ArticleNature medicine2016
A rapid pro-hemostatic approach to overcome direct oral anticoagulants.
Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 43 citations in OpenAlex.
- Andexanet Alfa-Associated Heparin Resistance in Cardiac Surgery: Mechanism and In Vitro Perspectives.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Engineering and evaluation of FXa bypassing agents that restore hemostasis following Apixaban associated bleeding.Nature communications · 2024Article
- Dual antithrombotic therapy dose-dependently alters hemostatic plug structure and function.Journal of thrombosis and haemostasis : JTH · 2024Article
- Blood Coagulation and Beyond: Position Paper from the Fourth Maastricht Consensus Conference on Thrombosis.Thrombosis and haemostasis · 2023Article
- Article
- Novel strategies in antithrombotic therapy: targeting thrombosis while preserving hemostasis.Frontiers in cardiovascular medicine · 2023Review
- Blood coagulation factor X: molecular biology, inherited disease, and engineered therapeutics.Journal of thrombosis and thrombolysis · 2021Review
- Current Clinical Applications of In Vivo Gene Therapy with AAVs.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- A Review of the Incidence Diagnosis and Treatment of Spontaneous Hemorrhage in Patients Treated with Direct Oral Anticoagulants.Journal of clinical medicine · 2020Review
- Deciphering the coagulation profile through the dynamics of thrombin activity.Scientific reports · 2020Article
- An Update on the Reversal of Non-Vitamin K Antagonist Oral Anticoagulants.Advances in hematology · 2020Review
- Protein-Engineered Coagulation Factors for Hemophilia Gene Therapy.Molecular therapy. Methods & clinical development · 2019Review
- The impact of prothrombin complex concentrates when treating DOAC-associated bleeding: a review.International journal of emergency medicine · 2018Review
- Combination of aptamer and drug for reversible anticoagulation in cardiopulmonary bypass.Nature biotechnology · 2018Article
- [Hemorrhage under direct oral anticoagulants : Occurrence and treatment in intensive care patients].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2018Review
- Reversal Strategies for Intracranial Hemorrhage Related to Direct Oral Anticoagulant Medications.Critical care research and practice · 2018Review
- Impact of Non-Vitamin K Antagonist Oral Anticoagulants From a Basic Science Perspective.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
- Engineered factor Xa variants retain procoagulant activity independent of direct factor Xa inhibitors.Nature communications · 2017Article
- Management of Spontaneous Intracerebral Hemorrhage.Current neurology and neuroscience reports · 2017Review
- Rendering factor Xa zymogen-like as a therapeutic strategy to treat bleeding.Current opinion in hematology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Direct inhibitors of coagulation factor Xa (FXa) or thrombin are promising oral anticoagulants that are becoming widely adopted. The ability to reverse their anticoagulant effects is important when serious bleeding occurs or urgent medical procedures are needed. Here, using experimental mouse models of hemostasis, we show that a variant coagulation factor, FXa(I16L), rapidly restores hemostasis in the presence of the anticoagulant effects of these inhibitors. The ability of FXa(I16L) to reverse the anticoagulant effects of FXa inhibitor depends, at least in part, on the ability of the active site inhibitor to hinder antithrombin-dependent FXa inactivation, paradoxically allowing uninhibited FXa to persist in plasma. Because of its inherent catalytic activity, FXa(I16L) is more potent (by >50-fold) in the hemostasis models tested than a noncatalytic antidote that is currently in clinical development. FXa(I16L) also reduces the anticoagulant-associated bleeding in vivo that is induced by the thrombin inhibitor dabigatran. FXa(I16L) may be able to fill an important unmet clinical need for a rapid, pro-hemostatic agent to reverse the effects of several new anticoagulants.
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Registered trials
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.