Department of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital, SE-171 76 Stockholm, Sweden; Center of Molecular Medicine, Karolinska University Hospital, SE-171 76 Stockholm, Sweden.
Department of Molecular Medicine and Surgery, Karolinska Institutet and University Hospital, SE-171 76 Stockholm, Sweden; Center of Molecular Medicine, Karolinska University Hospital, SE-171 76 Stockholm, Sweden; Institute of Clinical Chemistry and Laboratory Medicien, University Medical Center Hamburg-Eppendorf, D-20246 Hamburg, Germany.
Drug Discov Today. 2014 Sep;19(9):1459-64. doi: 10.1016/j.drudis.2014.06.024. Epub 2014 Jun 30.
Data from experimental animal models revealed an essential role for factor XII (FXII) in thrombotic occlusive diseases. In contrast to other blood coagulation factors, deficiency in the protease is not associated with abnormal bleeding from injury sites (hemostasis) in patients or in animals. Cumulatively, these findings suggest that FXII could be targeted as a new method of anticoagulation that is devoid of bleeding risks. An FXIIa-neutralizing antibody, 3F7, has been developed that inhibited thrombosis in an extracorporeal membrane oxygenation (ECMO) system as efficiently as heparin. However, in sharp contrast to heparin, 3F7 treatment was not associated with an increase in therapy-associated hemorrhage. In this review, we summarize current knowledge of FXII physiology and pharmacology.
从实验动物模型中获得的数据表明，因子 XII (FXII) 在血栓闭塞性疾病中起着重要作用。与其他凝血因子不同，蛋白酶缺乏症并不会导致患者或动物受伤部位（止血）异常出血。这些发现表明，FXII 可以作为一种新的抗凝方法，避免出血风险。已经开发出一种 FXIIa 中和抗体 3F7，它能像肝素一样有效地抑制体外膜氧合 (ECMO) 系统中的血栓形成。然而，与肝素形成鲜明对比的是，3F7 治疗不会增加与治疗相关的出血。在这篇综述中，我们总结了 FXII 生理学和药理学的最新知识。
