Ciraparantag, an anticoagulant reversal agent, is a small molecule specifically designed to bind non-covalently by charge-charge interaction to unfractionated heparin (UFH) and low molecular weight heparin (LMWH). It shows similar binding characteristics to the direct oral anticoagulants (DOAC). Dynamic light scattering methodology was used to demonstrate ciraparantag binding to the heparins and DOACs and its lack of binding to a variety of proteins including coagulation factors and to commonly used drugs. Ciraparantag reaches maximum concentration within minutes following intravenous (IV) administration with a half-life of 12 - 19 minutes. It is primarily hydrolyzed by serum peptidases into two metabolites, neither of which has substantial activity. Ciraparantag and its metabolites are recovered almost entirely in the urine. In animal models of bleeding (rat tail transection and liver laceration) a single IV dose of ciraparantag given at peak concentrations of the anticoagulant, but before the bleeding injury, significantly reduces the amount of blood loss. Ciraparantag given after the bleeding injury also significantly reduces blood loss. Ciraparantag appears to have substantial ability to reduce blood loss in animal models given a variety of anticoagulants and has potential as a useful DOAC reversal agent.