The present invention describes a novel application for for an existing CXCR4 antagonist, AMD3100, which was found to reduce pulmonary artery pressure and vessel remodeling in a neonatal model of pulmonary hypertension. Pulmonary Hypertension remains a significant cause of morbidity and mortality especially severe in neonates who have been perinatally exposed to hypoxia.

The main therapy currently utilized in neonates with pulmonary hypertension is nitric oxide. Unfortunately, this therapy is expensive, and does not reverse the vascular remodeling. Based on preliminary data, stem cells, as well as inflammation, play a significant role in the vascular remodeling that is evidenced during neonatal pulmonary hypertension. AMD3100 provides an alternative which is cheaper than inhaled nitric oxide and would decrease the vascular remodeling by addressing the root cause. Since patients with long standing pulmonary hypertension die because of irreversible vascular remodeling and right heart failure, this therapy will be significantly useful in reducing morbidity and mortality.

Neonatal Pulmonary Hypertension of various etiologies includes:

1.) Perinatal asphyxia
2.) Chronic lung disease of prematurity
3.) Congenital heart disease

Pulmonary Hypertension remains a significant cause of morbidity and mortality in humans and is especially severe in neonates who have been perinatally exposed to hypoxia. Inhaled Nitric Oxide is currently the standard of care for babies with pulmonary hypertension. Unfortunately, this therapy is expensive and does not significantly decrease the vascular remodeling or right ventricular heart failure evidenced chronically. AMD3100, an antagonist of CXCR4 (a marker found on inflammatory and stem cells), was found to reduce pulmonary artery pressure and vessel remodeling in a neonatal model of pulmonary hypertension. This therapy would be cheaper and could even be utilized as an outpatient option.