Results: Cmpd17b reduced MAP, SNS activity, cardiac and vascular adverse remodelling and dysfunction in hypertensive mice (Table ). Cutting-edge quantitative proteomics analysis revealed that hypertension-induced significant adverse structural remodelling (110 proteins in the heart and 60 proteins in the aorta) and mitochondrial dysregulation (38 in the heart and 91 in the aorta), consisted with function and pathology observed. Those changes were prevented by FPR agonism (53 structural cardiac proteins and 38 vascular structural proteins) and (24 cardiac mitochondrial proteins and 36 vascular mitochondrial proteins). Conclusions:Our study demonstrated for the first time that FPR prototype smallmolecule Cmpd17b reduced hypertension-induced cardiovascular damage, supporting the development of FPR-based therapy to treat cardiovascular complications in systemic hypertension.