|1.||Berioli, S: 2 articles (12/2001 - 01/2001)|
|2.||Fox, N L: 2 articles (12/2001 - 01/2001)|
|3.||Gibson, C M: 2 articles (09/2001 - 01/2001)|
|4.||Jain, R K: 1 article (07/2013)|
|5.||Sathyamurthy, I: 1 article (07/2013)|
|6.||Nair, T: 1 article (07/2013)|
|7.||Jadhav, U: 1 article (07/2013)|
|8.||Hiremath, J S: 1 article (07/2013)|
|9.||Kumbla, D: 1 article (07/2013)|
|10.||Iyengar, S S: 1 article (07/2013)|
12/01/2001 - "In the Assessment of the Safety and Efficacy of a New Thrombolytic (ASSENT)-2 trial, 16 949 patients with acute myocardial infarction were randomly assigned a single weight-adjusted bolus of TNK-tPA or a 90-min infusion of rt-PA. "
01/01/2001 - "TNK-tPA was evaluated in 4214 patients in two dose-ranging trials (Thrombolysis in Myocardial Infarction [TIMI] 10B and Assessment of the Safety and Efficacy of a New Thrombolytic Agent [ASSENT] I). "
01/21/1997 - "The thrombolysis in Myocardial Infarction (TIMI) 10A trial was a Phase 1, dose-ranging pilot trial designed to evaluate the pharmacokinetics, safety, and efficacy of TNK-TPA in patients with acute myocardial infarction. "
01/21/1997 - "One hundred thirteen patients with acute ST-segment elevation myocardial infarction presenting within 12 hours and without contraindications to thrombolysis were enrolled and treated with a single bolus of TNK-TPA over 5 to 10 seconds with doses ranging from 5 to 50 mg. TNK-TPA demonstrated a plasma clearance of 151 +/- 55 mL/min and a half-life of 17 +/- 7 minutes. "
09/01/2001 - "Furthermore, the results of TNK-tPA clinical trials showed that even at the highest weight-optimized dosage of 50 mg, ICH rates were among the lowest reported in clinical trials of thrombolytics for acute myocardial infarction. "
12/01/2004 - "These data suggest that the combination of IV 7E3 F(ab')2 (4 hours) and IA TNK-tPA (6 hours) extends the therapeutic window of thrombolysis to 6 hours after stroke."
12/01/2004 - "Rats subjected to embolic stroke were treated with IV 7E3 F(ab')2 (6 mg/kg) in combination with IA or IV TNK-tPA (5 mg/kg) at 4 and 6 hours after onset of stroke, respectively; IA TNK-tPA (5 mg/kg) alone at 6 hours after onset of stroke; or saline at 6 hours after onset of stroke. "
09/29/2000 - "Postischemic intracarotid treatment with TNK-tPA reduces infarct volume and improves neurological deficits in embolic stroke in the unanesthetized rat."
05/01/1999 - "No strokes occurred in the 73 patients treated with 50 mg TNK-tPA. "
09/29/2000 - "TNK-tPA (1.5 mg/kg) was administered intraarterially via the catheter at either 2 h or 4 h after stroke. "
|3.||Body Weight (Weight, Body)
11/01/1999 - "Thus, higher doses per unit body weight of TNK-tPA result in not only faster culprit artery flow, but also faster nonculprit, global, and post-PTCA flow, which may reflect earlier opening, reduced stunning, or improved microvascular function. "
11/01/1999 - "We hypothesized that higher doses of TNK-tissue plasminogen activator (tPA) per unit body weight would be related to improved flow at 90 minutes after thrombolytic administration. "
09/01/2001 - "However, data from TNK-tPA clinical trials suggest that body weight estimates can err by up to 20 kg (44 lb) without an increased risk of ICH or death. "
09/01/2001 - "In elderly female patients of low body weight, the use of weight-optimized TNK-tPA lowered the risk of ICH compared with the use of t-PA, expanding the potential use of thrombolytics to this high-risk patient population. "
09/01/2001 - "Weight-optimized TNK-tPA dosing requires body weight estimation, which may introduce the potential for medication error. "
09/29/2000 - "This study demonstrates that intraarterial administration of TNK-tPA at 2 h of ischemia in the unanesthesthetized rat is effective in reducing neurological deficits and ischemic lesion volume without increasing hemorrhagic transformation and that administration of TNK-tPA at 4 h of ischemia does not increase the incidence of hemorrhagic transformation."
12/01/2004 - "The combination of IV 7E3 F(ab')2 (4 hours) and IA TNK-tPA (6 hours) significantly (P<0.05) reduced infarct volume and improved neurological functional deficits, which was associated with significant (P<0.05) reductions in the size of embolus at the origin of the occluded middle cerebral artery and in down-stream microvascular platelet and fibrin deposition, and enhanced microvascular patency compared with saline-treated rats. "
|3.||Tissue Plasminogen Activator (Alteplase)
|6.||disufenton sodium (NXY 059)
|8.||TNK-tissue plasminogen activator
|9.||MB Form Creatine Kinase
|3.||Medication Errors (Medication Error)