ArticleCommunications biology2026
Von Willebrand factor A1 blockade prevents platelet-mediated sustained occlusion for the treatment of arterial thrombosis.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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8 authors.
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Abstract
Arterial thrombosis is a leading cause of death and disability worldwide. Administration of tissue plasminogen activator (tPA) remains the current noninvasive clinical gold standard but is ineffective for many patients. Von Willebrand factor (VWF) is mechanistically critical in arterial thrombosis and has been studied as an alternative target for thrombolytic therapy. This study utilizes a microfluidic system of arterial thrombosis to evaluate VWF-A1 domain inhibitor aptamer (BB-031), aiming to understand VWF-mediated recanalization (vessel reopening) and compare efficacy of BB-031 to Alteplase and Tenecteplase. Thrombotic occlusion is simulated in a microfluidic device, and thrombi are allowed to retract and remodel for up to 6 hr. During a subsequent 2 h treatment reperfusion period (not disruptive to the original thrombus), thrombus morphology, composition, and channel patency (openness) are analyzed. Thrombi substantially remodel post-occlusion. BB-031 treatment results in an inability to maintain thrombus and significantly improves microfluidic patency compared to vehicle and tPA. Acute ischemic stroke patient samples demonstrate improved microfluidic patency with BB-031 compared to vehicle. Here we establish an in vitro/ex vivo platform to study arterial occlusion, clot retraction, drug delivery, and recanalization/patency, and implement this platform to demonstrate BB-031 could be a safe and efficacious therapeutic alternative to tPA.
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