Soliris MOA

Soliris specifically inhibits chronic, uncontrolled complement activation1-3

First and only targeted complement inhibitor to reduce chronic hemolysis

The optimal approach to complement inhibition

  • Targets and blocks activation of the terminal complement pathway at C5, preserving the immune response of the proximal pathway, which is responsible for clearing microbial opsonization, immune complex clearance, and has weak anaphylatoxin properties2,3
  • Binds to C5 with high affinity; inhibits cleavage of C53
References: 
1. Hill A, Richards S, Hillmen P. Recent developments in the understanding and management of paroxysmal nocturnal haemoglobinuria. Br J Haematol. 2007;137:181-192. 2. Kelly R, Richards S, Hillmen P, Hill A. The pathophysiology of paroxysmal nocturnal hemoglobinuria and treatment with eculizumab. Ther Clin Risk Manag. 2009;5:911-921. 3. Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. JAMA. 2005;293:1653-1662. 4. Rother RP, Rollins SA, Mojcik CF, Brodsky RA, Bell L. Discovery and development of the complement inhibitor eculizumab for the treatment of paroxysmal nocturnal hemoglobinuria [published correction appears in Nat Biotechnol. 2007;25:1488]. Nat Biotechnol. 2007;25:1256-1264. 5. Walport MJ. Complement Part 1. N Engl J Med. 2001;344:1058-1066. 6. Walport MJ. Complement Part 2. N Engl J Med. 2001;344:1140-1144. 7. Noris M, Remuzzi G. Medical progress atypical hemolyticuremic syndrome. N Engl J Med. 2009;361:1676-1687. 8. Rosse W, Hillmen P, Schreiber A. Immune-mediated hemolytic anemia. Hematol. 2004:48-62.