The PAH Challenge

PAH (Pulmonary Arterial Hypertension) — a pressing challenge.

There is a pressing unmet need for a different approach, better options and more effective treatment for Pulmonary Arterial Hypertension (PAH), an incurable disease that has been challenging the medical profession and the pharmaceutical industry. Pulmokine is developing a new class of drugs (kinase inhibitors) to address this challenge.

The pathology of PAH

Pulmonary arterial hypertension (PAH) is a pulmonary vascular disease characterized by high pressure in the blood supply to the lungs. It is a progressive disease associated with a high morbidity. If untreated, patients with PAH suffer from shortness of breath,heart failure, and decreased life expectancy.

PAH is caused by a constellation of diseases that affect the pulmonary vasculature. These include primary genetic abnormalities, systemic sclerosis (scleroderma), mixed connective tissue disease, uncorrected congenital heart disease, portal hypertension, HIV infection, and other disorders.

The pathology of PAH consists of proliferation of cells in small pulmonary arterioles. It has been proposed that PAH is a “cancer” of pulmonary arteriolar endothelial cells. The paradigm of PAH as a neoplastic process provides a rationale to develop anti-proliferative kinase inhibitors for this disease.

Limitations of current therapies

Current therapies for PAH consist of vasodilators, which help relax constricted pulmonary blood vessels, but which do not fully address the underlying cause of the disease. These drugs can have adverse side effects and do not stop the progression of the disease. Even with the latest advances, a significant number of patients plateau or get worse. More effective therapies are needed.

Learn more about PAH

If you are interested in learning more about PAH we recommend contacting the Pulmonary Hypertension Association or going to their website at

If you have any questions for us contact please contact Lawrence S. Zisman, MD;; phone: 518-573-8315 or click here.