Evidence map›Paper›PMID 26605293›Full record

ReviewAnnals of translational medicine2015

The factor XIIa blocking antibody 3F7: a safe anticoagulant with anti-inflammatory activities.

Marie Worm, Elodie C Köhler, Rachita Panda, Andy Long, Lynn M Butler, Evi X Stavrou, Katrin F Nickel, Tobias A Fuchs, Thomas Renné

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Annals of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Antifouling Zwitterionic Polymer Coatings for Blood-Bearing Medical Devices.Langmuir : the ACS journal of surfaces and colloids · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Coming soon to a pharmacy near you? FXI and FXII inhibitors to prevent or treat thromboembolism.Hematology. American Society of Hematology. Education Program · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. [Hereditary angioedema].Der Internist · 2019
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. 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 1 institution in 1 country.

Marie Worm1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Elodie C Köhler1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Rachita Panda1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Andy Long1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Lynn M Butler1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Evi X Stavrou1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Katrin F Nickel1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Tobias A Fuchs1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Thomas Renné1 Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany ; 2 Division of Clinical Chemistry, Department of Molecular Medicine and Surgery and Center of Molecular Medicine, Karolinska Institutet and University Hospital, Stockholm, Sweden ; 3 Division of Hematology and Oncology, Department of Medicine, Case Western Reserve University, Cleveland, Ohio, USA ; 4 Department of Medicine, Louis Stokes Veterans Administration Hospital, Cleveland, Ohio, USA.
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The plasma protein factor XII (FXII) is the initiating protease of the procoagulant and proinflammatory contact system. FXII activates both the bradykinin (BK) producing kallikrein-kinin system and the intrinsic pathway of coagulation. Contact with negatively charged surfaces induces auto-activation of zymogen FXII that results in activated FXII (FXIIa). Various in vivo activators of FXII have been identified including heparin, misfolded protein aggregates, nucleic acids and polyphosphate. Murine models have established a central role of FXII in arterial and venous thromboembolic diseases. Despite the central function of FXII in pathologic thrombosis, its deficiency does not impair hemostasis in animals or humans. The selective role of FXIIa in thrombosis, but not hemostasis, offers an exciting novel strategy for safe anticoagulation based on interference with FXIIa. We have generated the recombinant fully human FXIIa-blocking antibody 3F7, which abolished FXIIa enzymatic activity and prevented thrombosis in a cardiopulmonary bypass system in large animals, in the absence of increased therapy-associated bleeding. Furthermore, 3F7 also interfered with BK-driven edema in the severe swelling disorder hereditary angioedema (HAE) type III. Taken together, targeting FXIIa with 3F7 appears to be a promising approach to treat edema disorders and thrombosis.

Indexed as

angioedemaanticoagulationCardiovascularcoagulationfactor XII (FXII)hereditary angioedema (HAE) type IIIthrombosis

Identifiers

PMID26605293
PMCPMC4620089
OpenAlexW1752012283

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.