Evidence mapPaperPMID 32636459Full record

ArticleScientific reports2020

The aptamer BT200 effectively inhibits von Willebrand factor (VWF) dependent platelet function after stimulated VWF release by desmopressin or endotoxin.

Katarina D Kovacevic, Nina Buchtele, Christian Schoergenhofer, Ulla Derhaschnig, Georg Gelbenegger, Christine Brostjan, Shuhao Zhu, James C Gilbert, Bernd Jilma

Open access · goldAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Recent Advances in Aptamer-Based Applications in Cardiology.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Aptamers Regulating the Hemostasis System.Molecules (Basel, Switzerland) · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. The Intriguing Relationships of von Willebrand Factor, ADAMTS13 and Cardiac Disease.Journal of cardiovascular development and disease · 2021
    Review
  17. Article
  18. Article
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Katarina D KovacevicDepartment of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Nina BuchteleDepartment of Internal Medicine I, Medical University of Vienna, Vienna, Austria.
Christian SchoergenhoferDepartment of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Ulla DerhaschnigDepartment of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Georg GelbeneggerDepartment of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Christine BrostjanDivision of Vascular Surgery and Surgical Research Laboratories, Department of Surgery, Medical University of Vienna, Vienna, Austria.
Shuhao ZhuGuardian Therapeutics, Lexington, MA, USA.
James C GilbertGuardian Therapeutics, Lexington, MA, USA.
Bernd JilmaDepartment of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. bernd.jilma@meduniwien.ac.at.
Medical University of Vienna · ATGuardian Industries (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Platelet AggregationAdenosine DiphosphateAdultAptamers, NucleotideBlood PlateletsCells, CulturedCollagenDeamino Arginine VasopressinFemaleHumansLipopolysaccharidesMaleMiddle Agedvon Willebrand FactorAdenosine DiphosphateAptamers, NucleotideCollagenDeamino Arginine VasopressinLipopolysaccharidesvon Willebrand Factor

Identifiers

PMID32636459
PMCPMC7341806
OpenAlexW3039882541

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.