Pharmacological reduction of coagulation factor XI reduces macrophage accumulation and accelerates deep vein thrombosis resolution in a mouse model of venous thrombosis.

ABSTRACT:

Background

Deep vein thrombosis (DVT) and post-thrombotic syndrome (PTS) remain highly prevalent despite modern medical therapy. Contact activation is a promising target for safe antithrombotic anticoagulation. The anti-factor XI (FXI) monoclonal antibody 14E11 reduces circulating levels of FXI without compromising hemostasis. The human recombinant analog, AB023, is in clinical development. The role of FXI in mediation of inflammation during DVT resolution is unknown.

Objectives

Investigate the effects of pharmacological targeting of FXI with 14E11 in an experimental model of venous thrombosis.

Methods

Adult wild-type CD1 mice were treated with subcutaneous anti-FXI antibody (14E11, 5 mg/kg) versus saline prior to undergoing surgical constriction of the inferior vena

SUBMITTER: Jordan KR 

PROVIDER: S-EPMC9580566 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature