|
|
 |
| |
Tracleer® - The Endothelin Receptor Antagonist
|
THE ACTELION ANNUAL REPORT 2002 |
|
|
|
| |
|
|
|
|
|
|
|
Endothelin, the molecular target of Tracleer®
|
| |
Tracleer® represents the first and only approved drug of a new pharmaceutical class that blocks the detrimental effects of endothelin (ET). Tracleer® is an orally active dual endothelin receptor antagonist (ERA). It works by blocking the binding of ET to both of its receptors, ETA and ETB, thereby preventing the deleterious effects of ET. Levels of ET are often elevated in certain disease settings. ET is produced and secreted by the endothelium, a single layer of cells covering the inner surface of blood vessels that regulate blood flow by causing blood vessels to narrow (vasoconstriction). In addition to vasoconstriction, ET has other deleterious effects, such as stiffening blood vessels by promoting the accumulation of connective tissue (fibrosis), changing the vessel’s shape (remodeling) and size (hypertrophy) and predisposing them to inflammation. The over-production of ET as a key pathogenic mediator plays a critical role in chronic diseases such as pulmonary arterial hypertension, connective tissue diseases (e.g.
scleroderma), pulmonary fibrosis and acute heart failure, where it has been shown to correlate with the disease’s severity.
|
|
|
| |
|
|
|
|
|
|
| Endothelin (ET) is a key pathogenic mediator, which, in addition to vasoconstriction, has direct deleterious effects that include fibrosis, vascular hypertrophy and inflammation. Overexpression of ET plays a critical role in diseases such as pulmonary arterial hypertension (PAH). Tracleer®, the orally active dual endothelin receptor antagonist (ERA), “loosens the grip” of ET by blocking its pathological effects. |
|
|
|
|
