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Small-molecule factor B inhibitor for the treatment of complement-mediated diseases
Journal article   Open access   Peer reviewed

Small-molecule factor B inhibitor for the treatment of complement-mediated diseases

Anna Schubart, Karen Anderson, Nello Mainolfi, Holger Sellner, Takeru Ehara, Christopher M Adams, Aengus Mac Sweeney, Sha-Mei Liao, Maura Crowley, Amanda Littlewood-Evans, …
Proceedings of the National Academy of Sciences - PNAS, Vol.116(16), pp.7926-7931
04/16/2019
DOI: 10.1073/pnas.1820892116
PMCID: PMC6475383
PMID: 30926668
url
https://doi.org/10.1073/pnas.1820892116View
Published (Version of record) Open Access

Abstract

Dysregulation of the alternative complement pathway (AP) predisposes individuals to a number of diseases including paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, and C3 glomerulopathy. Moreover, glomerular Ig deposits can lead to complement-driven nephropathies. Here we describe the discovery of a highly potent, reversible, and selective small-molecule inhibitor of factor B, a serine protease that drives the central amplification loop of the AP. Oral administration of the inhibitor prevents KRN-induced arthritis in mice and is effective upon prophylactic and therapeutic dosing in an experimental model of membranous nephropathy in rats. In addition, inhibition of factor B prevents complement activation in sera from C3 glomerulopathy patients and the hemolysis of human PNH erythrocytes. These data demonstrate the potential therapeutic value of using a factor B inhibitor for systemic treatment of complement-mediated diseases and provide a basis for its clinical development.
Animals Complement Factor B - antagonists & inhibitors Complement Pathway, Alternative - drug effects Disease Models, Animal Drug Discovery - methods Glomerulonephritis, Membranous - physiopathology Humans Immunologic Factors - pharmacology Male Mice Mice, Inbred C57BL Rats, Sprague-Dawley

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