Autoantibodies against the second extracellular loop of β₁-adrenergic receptor (β₁-AA) have been shown to be involved in the development of cardiovascular diseases. Recently, there has been considerable interest in strategies to remove these autoantibodies, particularly therapeutic peptides to neutralize β₁-AA. Researchers are investigating the roles of cyclic peptides that mimic the structure of relevant epitopes on the β₁-AR-EC_II in a number of immune-mediated diseases. Here, we used a cyclic peptide, namely, RD808, to neutralize β₁-AA, consequently alleviating β₁-AA-induced myocardial injury. We investigated the protective effects of RD808 on the myocardium both in vitro and in vivo. RD808 was found to increase the survival rate of cardiomyocytes; furthermore, it decreased myocardial necrosis and apoptosis and improved the cardiac function of BalB/c mice in a β₁-AA transfer model. In vitro and in vivo experiments showed that myocardial autophagy was increased in the presence of RD808, which might contribute to its cardioprotective effects. Our findings indicate that RD808 reduced myocardial injury induced by β₁-AA.