In 1995, GlaxoSmithKline’s Flolan (epoprostenol) became the first therapy to be specifically approved for the orphan disease of pulmonary arterial hypertension (PAH). As a prostaglandin analog, the drug acts as a potent vasodilator and platelet aggregation inhibitor through binding of the prostaglandin I2 (PGI2) receptor. In PAH, the production of PGI2 is chronically impaired and this plays a crucial role in the excessive vasoconstriction, pulmonary vasculature remodeling, and thrombosis formation associated with the disease pathology.
Despite demonstrating a significant improvement in survival, Flolan (epoprostenol; GlaxoSmithKline) usage is limited by the drug’s unfavorable administration (Barst et al., 1996). As such, the drug is the leading therapy for patients with the highest disease burden. The drug’s high price point has also negatively impacted on uptake, but increasing generic competition should help to improve access to treatment.
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