ArticleScientific reports2020
The aptamer BT200 effectively inhibits von Willebrand factor (VWF) dependent platelet function after stimulated VWF release by desmopressin or endotoxin.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- A randomized placebo-controlled trial in healthy volunteers examining the effects of acetaminophen and NO-acetaminophen NCX 701 in human endotoxemia.Scientific reports · 2025Trial
- The von Willebrand factor A-1 domain binding aptamer BT200 elevates plasma levels of von Willebrand factor and factor VIII: a first-in-human trial.Haematologica · 2022Trial
- Von Willebrand Factor as a Therapeutic Target in Thrombotic Disorders.Thrombosis and haemostasis · 2026Review
- Recent Advances in Aptamer-Based Applications in Cardiology.International journal of molecular sciences · 2026Review
- Emerging role of nucleic acid aptamers in sepsis-induced coagulopathy: Future perspectives in diagnostics and therapeutics.Annals of intensive care · 2026Review
- Conformation-specific RNA aptamers for phenotypic distinction between normal von Willebrand factor and type 2B von Willebrand disease.NAR molecular medicine · 2024Article
- The aptamer BT200 blocks interaction of K1405-K1408 in the VWF-A1 domain with macrophage LRP1.Blood · 2024Article
- Kinetic Modeling for BT200 to Predict the Level of Plasma-Derived Coagulation Factor VIII in Humans.The AAPS journal · 2024Article
- Aptamers Regulating the Hemostasis System.Molecules (Basel, Switzerland) · 2022Review
- Hypoxia inducible factor-1α mediates the mechanism of the Hedgehog pathway in tendinopathy repair by Asperosaponin VI.Regenerative therapy · 2022Review
- Factors Associated with Platelet Activation-Recent Pharmaceutical Approaches.International journal of molecular sciences · 2022Review
- Structure-Based Cyclic Glycoprotein Ibα-Derived Peptides Interfering with von Willebrand Factor-Binding, Affecting Platelet Aggregation under Shear.International journal of molecular sciences · 2022Article
- Von Willebrand factor in diagnostics and treatment of cardiovascular disease: Recent advances and prospects.Frontiers in cardiovascular medicine · 2022Review
- Inflammatory Mediators of Platelet Activation: Focus on Atherosclerosis and COVID-19.International journal of molecular sciences · 2021Review
- Age-Associated Increase in Thrombogenicity and Its Correlation with von Willebrand Factor.Journal of clinical medicine · 2021Review
- The Intriguing Relationships of von Willebrand Factor, ADAMTS13 and Cardiac Disease.Journal of cardiovascular development and disease · 2021Review
- The aptamer BT200 blocks von Willebrand factor and platelet function in blood of stroke patients.Scientific reports · 2021Article
- Association of ABO blood group with bleeding severity in patients with bleeding of unknown cause.Blood advances · 2020Article
- Shear Stress-Induced Activation of von Willebrand Factor and Cardiovascular Pathology.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Von Willebrand factor (VWF) plays a major role in arterial thrombosis. Antiplatelet drugs induce only a moderate relative risk reduction after atherothrombosis, and their inhibitory effects are compromised under high shear rates when VWF levels are increased. Therefore, we investigated the ex vivo effects of a third-generation anti-VWF aptamer (BT200) before/after stimulated VWF release. We studied the concentration-effect curves BT200 had on VWF activity, platelet plug formation under high shear rates (PFA), and ristocetin-induced platelet aggregation (Multiplate) before and after desmopressin or endotoxin infusions in healthy volunteers. VWF levels increased > 2.5-fold after desmopressin or endotoxin infusion (p < 0.001) and both agents elevated circulating VWF activity. At baseline, 0.51 µg/ml BT200 reduced VWF activity to 20% of normal, but 2.5-fold higher BT200 levels were required after desmopressin administration (p < 0.001). Similarly, twofold higher BT200 concentrations were needed after endotoxin infusion compared to baseline (p < 0.011). BT200 levels of 0.49 µg/ml prolonged collagen-ADP closure times to > 300 s at baseline, whereas 1.35 µg/ml BT200 were needed 2 h after desmopressin infusion. Similarly, twofold higher BT200 concentrations were necessary to inhibit ristocetin induced aggregation after desmopressin infusion compared to baseline (p < 0.001). Both stimuli elevated plasma VWF levels in a manner representative of thrombotic or pro-inflammatory conditions such as arterial thrombosis. Even under these conditions, BT200 potently inhibited VWF activity and VWF-dependent platelet function, but higher BT200 concentrations were required for comparable effects relative to the unstimulated state.
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Registered trials
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