Mitochondrial dysfunction in intestinal epithelial cells (IEC) is a critical driver in the failure to heal chronic ulceration in IBD(1). OXPHOS is important for differentiation and cell polarity in repairing IEC(2,3). The development of new IBD drugs that improve mitochondria function would potentially accelerate mucosal repair and enhance overall clinical management of refractory patients. For this study, we tested the efficacy of a novel oral agent (AuPhos) that localized to mitochondria where it increases respiration (Wempe et al CCC, 2022) and mitochondrial energy production.