Selective CXCR2 antagonist. Its use is capable of reducing BP, reducing the duration of arterial fibrillation and promoting atrial remodeling, in addition to decreasing macrophage recruitment, reducing superoxide production associated with multiple pathways, such as TGF-b1/Smad2/3, NFkB-p65, NOX1, NOX2, Kir 2.1, Kvl.5, and Cx43, in SHR rats. It has also been reported to reduce fibrosis and pulmonary hypertension in mice. Here, GJA1 is linked to pulmonary hypertension.