Literature DB >> 20865643

Therapeutic complement inhibition: new developments.

Woodruff Emlen1, Wenhan Li, Michael Kirschfink.   

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. © Thieme Medical Publishers.

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Year:  2010        PMID: 20865643     DOI: 10.1055/s-0030-1262888

Source DB:  PubMed          Journal:  Semin Thromb Hemost        ISSN: 0094-6176            Impact factor:   4.180


  15 in total

Review 1.  Complement in the immunopathogenesis of rheumatic disease.

Authors:  Gunnar Sturfelt; Lennart Truedsson
Journal:  Nat Rev Rheumatol       Date:  2012-06-05       Impact factor: 20.543

2.  Design and development of TT30, a novel C3d-targeted C3/C5 convertase inhibitor for treatment of human complement alternative pathway-mediated diseases.

Authors:  Masha Fridkis-Hareli; Michael Storek; Istvan Mazsaroff; Antonio M Risitano; Ante S Lundberg; Christopher J Horvath; V Michael Holers
Journal:  Blood       Date:  2011-08-22       Impact factor: 22.113

3.  C1 inhibitor-mediated myocardial protection from chronic intermittent hypoxia-induced injury.

Authors:  Jinrong Fu; Furong Guo; Cheng Chen; Xiaoman Yu; Ke Hu; Mingjiang Li
Journal:  Exp Ther Med       Date:  2016-08-12       Impact factor: 2.447

4.  Cell surface complement regulators moderate experimental myasthenia gravis pathology.

Authors:  Linda L Kusner; Jose A Halperin; Henry J Kaminski
Journal:  Muscle Nerve       Date:  2012-10-05       Impact factor: 3.217

5.  Therapeutic inhibition of the alternative complement pathway attenuates chronic EAE.

Authors:  Xianzhen Hu; V Michael Holers; Joshua M Thurman; Trent R Schoeb; Theresa N Ramos; Scott R Barnum
Journal:  Mol Immunol       Date:  2013-01-20       Impact factor: 4.407

6.  New analogs of the clinical complement inhibitor compstatin with subnanomolar affinity and enhanced pharmacokinetic properties.

Authors:  Hongchang Qu; Daniel Ricklin; Hongjun Bai; Hui Chen; Edimara S Reis; Mateusz Maciejewski; Apostolia Tzekou; Robert A DeAngelis; Ranillo R G Resuello; Florea Lupu; Paul N Barlow; John D Lambris
Journal:  Immunobiology       Date:  2012-06-17       Impact factor: 3.144

7.  Low ficolin-3 levels in early follow-up serum samples are associated with the severity and unfavorable outcome of acute ischemic stroke.

Authors:  George Füst; Lea Munthe-Fog; Zsolt Illes; Gábor Széplaki; Tihamér Molnar; Gabriella Pusch; Kristóf Hirschberg; Robert Szegedi; Zoltán Széplaki; Zoltán Prohászka; Mikkel-Ole Skjoedt; Peter Garred
Journal:  J Neuroinflammation       Date:  2011-12-29       Impact factor: 8.322

Review 8.  Atypical hemolytic uremic syndrome.

Authors:  Chantal Loirat; Véronique Frémeaux-Bacchi
Journal:  Orphanet J Rare Dis       Date:  2011-09-08       Impact factor: 4.123

9.  Soluble CD59 expressed from an adenovirus in vivo is a potent inhibitor of complement deposition on murine liver vascular endothelium.

Authors:  Jarel Gandhi; Siobhan M Cashman; Rajendra Kumar-Singh
Journal:  PLoS One       Date:  2011-06-24       Impact factor: 3.240

Review 10.  Complement activation and inhibition in wound healing.

Authors:  Gwendolyn Cazander; Gerrolt N Jukema; Peter H Nibbering
Journal:  Clin Dev Immunol       Date:  2012-12-30
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