ArticleResearch and practice in thrombosis and haemostasis2026
Factor VIII
Article in Research and practice in thrombosis and haemostasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Personalized Treatment of Hemophilia: Matching Therapies to Patient Needs in a Rapidly Evolving Landscape.Drugs · 2026Review
- Divergent molecular strategies of next-generation activated factor VIII mimetics: insights from a direct comparative analysis.Research and practice in thrombosis and haemostasis · 2026Article
- Mechanism of action and impact on thrombin generation of denecimig (Mim8), emicizumab, and zemocimig (NXT007): comparative analysis using sequence-identical analogs.Research and practice in thrombosis and haemostasis · 2026Article
- Estimating the Factor VIII-Equivalent Activity of Emicizumab Using Global Assays of Haemostasis.Haemophilia : the official journal of the World Federation of Hemophilia · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Denecimig (Mim8, Novo Nordisk A/S) is a next-generation bispecific antibody designed to mimic activated factor (F)VIII and restore hemostasis in persons with hemophilia A. The extent to which activated FVIII mimetics, such as denecimig and emicizumab, can correct clotting deficiency remains unclear. Objectives: To assess the Methods: Thrombin generation was analyzed in severe hemophilia A platelet-poor plasma, spiked with various levels of FVIII or with clinical doses of denecimig (5 μg/mL) or emicizumab (50 μg/mL), using a sequence-identical analog (SIA). TGA used 4 trigger conditions: tissue factor (TF), activated FXI, a combination of TF and activated FXI, or activated FIX. Results: The average FVIII bioequivalence estimate using 1 pM TF trigger was 42 IU/dL (SD, 14) for 5 μg/mL denecimig and 14 IU/dL (SD, 5) for 50 μg/mL emicizumab-SIA using peak thrombin. The FVIII bioequivalence estimates of denecimig and emicizumab-SIA for hemostatic activity were generally highest for endogenous thrombin potential, followed by peak thrombin and velocity index across trigger concentrations. FVIII bioequivalence increased with decreasing trigger concentrations. Denecimig demonstrated a higher thrombin peak in conditions with limited activated FIX compared with emicizumab-SIA, suggesting differences in mechanisms of action. Conclusion: Estimation of denecimig
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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.