EC Number   |
Application |
Reference |
|---|
   3.4.21.68 | diagnostics |
alterations in tPA activity levels can be used as a biomarker for perturbations in brain homeostasis |
-, 718064 |
| 3.4.21.68 | drug development |
antifibrinolytic agents may be useful for protecting neurons when tPA-mediated damage is anticipated |
695293 |
| 3.4.21.68 | drug development |
both TPA-antibiotic locks and heparin-antibiotic locks used in conjunction with systemic antibiotics can effectively clear catheter-related bacteraemia in children without significant late recurrence at 6 weeks. The mean infection-free survival of the catheters following TPA-antibiotic locks treatment is shorter than that following heparinantibiotic locks treatment, but is not statistically significant |
700404 |
| 3.4.21.68 | drug development |
neutrophils are good candidates to be the main source of metalloproteinase-9 following t-PA stroke treatment and in consequence, are partially responsible for thrombolysis-related brain bleedings. Combined therapy of t-PA with a metalloproteinase-9 or a neutrophil degranulation inhibitor may improve safety and efficacy of thrombolytic therapy in the acute phase of stroke |
699407 |
| 3.4.21.68 | medicine |
although rtPA enhances ischemic damage, the dose of recombinant tPA used in clinics does not affect the powerful neuroprotection by the JNK inhibitor XG-102 |
697246 |
| 3.4.21.68 | medicine |
combining antithrombin III, R-TPA and supportive care is more advantageous in treating the clinical manifestations of disseminated intravascular coagulation in this neonatal pig model than either single modality or supportive care alone |
684083 |
| 3.4.21.68 | medicine |
desmoteplase has additional advantages to human tPA, it is not neurotoxic and is unaffected by beta-amyloid. Desmoteplase antagonizes the neurotoxicity induced by vascular tPA possibly by competing with tPA for the low-density lipoprotein receptorrelated protein-1 binding at the BBB and thus preventing tPA access to the brain parenchyma. A phase III clinical trial of desmoteplase is halted since it has failed to demonstrate any beneficial effects in terms of neurological improvements and survival |
697441 |
| 3.4.21.68 | medicine |
dogs with femoral artery thrombosis are given either M5, a single site mutant of prourkinase or tPA by i.v. infusion. Thrombolysis is comparably effective by both activators. Blood loss is 10-fold higher with t-PA than with M5 and occurred at more multiple sites. This effect is postulated to be related to differences in the mechanism of plasminogen activation by t-PA and M5 in which the latter is promoted by degraded rather than intact (hemostatic) fibrin |
683822 |
| 3.4.21.68 | medicine |
effects of intravenous administration of tPA on serum levels of IGF-1 and IGF-binding protein-3 in patients with acute ischemic stroke are investigated by radioimmunoassay in 10 patients. During tPA treatment, total IGF-1 and IGFBP-3 serum levels do not change, but there was an 70% increase in free IGF-1 serum levels at the end of the 1-h infusion. Intravenous therapy with tPA enhances the bioavailability of IGF-1 |
684067 |
| 3.4.21.68 | medicine |
enzyme has important thrombolytic properties due to its high fibrin affinity, it is approved for treating acute myocardial infarction, or heart attacks, and later for acute ischemic stroke, and acute, massive pulmonary embolism |
707127 |
