9 By binding to DOACs and heparin via non-covalent hydrogen bonds and charge–charge interactions, ciraparantag reverses their anticoagulant effects by displacing them from FXa and thrombin. 8 Therefore, there remains a need for effective and relatively low-cost reversal agents for oral FXa inhibitors.Ĭiraparantag, a small water-soluble synthetic molecule, has the potential to fill this gap (see Table 1). Instead, four-factor prothrombin complex concentrate (PCC) is often used for urgent reversal of apixaban or rivaroxaban based on data from cohort studies suggesting that it is effective. 6 However, andexanet is not approved in Canada and the UK, is only available in ∼12% of hospitals in the USA, 7 and enthusiasm for its use is limited by its high cost.

5 Andexanet, a recombinant FXa variant, is licensed in Europe and the USA for reversal of apixaban and rivaroxaban. Idarucizumab, an antibody fragment that binds dabigatran with high affinity, is widely available for rapid dabigatran reversal. Consequently, agents that rapidly reverse the anticoagulant effects of the DOACs could streamline management and improve outcomes of patients presenting with serious bleeding or requiring urgent interventions or surgery. 4 Although the DOACs are associated with less serious bleeding than VKAs, particularly less intracranial haemorrhage, bleeding remains the major side effect of the DOACs. 1–3 Of the DOACs, apixaban and rivaroxaban are the most widely used.

Use of the DOACs increased when guidelines gave preference to them over vitamin K antagonists (VKAs) such as warfarin for stroke prevention in patients with non-valvular atrial fibrillation and for treatment of venous thrombo-embolism.

Ciraparantag binds to apixaban, edoxaban, enoxaparin, and rivaroxaban and reverses their anticoagulant activity.ĭirect oral anticoagulants (DOACs) include dabigatran, which inhibits thrombin, and apixaban, edoxaban, and rivaroxaban, which inhibit factor Xa (FXa).

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