetes and cardiovascular disease)
  • Inflammatory Bowel Disease (IBD), ulcerative colitis
  • Autoimmune diseases (e.g. lupus, multiple sclerosis)
  • Neurodegenerative diseases
  • Cancers.

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