Therapeutic complement inhibition: new developments.

Abstract

Activation of the complement system significantly contributes to the pathogenesis of various acute and chronic inflammatory diseases. Current strategies to inhibit complement include the replacement or substitution of endogenous soluble complement inhibitors (e.g., C1 inhibitor [C1 inh], recombinant soluble complement receptor 1, TP10), the administration of antibodies to block key proteins of the cascade reaction (e.g., C5) or to neutralize the action of the complement-derived anaphylatoxins, or blockade of complement receptors (e.g., C5aR, CD88). The recent approvals of anti-C5 for the treatment of paroxysmal nocturnal hemoglobinuria as well as of C1 inh for the treatment of hereditary angioedema beyond European countries have provided a resurgence of interest in the potential of complement therapeutics for the treatment of disease.

• Authors: Woodruff Emlen, Wenhan Li, Michael Kirschfink
• Journal: Seminars in thrombosis and hemostasis (Semin Thromb Hemost) Vol. 36 Issue 6 Pg. 660-8 (Sep 2010) ISSN: 1098-9064 [Electronic] United States
• PMID: 20865643 (Publication Type: Journal Article, Review)
• Copyright: © Thieme Medical Publishers.

Chemical References

• Antibodies, Monoclonal
• Complement C1 Inhibitor Protein
• Complement System Proteins

Topics

• Angioedemas, Hereditary (drug therapy, immunology)
• Animals
• Antibodies, Monoclonal (therapeutic use)
• Complement Activation (drug effects, immunology)
• Complement C1 Inhibitor Protein (therapeutic use)
• Complement Pathway, Alternative (drug effects, immunology)
• Complement System Proteins (immunology)
• Humans