Development

Since Alexion's founding in 1992, the company's research efforts have focused primarily on complement inhibition – the selective blocking of the complement cascade. In 2007, Alexion became the first company to discover, develop and successfully commercialize a terminal complement inhibitor.

The complement cascade consists of a series of proteins that form an important component of the immune system, but when unregulated can cause harmful inflammation and numerous clinical consequences if inappropriately activated.25 Naturally-occurring but highly specialized proteins are designed to ensure that the complement system does not get out of control, and these proteins are vital to prevent potentially harmful effects. In some life-threatening diseases, the absence of these specialized regulatory or protective proteins lead to severe clinical disorders.

Based on research conducted in the 1980s and early 1990s, researchers at Alexion believed that selective targeting of the complement system was the key to treating certain autoimmune and inflammatory diseases. In the design of the complement inhibitor Soliris, complement protein C5 was identified as the most appropriate protein to block in the complement pathway, because it is common to all activation pathways of the complement system. Blockade at C5 also preserves critical protective functions of the complement system while preventing the generation of the activation products C5a and C5b-9 which cause inflammation and destruction of cells and tissues.23

In 2002 the company began to focus on the treatment of patients with paroxysmal nocturnal hemoglobinuria (PNH). PNH is a rare and life-threatening blood disorder characterized by complement-mediated hemolysis, the destruction of a person's red blood cells, due to absence of a complement inhibitor.7 In patients with PNH, hemolysis can cause thromboses (blood clots), kidney disease, liver failure, disabling fatigue, impaired quality of life, recurrent pain, shortness of breath, increased pressure in the blood vessels of the lungs, intermittent episodes of dark colored urine (hemoglobinuria), and anemia.2,4,6,8

In May 2002 the first patient with PNH was dosed with Soliris in an 11-patient, open-label pilot study to test the efficacy and safety of Soliris as a treatment for PNH. The PNH clinical studies demonstrated that Soliris reduced hemolysis in every treated patient and led to positive outcomes for patients suffering from PNH. This data is the basis for regulatory approval of Soliris for the treatment of patients with PNH in both the United States and European Union in 2007.23



IMPORTANT SAFETY INFORMATION

Soliris increases the risk of meningococcal infections. Meningococcal infection may become rapidly life-threatening or fatal if not recognized and treated early

Soliris® increases the risk of meningococcal infections

  • Vaccinate patients with a meningococcal vaccine at least 2 weeks prior to receiving the first dose of Soliris; revaccinate according to current medical guidelines for vaccine use
  • Monitor patients for early signs of meningococcal infections, evaluate immediately if infection is suspected, and treat with antibiotics if necessary

The effect of anticoagulant withdrawal during Soliris treatment has not been studied. Therefore, treatment with Soliris should not alter anticoagulant management.

Soliris is generally well tolerated. The most frequent adverse events observed in clinical studies were headache, a runny nose (nasopharyngitis), back pain, nausea, and tiredness (fatigue).