TNFα is a master regulator of inflammation. Excessive production of TNFα drives the damaging inflammation characteristic of many inflammatory diseases.

Small molecule anti-TNFα

Inhibition of the effects of TNFα is efficacious in the treatment of rheumatoid arthritis, ankylosing spondylitis, polyarticular juvenile idiopathic arthritis, psoriatic arthritis, plaque psoriasis, Crohn’s disease, and ulcerative colitis. There is the potential for the use of TNFα-directed therapy in many other inflammatory disorders where TNFα is a key factor.

Our programme focuses on small molecule TNFα suppressors which could potentially avoid the inconvenience, unwanted effects and the development of drug-resistance associated with anti-TNFα biologic therapies. Our molecules are designed to regulate TNFα transcription and post-transcriptional TNFα expression.

Our lead compounds are small molecules with:

  • good variability in chemotypes
  • synthetic tractability
  • good drug-like characteristics
  • no significant toxicity in initial screens
  • reduce TNFα titres to zero in LPS-induced PBMCs