Possibility of Using Asundexian, a Factor XI Inhibitor, to Prevent Stroke in Patients with Atrial Fibrillation
|
Reviewed by Dat Tien Nguyen, B.A, ScM.
Translated by Nhi Phuong Quynh Le, B.A |
Posted on February 05th, 2025
|
The irregular cardiac muscle contractions in patients with atrial fibrillation increase the risk of blood clot formation, which, in turn, raises the likelihood of stroke. While the condition can typically be managed with anticoagulants, individuals at higher risk of bleeding are unable to use this form of treatment, creating a need for alternative therapies. A recent article published in the New England Journal of Medicine explored the use of asundexian, a factor XI inhibitor, to prevent stroke in patients with atrial fibrillation.
The phase 3 clinical trial involved 14,810 participants with an average age of 73.9 years, all diagnosed with atrial fibrillation. The participants were randomly assigned to receive either 50 mg of asundexian daily or the standard regimen of 5 mg of apixaban twice daily. Asundexian works by binding to and inhibiting the activated form of factor XI, which plays a role in amplifying the clotting pathway triggered by vascular endothelial damage. Since it does not affect the extrinsic clotting cascade, individuals with factor XI deficiency have a lower risk of spontaneous bleeding and hematoma formation. The researchers found that patients treated with asundexian had a significantly higher risk of stroke and systemic embolism compared to those receiving the standard anticoagulant, apixaban, which resulted in an early termination of the study. The researchers hypothesized that the 50-mg dose of asundexian tested in the trial may not be sufficient to prevent thrombosis.
The phase 3 clinical trial involved 14,810 participants with an average age of 73.9 years, all diagnosed with atrial fibrillation. The participants were randomly assigned to receive either 50 mg of asundexian daily or the standard regimen of 5 mg of apixaban twice daily. Asundexian works by binding to and inhibiting the activated form of factor XI, which plays a role in amplifying the clotting pathway triggered by vascular endothelial damage. Since it does not affect the extrinsic clotting cascade, individuals with factor XI deficiency have a lower risk of spontaneous bleeding and hematoma formation. The researchers found that patients treated with asundexian had a significantly higher risk of stroke and systemic embolism compared to those receiving the standard anticoagulant, apixaban, which resulted in an early termination of the study. The researchers hypothesized that the 50-mg dose of asundexian tested in the trial may not be sufficient to prevent thrombosis.