ArticleJournal of thrombosis and haemostasis : JTH2025
Protective effects of factor XI inhibition by abelacimab in a baboon model of live Staphylococcus aureus sepsis.
Article in Journal of thrombosis and haemostasis : JTH, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- A Suspension-Trapping Protocol for Bottom-Up Proteomics Sample Preparation.Bio-protocol · 2026Article
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Authors and funding
21 authors.
Funding
Abstract
backgroundSepsis remains a major clinical challenge characterized by dysregulated immune response, coagulation abnormalities, and multiorgan failure, leading to high morbidity and mortality.
objectivesThis study investigated the therapeutic potential of abelacimab, a monoclonal antibody targeting the plasma zymogen factor (F)XI, in a new baboon model of Staphylococcus aureus sepsis.
methodsHealthy Papio anubis baboons were randomly assigned to control or abelacimab treatment groups. Both groups (n = 6, each) were intravenously infused with a median lethal (LD
resultsAll 6 abelacimab-treated baboons survived until the 7-day endpoint, while 3 out of 6 untreated controls succumbed to sepsis within 102 hours. Abelacimab significantly attenuated sepsis-induced coagulopathy without signs of bleeding, as evidenced by biochemical tests and pathology analysis. Treated animals exhibited decreased proinflammatory cytokines, diminished neutrophil activation, and preservation of endothelial integrity, collectively conferring robust protection against organ damage. Proteomic analysis revealed that abelacimab modulated pathways related to coagulation, inflammation, and tissue injury, contributing to improved survival outcomes.
conclusionFXI inhibition by abelacimab offers significant protection by attenuating activation of coagulation, reducing inflammation, and preventing organ failure. Targeting FXI may be a promising therapeutic strategy for managing sepsis by addressing multiple facets of its complex pathophysiology.
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Registered trials
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