Anti-TFPI for hemostasis induction in patients with rare bleeding disorders, an ex vivo thrombin generation (TG) guided pilot study.


Journal

Blood cells, molecules & diseases
ISSN: 1096-0961
Titre abrégé: Blood Cells Mol Dis
Pays: United States
ID NLM: 9509932

Informations de publication

Date de publication:
07 2022
Historique:
received: 06 03 2022
revised: 07 04 2022
accepted: 08 04 2022
pubmed: 8 5 2022
medline: 25 5 2022
entrez: 7 5 2022
Statut: ppublish

Résumé

Rare bleeding disorders (RBD) are inherited coagulopathies, whose hemostatic control is based upon replacement therapy. Marstacimab (PF-06741086) is a human monoclonal IgG that targets the Kunitz2 domain of tissue factor pathway inhibitor [TFPI]. Marstacimab is currently in development for bleeding prophylaxis in patients with hemophilia. To assess the potential impact of Marstacimab upon thrombin generation (TG) in RBD patients' plasma samples. Our cohort included 18 RBD patients, with severe deficiencies: 5 Von Willebrand Disease (VWD) type 3, 4 FVII, 3 FXI, 2 FXIII deficiency and 1 patient with: FX, FV + FVIII, Fibrinogen, combined vitamin K dependent factors' deficiency. Citrated samples from RBD patients were collected and spiked with Marstacimab, TG was measured by calibrated automated thrombogram. Among all patients a reduced baseline TG was observed as compared to controls. Improvement of median (lag time, peak and ETP was observed in Marstacimab spiked samples from 8 min, 99 nM, 1116 nMx min to 5.5 min, 194 nM,1614 nMx min, respectively. None of the values measured among RBD patients exceeded normal controls. These in vitro data suggest that Marstacimab may serve as a promising approach for restoring the hemostatic balance in various RBD, though potential clinical implications should be further investigated.

Sections du résumé

BACKGROUND
Rare bleeding disorders (RBD) are inherited coagulopathies, whose hemostatic control is based upon replacement therapy. Marstacimab (PF-06741086) is a human monoclonal IgG that targets the Kunitz2 domain of tissue factor pathway inhibitor [TFPI]. Marstacimab is currently in development for bleeding prophylaxis in patients with hemophilia.
OBJECTIVES
To assess the potential impact of Marstacimab upon thrombin generation (TG) in RBD patients' plasma samples.
RESULTS
Our cohort included 18 RBD patients, with severe deficiencies: 5 Von Willebrand Disease (VWD) type 3, 4 FVII, 3 FXI, 2 FXIII deficiency and 1 patient with: FX, FV + FVIII, Fibrinogen, combined vitamin K dependent factors' deficiency. Citrated samples from RBD patients were collected and spiked with Marstacimab, TG was measured by calibrated automated thrombogram. Among all patients a reduced baseline TG was observed as compared to controls. Improvement of median (lag time, peak and ETP was observed in Marstacimab spiked samples from 8 min, 99 nM, 1116 nMx min to 5.5 min, 194 nM,1614 nMx min, respectively. None of the values measured among RBD patients exceeded normal controls.
CONCLUSION
These in vitro data suggest that Marstacimab may serve as a promising approach for restoring the hemostatic balance in various RBD, though potential clinical implications should be further investigated.

Identifiants

pubmed: 35525014
pii: S1079-9796(22)00020-1
doi: 10.1016/j.bcmd.2022.102663
pii:
doi:

Substances chimiques

Hemostatics 0
Lipoproteins 0
lipoprotein-associated coagulation inhibitor 0
Thrombin EC 3.4.21.5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

102663

Informations de copyright

Copyright © 2022. Published by Elsevier Inc.

Auteurs

Assaf A Barg (AA)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Tami Brutman-Barazani (T)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Einat Avishai (E)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Ivan Budnik (I)

Department of Pathophysiology, Sechenov First Moscow State Medical University (Sechenov University), Russia.

Omri Cohen (O)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Rima Dardik (R)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Sarina Levy-Mendelovich (S)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Tami Livnat (T)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel.

Gili Kenet (G)

National Hemophilia Center, Sheba Medical Center, Tel Hashomer, Israel; Amalia Biron Research Institute of Thrombosis and Hemostasis, Sackler School of Medicine, Tel Aviv University, Israel. Electronic address: gili.kenet@sheba.health.gov.il.

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Classifications MeSH