Kouns W C, Kirchhofer D, Hadváry P, Edenhofer A, Weller T, Pfenninger G, Baumgartner H R, Jennings L K, Steiner B
Pharma Division, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Blood. 1992 Nov 15;80(10):2539-47.
Platelet glycoprotein (GP) IIb-IIIa inhibitors may become useful antithrombotic agents. Ro 43-5054 is a low molecular weight, noncyclic, peptidomimetic inhibitor that is three orders of magnitude more potent than RGDS in inhibiting fibrinogen binding to purified GPIIb-IIIa and in preventing platelet aggregation. Comparisons of RGDS and Ro 43-5054 in cell adhesion assays showed that, in contrast to RGDS, Ro 43-5054 was highly selective GPIIb-IIIa inhibitor. Effects of RGDV and Ro 43-5054 on the conformation and activation state of GPIIb-IIIa were also examined. RGDV and Ro 43-5054 induced conformational changes in purified inactive GPIIb-IIIa as determined by binding of the monoclonal antibody D3GP3 (D3). These conformational alterations were not reversed after inhibitor removal, as indicated by the continued exposure of the D3 epitope and a newly acquired ability to bind fibrinogen. Similarly, RGDV and Ro 43-5054 induced conformational changes in GPIIb-IIIa on the intact platelet. However, after removal of the inhibitors, exposure of the D3 epitope was fully reversed and the platelets did not aggregate in the absence of agonist. Thus, while RGD(X) peptides and Ro 43-5054 transformed purified inactive GPIIb-IIIa into an irreversibly activated conformer, the effects of these inhibitors were reversible on the intact platelet. This suggests that factors present in the platelet membrane or cytoplasm may regulate in part the ability of the complex to shift between active and inactive conformers.
血小板糖蛋白(GP)IIb-IIIa抑制剂可能会成为有用的抗血栓形成药物。Ro 43-5054是一种低分子量、非环状的拟肽类抑制剂,在抑制纤维蛋白原与纯化的GPIIb-IIIa结合以及防止血小板聚集方面,其效力比RGDS强三个数量级。在细胞黏附试验中对RGDS和Ro 43-5054进行比较,结果显示,与RGDS不同,Ro 43-5054是一种高度选择性的GPIIb-IIIa抑制剂。还研究了RGDV和Ro 43-5054对GPIIb-IIIa构象和活化状态的影响。如通过单克隆抗体D3GP3(D3)的结合所测定,RGDV和Ro 43-5054可诱导纯化的无活性GPIIb-IIIa发生构象变化。抑制剂去除后,这些构象改变并未逆转,这表现为D3表位持续暴露以及新获得的结合纤维蛋白原的能力。同样,RGDV和Ro 43-5054可诱导完整血小板上的GPIIb-IIIa发生构象变化。然而,去除抑制剂后,D3表位的暴露完全逆转,并且在没有激动剂的情况下血小板不会聚集。因此,虽然RGD(X)肽和Ro 43-5054可将纯化的无活性GPIIb-IIIa转化为不可逆活化的构象体,但这些抑制剂对完整血小板的作用是可逆的。这表明血小板膜或细胞质中存在的因子可能部分调节该复合物在活性和非活性构象体之间转换的能力。