ArticleResearch and practice in thrombosis and haemostasis2025
Impact of asundexian on a panel of coagulation assays.
Article in Research and practice in thrombosis and haemostasis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- A comprehensive multicenter study assessing the impact of abelacimab, asundexian, and milvexian on coagulation assays.Blood advances · 2026Article
- Translational Development of Oral FXIa Inhibitors: A Systematic Review of Molecular Design, Pharmacology, and Indication-Specific Clinical Evidence.Pharmaceuticals (Basel, Switzerland) · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: During the last few years, the small, oral, activated factor XI inhibitor, asundexian, has been investigated in different cardiovascular disorders. However, little is known about its impact on laboratory coagulation assays. Objectives: To describe the effects of asundexian on a panel of laboratory coagulation assays. Methods: The following assays were performed in normal pooled plasma spiked with increasing concentrations of asundexian (0-2000 ng/mL): activated partial thromboplastin time (aPTT), prothrombin time (PT), fibrinogen quantification (PT-derived and Clauss method), one-stage aPTT and PT-based coagulation factor assays, chronometric protein C and immunoturbidimetric protein S assays, reptilase time, chromogenic ecarin assay, dilute Russell's viper venom time assays, thrombin generation assay initiated by tissue factor (1, 5, and 20 pM) and ellagic acid (0.42 μM), rotational thromboelastometry intrinsically- and extrinsically-triggered assays, kaolin-activated clotting time, and glass bead-activated clotting time. This latter assay was also carried out in whole blood. Results: Asundexian up to 2000 ng/mL impacted aPTT and one-stage aPTT-based coagulation factor assays, with high variability between reagents and methodologies. Asundexian reduced thrombin generation triggered by ellagic acid and 1 or 5 pM tissue factor. The rotational thromboelastometry intrinsically-triggered assays and kaolin- and glass bead-activated clotting time assays were affected by asundexian 2000 ng/mL, while overall, no significant interference was observed with any of the remaining assays. Conclusion: Despite this study including a comprehensive panel of coagulation assays, asundexian may still affect other coagulation assays not assessed here. Further investigations in patients treated with asundexian are therefore warranted.
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