Using state-of-the-art scientific methodology to validate a platform of clinical opportunities and progress small molecule drugs to the clinic and patients

• Inhibition of a GPR35-driven epithelial growth program upregulated in digestive system metaplasia, dysplasia and cancer
• Potent risk factors for digestive system metaplasia, dysplasia and cancer include strong genetic associations and environmental factors, including poor diet
• GPR35 polymorphisms are significantly associated with inflammatory bowel diseases, including ulcerative colitis, Crohn’s disease and primary sclerosing cholangitis, which pre-dispose patients to digestive tract adenocarcinomas
• GPR35 is expressed in digestive tract epithelial tissues, where it drives a cell growth program, and key GPR35 polymorphisms have been associated with increased expression and function
• GPR35 is activated by carboxylate-containing agonists in the gut and we have discovered a novel, potent endogenous agonist of GPR35 that is associated with high fat, obesogenic diets, a key disease risk factor for gut disease
• GPR35 is overexpressed uniquely in adenocarcinomas of the digestive tract and high expression can confer poorer prognosis to patients