MP2000

Our target: cardiac muscle metabolism

MP2000 denotes a range of closely related drug compounds which are specific inhibitors of an enzyme called CPT1. These drugs inhibit the use of fatty-acids as primary energy source of the heart muscle and shift the heart metabolism towards the use of glucose as an alternative energy source. “Burning” of glucose needs less oxygen for the same amount of muscle energy.

Thus in patients with coronary disease and a reduced oxygen supply of the heart, the use of CPT1-inhibitors gives more pumping power to the heart without the need for more oxygen. This is especially valuable in patients with severe heart failure (NYHA grade IV).
50% of these patients die within one year and there is a high medical need for additional pharmacologic treatment options. Leading cardiologists have noted that the therapeutic principle of drugs like MP2000 will lead to a new era of pharmacological treatment of heart disease¹. The MP2000 class of molecules are the most specific and potent drugs known for this new treatment approach to chronic heart failure.

Mode of action

The pumping capacity of the heart depends on metabolic energy and ample oxygen supply. The primary energy source for the heart muscle cells are fatty acids. Fatty acids are transported via the enzyme carnitine palmitoyltransferase 1(CPT 1) into the mitochondria (the cell’s “power plants”). Fatty acids are metabolized within the mitochondria via beta-oxidation, a process by which energy is released. This process needs ample oxygen supply, which in the case of ischemia or coronary heart disease¹ is diminished. The ensuing reduced pumping capacity of the heart is the cause of chronic heart failure.

MP2000 inhibits the uptake of fatty acids into the mitochondria by blocking CPT1. The heart muscle cells start using glucose as their primary source of energy. The metabolic pathway to generate cellular energy from glucose inherently needs less oxygen than the metabolism of fatty acids for the same amount of energy.