Myocardial infarction (MI) is the leading cause of death in both men and women and represents one of the most severe health problem in a modern world. Myocardial necrosis is caused by critical imbalance between the coronary oxygen supply and the demand of the myocardium. Heart failure after MI is a common clinical syndrome with high mortality. Left ventricular remodeling after MI involves expansion of the infarcted area, ventricular dilatation and thinning of the ventricular wall. The main goals of standard therapy are rapid thrombolysis, optimization of oxygen, reduction of cardiac workload and pain control. There is great need for novel, powerful antifibrotic therapy. Bone morphogenetic proteins (BMP) are molecules discovered in bones and other different tissues. BMP1 isoforms were discovered in healthy humans and in patients with numerous diseases. In rats with chronic kidney disease administration of BMP1-3 increased renal fibrosis, while therapy with BMP1-3 neutralizing antibody reduced renal fibrosis. BMP1 isoforms were also identified in patients with acute myocardial infarction. We succeeded in performing the inhibition of the BMP1-3 isoforme with specific antibody as a key role molecule in fibrose process in an acute myocardial infarction in rats. Our results confirmed high efficiency in reducing the area of the heart muscle affected by fibrous changes, noted reduced effect of heart remodeling as well as a significant improvement in heart function. We evaluated the therapy by using the measurement of cardiac enzyme levels, echocardiographic analysis of cardiac function and histological analysis of the heart muscle after coronary artery ligation and initiation of the therapy.