Introduction: Non-alcoholic steatohepatitis (NASH) is a serious form of non-alcoholic fatty liver disease (NAFLD) for which there is no marketed treatments. NAFLD is initiated by excess intake of nutrients and recent evidence has pinpointed the mitochondrial pyruvate carrier (MPC) as a mediator of the nutritional overload signals. Areas covered: An overview is given of MSDC-0602K, a new agent in development that modulates the MPC and as such treats the symptoms of fatty liver including dysfunctional lipid metabolism, inflammation, and insulin resistance as well as the key liver pathology including fibrosis.
Methodology: The current evaluation is written from the direct experience of the authors and review of published literature using standard search techniques. Expert Opinion: The mechanism of action of MSDC-0602K appears to be suited for treatment of the NASH pathophysiology. An ongoing phase 2b dose-ranging trial should demonstrate whether or not MSDC-0602K has the potential to be a cornerstone metabolic therapy for the treatment of NASH.
Keywords: Insulin resistance; MPC; MSDC-0602K; NAFLD; NASH.