ArticleResearch and practice in thrombosis and haemostasis2026
Mechanism and kinetics study of MG1113, an anti-tissue factor pathway inhibitor antibody promoting hemostasis in hemophilia.
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. Not yet cited in PubMed.
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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Targeting tissue factor pathway inhibitor (TFPI) is an emerging hemostatic rebalancing strategy for hemophilia. MG1113 is a humanized monoclonal antibody designed to specifically bind the Kunitz domain (KD)2 of TFPI. Objectives: This study elucidated the detailed pharmacologic mechanism of action and the preclinical hemostatic efficacy of MG1113. Methods: Results: In acquired HA monkeys, a single dose of MG1113 (3 mg/kg) reduced free TFPI levels by 98.8%, shortened the modified prothrombin time and restored thrombin peak height to ∼78% of normal levels. Mechanistically, MG1113 successfully prevented TFPI-mediated inhibition of the extrinsic tenase complex-specifically in the presence of FXa-despite targeting only KD2. MG1113 restored the FXa amplification loop and simultaneously neutralized both plasma-derived TFPI-α and cell-surface TFPI-β. However, despite sufficiently restoring FXa generation, clot waveform analysis revealed that MG1113 exhibited a broader, less intense, and more prolonged coagulation profile compared with the rapid burst characteristic of factor replacement therapy. Conclusion: MG1113 effectively restores hemostasis by blocking the TFPI/FXa interaction. By systematically lowering the threshold for tissue factor-mediated initiation, MG1113 facilitates physiological restoration of hemostasis. This mechanistic profile-combined with gradual clot kinetics and the advantages of a monoclonal antibody-makes MG1113 suited for routine prophylaxis.
Indexed as
Identifiers
What OpenQuestion holds
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.