Heart failure is a clinical syndrome characterized by the inability of the heart to sufficiently pump blood to meet the body’s metabolic needs.

This results in fatigue and shortness of breath and everyday activities such as walking, climbing stairs or carrying groceries can become very difficult. According to the American Heart Association, approximately 6 million Americans have been diagnosed with heart failure and an additional 670,000 new cases are diagnosed annually. Although there is no cure for heart failure, people can lead a full life when the condition is managed with heart failure medicines and healthy lifestyle changes.

Therapeutic strategies for chronic heart failure have traditionally focused on the modification of hemodynamic alterations that occur in the failing heart. However, heart failure is also associated with significant alterations in cardiac metabolism (Neubauer, 2007). The failing heart faces an energy deficit, primarily because of a decrease in mitochondrial oxidative capacity. Pharmacological targeting of the energy metabolic pathways that improve cardiac energetics has emerged as a novel therapeutic approach to improving cardiac efficiency, decreasing the energy deficit and improving cardiac function in the failing heart.

Part 2 of our two-part Phase 2 trial is assessing the impact of ninerafaxstat on cardiac energetics, diastolic function, functional capacity and heart failure symptoms.

References: Neubauer S. The failing heart — an engine out of fuel. N Engl J Med. 2007;356:1140–1151; Lopaschuk G et al. Cardiac Energy Metabolism in Heart Failure. Circulation Research. Volume 128, Issue 10, 14 May 2021; Pages 1487-1513.