Upon activation by thrombin(-thrombomodulin) or plasmin, the key-enzymes of the coagulation and fibrinolysis respectively, the zymogen is converted into a potent attenuator of fibrinolysis: carboxypeptidase U (CPU, TAFIa, CPB2). The basic carboxypeptidase zymogen procarboxypeptidase U (proCPU), also known as thrombin-activatable fibrinolysis inhibitor (TAFI), procarboxypeptidase R (proCPR) or plasma procarboxypeptidase B (proCPB), is predominantly synthesized by the liver and secreted into plasma. In this paper, an overview is given of the methods available for measuring proCPU, CPU, and inactivated CPU (CPUi), together with a summary of the clinical data generated so far, ranging from the current knowledge on proCPU concentrations and polymorphisms as potential thromboembolic risk factors to the positioning of different CPU forms (proCPU, CPU, and CPUi) as diagnostic markers for thromboembolic disease, and the potential benefit of pharmacological inhibition of the CPU pathway. Furthermore, extensive research has been conducted on the in vivo role of CPU in (the acute phase of) thromboembolic disease, as well as on the hypothesis that high proCPU levels and the Thr/Ile325 polymorphism may cause a thrombotic predisposition. As CPU forms a molecular link between coagulation and fibrinolysis, the development of CPU inhibitors as profibrinolytic agents constitutes an attractive new concept to improve endogenous fibrinolysis or to increase the efficacy of thrombolytic therapy in thromboembolic diseases. Procarboxypeptidase U (proCPU, TAFI, proCPB2) is a basic carboxypeptidase zymogen that is converted by thrombin(-thrombomodulin) or plasmin into the active carboxypeptidase U (CPU, TAFIa, CPB2), a potent attenuator of fibrinolysis.

Cpu models created by cpusim