A heart attack, or myocardial infarction (MI), is permanent damage to heart muscles. It affects millions of people worldwide each year. Current therapeutic treatments are mainly used for the prevention but not the post-treatment of heart attack. They do nothing to protect heart muscle cells from death after heart attack. Therefore, we developed a potent drug candidate PP-002 that can be used as an effective post-treatment to stop the cell death signaling pathway in heart muscle cells after heart attack. PP-002 is water soluble and membrane permeable. Post-treatment with PP-002 effectively restored heart function in a rat model of heart attack compared with the saline-treated group.
*** p﹤0.001 VS the saline group.
Data are presented as Mean±SD
LVSP: left ventricular systolic pressure;
LVEDP: left ventricular end diastolic pressure;
±dp/dtmax: The rate (dP/dt max) of left ventricle (LV) pressure rise in early systole is one of the oldest measures of LV global contractility. The greater the contractile force exerted, the greater the rate of increase in left ventricular pressure.