Recombinant activated factor VII (rFVIIa) was initially developed to treat bleeding episodes in patients with congenital haemophilia and inhibitors. The story of its development began in the 1970s, when FVIIa was identified as one of the activated coagulation factors that has minimal potential for inducing thromboembolic side-effects. Extensive research over the last 30 years has greatly increased our knowledge of the characteristics of FVII, its activation, and the mechanisms by which rFVIIa restores haemostasis. In haemophilia, the haemostatic effect of rFVIIa is mediated via binding to thrombin-activated platelets at the site of injury, thereby enhancing thrombin generation also in the absence of factor (F) VIII or FIX. The mechanism of action of rFVIIa has also allowed its successful use in other clinical scenarios characterised by impaired thrombin generation, and its licensed uses have now been extended to acquired haemophilia, congenital FVII deficiency and Glanzmann's thrombasthenia.

中文翻译：

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重组活化因子VII：30年的研究和创新。

重组活化因子VII（rFVIIa）最初被开发用于治疗先天性血友病和抑制剂患者的出血发作。它的发展始于1970年代，当时FVIIa被认为是活化凝血因子之一，具有最小的诱发血栓栓塞副作用的潜力。在过去的30年中，广泛的研究极大地增加了我们对FVII的特征，其激活以及rFVIIa恢复止血的机制的认识。在血友病中，rFVIIa的止血作用是通过与损伤部位的凝血酶活化血小板结合而介导的，从而在不存在因子（F）VIII或FIX的情况下也增强了凝血酶的产生。