Question

kohs tcl, lorentz cu, johnson j, et al. development of coagulation factor xii antibodies for inhibiting vascular device-related thrombosis. cell mol bioeng. 2021;14(2):161-175.

Answer 1

Blood coagulation can be triggered by vascular devices including stents, hemodialyzers, and membrane oxygenators; as a result, systemic anticoagulants are frequently needed to prevent specific intravascular thrombotic/embolic events or extracorporeal device failure. Vascular device surface-initiated thrombus development has been demonstrated to be significantly influenced by coagulation factor (F)XII of the contact activation system. Targeting the contact activation system shows promise as a substantially safer method than conventional antithrombotic for avoiding vascular device-associated thrombosis because FXII is not required for hemostasis. Create and describe anti-FXII monoclonal antibodies that block the activation or activity of the enzyme. Methods: In FXII-deficient animals, monoclonal antibodies against FXII were produced, and their binding and anticoagulant abilities were examined in purified plasma systems, whole blood flow-based tests, and an in vitro experiment.

thrombus development caused by a vascular device in a living non-human primate animal. Results: Over 400 candidates were selected from an FXII antibody screen and tested in binding and clotting experiments. Six inhibitor antibodies and one non-inhibitor antibody were chosen for functional test evaluation. The most effective inhibitory antibody, 1B2, has been shown to lengthen clotting durations, inhibit fibrin development on collagen under shear, and inhibit platelet deposition and fibrin formation in an extracorporeal membrane oxygenator used in a non-human primate. Conclusion: Selective contact activation inhibitors have the potential to be helpful research tools as well as secure and efficient thrombosis inhibitors for vascular devices.

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