Fitzpatrick Ella K, Fredenburgh James C, Weitz Jeffrey I
Thrombosis and Atherosclerosis Research Institute and Hamilton Health Sciences, Hamilton, Ontario, Canada; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
Thrombosis and Atherosclerosis Research Institute and Hamilton Health Sciences, Hamilton, Ontario, Canada; Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
J Thromb Haemost. 2025 Sep;23(9):2830-2836. doi: 10.1016/j.jtha.2025.05.032. Epub 2025 Jun 6.
Asundexian and milvexian are small-molecule factor (F)XIa inhibitors, whereas abelacimab is an antibody that binds FXI and blocks its activation and activity. All 3 FXI inhibitors are currently undergoing phase 3 evaluation. Similar to heparin and dabigatran, asundexian, milvexian, and abelacimab prolong the activated partial thromboplastin time (APTT) in a concentration-dependent manner. DOAC-Stop (DS) is an activated charcoal-based compound that adsorbs direct oral anticoagulants such as dabigatran, but not heparin, from plasma. It is unknown whether DS also neutralizes asundexian and milvexian.
This study aimed to determine whether DS reverses the prolongation of the APTT caused by asundexian or milvexian. Dabigatran was used as a positive control, while abelacimab and heparin served as negative controls.
The APTT in human plasma, with or without asundexian, milvexian, abelacimab, dabigatran, or heparin, was determined before and after DS treatment.
As expected, all drugs produced concentration-dependent prolongation of the APTT. DS returned the APTT to baseline values with asundexian, milvexian, and dabigatran, but not with abelacimab or heparin. The APTT was prolonged in a more than additive manner with the combination of 2.5 μM milvexian and 0.125 U/mL heparin. However, DS reversed only the APTT prolongation induced by milvexian, but not that by heparin.
DS reverses the effect of asundexian and milvexian on the APTT and distinguishes between the APTT effects of milvexian and heparin.
阿孙西单抗和米尔维单抗是小分子因子(F)XIa抑制剂,而阿贝西单抗是一种结合FXI并阻断其激活和活性的抗体。目前,这三种FXI抑制剂均在进行3期评估。与肝素和达比加群类似,阿孙西单抗、米尔维单抗和阿贝西单抗以浓度依赖性方式延长活化部分凝血活酶时间(APTT)。DOAC-Stop(DS)是一种基于活性炭的化合物,可从血浆中吸附达比加群等直接口服抗凝剂,但不能吸附肝素。尚不清楚DS是否也能中和阿孙西单抗和米尔维单抗。
本研究旨在确定DS是否能逆转阿孙西单抗或米尔维单抗引起的APTT延长。达比加群用作阳性对照,阿贝西单抗和肝素用作阴性对照。
在DS治疗前后,测定添加或未添加阿孙西单抗、米尔维单抗、阿贝西单抗、达比加群或肝素的人血浆中的APTT。
正如预期的那样,所有药物均使APTT呈浓度依赖性延长。DS使阿孙西单抗、米尔维单抗和达比加群处理后的APTT恢复到基线值,但对阿贝西单抗或肝素处理后的APTT无此作用。2.5 μM米尔维单抗和0.125 U/mL肝素联合使用时,APTT延长超过相加效应。然而,DS仅逆转了米尔维单抗诱导引起的APTT延长,而未逆转肝素诱导引起的APTT延长。
DS可逆转阿孙西单抗和米尔维单抗对APTT的影响,并区分米尔维单抗和肝素对APTT的影响。