Pediatric heart failure is an important cause of death in childhood; however, therapeutic drugs specific for pediatric heart failure have not been developed. Angiotensin II modulates cellular function by associating with its receptor, mainly angiotensin II type 1 receptor (AT₁R) and activates G protein or β-arrestin signaling. We reported that a β-arrestin-biased AT₁R agonist (BBA) peptide, TRV027 induced a strong inotropic effect on preweaning mice suffering from congenital dilated cardiomyopathy (DCM). Remarkably, this inotropic effect was not associated with either arrhythmia or an increase in cardiac oxygen consumption. Here, we examined the prosurvival effect of TRV027 in DCM model mice. Daily subcutaneous administration of TRV027, but not an AT₁R blocker from postnatal day 1 significantly improved the survival rate and contractility of the left ventricle. Hematologic and pathological analyses revealed no detectable abnormalities in TRV027-treated DCM model mice except for hypertrophic heart. These results suggested that TRV027 has a beneficial effect to prolong healthy lifespan of pediatric heart failure patients. We also performed a high-throughput screening of one million compounds in order to discover small molecule BBA and found some hit compounds.