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Experimental autoimmune myocarditis (EAM) is an animal model of human idiopathic dilated cardiomyopathy (IDC) and can be induced in susceptible mice using various autoantigens. In the current study, we assessed the ability of the new quinazolinone, RO5126766, a potent and selective phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase kinase (MEK) inhibitor to inhibit experimental autoimmune myocarditis (EAM) induced in C57BL/6 mice by either autoantigen-adjuvant combination A (S100A8/A9) and alum or by autoantigen-antibody combination B (cardiac myosin). We determined the effects of RO5126766 on cardiac dysfunction and cardiomyocyte hypertrophy in EAM, and on cardiac remodeling in non-EAM. EAM was induced by a single subcutaneous (s.c.) injection of 100 μg of S100A9 and 10 mg of alum. The animals were treated s.c. with 50 mg/kg of RO5126766 three times a week until endpoint (day 28). We found that the administration of RO5126766 significantly reduced the incidence of EAM, and improved the survival rate. Inhibition of myocarditis by RO5126766 was accompanied by a reduction in cardiac inflammation, lymphocytic infiltration, microvascular damage, and a significant reduction in cardiac myocyte hypertrophy. We conclude that the quinazolinone RO5126766 is effective in preventing and treating EAM induced in C57BL/6 mice by two different autoant System Requirements For X-Eclipse: Minimum: - Windows 7, Windows 8/8.1 (64-bit), Windows 10 (64-bit) - Intel Core 2 Duo, 2.6 GHz or better - 4 GB RAM (8 GB RAM for the DOS version) - 300 MB free hard disk space - 128 MB VRAM - DirectX 9.0c Recommended: - Intel Core i3, 2.
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