Disease relevance of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• There were no significant differences in the rates of major bleeding complications or transfusions, but tirofiban was associated with a lower rate of minor bleeding episodes and thrombocytopenia [1].
• Tirofiban in unstable coronary disease [2].
• The Thrombolysis In Myocardial Infarction (TIMI) major hemorrhage rate was 1.5% for enoxaparin versus 1.3% for UFH (odds ratio 1.16 [95% CI 0.44 to 3.02]) and 1.8% versus 1% for tirofiban versus placebo (odds ratio 1.82 [95% CI 0.67 to 4.95]) [3].
• All patients received an initial bolus (10 microg/kg body weight over 3 min), followed by a 36-h infusion (0.15 microg/kg per min) of either tirofiban or placebo [4].
• In the acute coronary syndromes without ST segment elevation, absolute 1.5% to 3.2% reductions in 30-day rates of death or myocardial (re-) infarction have been achieved with two to four day courses of eptifibatide or tirofiban [5].

Psychiatry related information on L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• Seventy of these lesions were in the standard therapy group and 58 in the tirofiban group [6].

High impact information on L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• The same effect was observed when normal platelets were pretreated with the commercially available anti-alpha IIb beta 3 drugs abciximab, eptifibatide, or tirofiban [7].
• We studied 9 patients who developed severe thrombocytopenia (platelets less than 25 x 10(9)/L) within several hours of treatment with the GPIIb/IIIa inhibitors tirofiban (4 patients) and eptifibatide (5 patients) [8].
• Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80% [9].
• METHODS: Outcomes among 4,809 patients randomized to tirofiban or abciximab during PCI with stent placement were compared according to whether they received 300 mg of clopidogrel before PCI (93.1%) versus immediately after the procedure [10].
• METHODS: Sixty patients undergoing coronary stenting were randomly assigned to abciximab (bolus 0.25 mg/kg body weight, infusion 10 microg per min for 12 h), tirofiban (bolus 10 microg/kg, infusion 0.15 microg/kg per min for 72 h) or eptifibatide (bolus 180 microg/kg, infusion 2 microg/kg per min for 72 h) [11].

Chemical compound and disease context of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• The findings indicate that acute thrombocytopenia after the administration of tirofiban or eptifibatide can be caused by drug-dependent antibodies that are "naturally occurring" or are induced by prior exposure to drug [8].
• An in-vitro model to study device-induced thrombosis and embolism: evaluation of the efficacy of tirofiban, aspirin, and dipyridamole [12].
• We sought to determine the efficacy and safety of single high-dose bolus (HDB) tirofiban with high-dose clopidogrel loading in primary PCI in acute ST elevation myocardial infarction [13].
• The Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy (TACTICS) Thrombolysis in Myocardial Infarction (TIMI)-18 Trial treated all patients with upstream intravenous tirofiban and heparin for 48 hours or until revascularization, and randomized subjects to an invasive or conservative approach [14].
• Images in Cardiovscular Medicine. Tirofiban for cocaine-induced coronary artery thrombosis: a novel therapeutic approach [15].

Biological context of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• FK419 and tirofiban similarly inhibited platelet aggregation in vitro (IC50 values: 0.43+/-0.076 and 0.41+/-0.053 micromol/L) and dispersed aggregated platelets (EC50 values: 2.3+/-0.88 and 2.0+/-0.81 micromol/L) [16].
• Sedimentation equilibrium demonstrated that both echistatin ligands induced substantial alphaIIbbeta3 dimerization. van't Hoff analysis revealed a pattern of entropy/enthalpy compensation similar to tirofiban, a small RGD ligand-mimetic that binds tightly to alphaIIbbeta3, but yields smaller conformational perturbations than echistatin [17].
• Tirofiban prolonged bleeding time both in period 1 and in period 2 [18].
• Effect of fibrinogen concentration and platelet count on the inhibitory effect of abciximab and tirofiban [19].
• This review updates what is known about the pharmacokinetics of tirofiban in humans, especially in comparison with the monoclonal antibody against the IIb/IIIa receptor, abciximab [20].

Anatomical context of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• When FK419 or tirofiban were administered after photochemically induced middle cerebral artery (MCA) occlusion in guinea-pigs, they dose-dependently improved MCA patency [16].
• FK419 inhibited retention of platelets and neutrophils in a collagen-coated bead column with greater potency than tirofiban (IC50 values of 0.90+/-0.133 and 2.4+/-0.21 micromol/L for platelet retention and 0.32+/-0.078 and 0.57+/-0.180 micromol/L for neutrophil retention) [16].
• Tirofiban reduced platelet adhesion (23+/-4/field vs. 61+/-2/field in wild-type hearts) and leukocyte recruitment (34+/-2/field), improving LVDP (63+/-4 mmHg) [21].
• In four patients with acute basilar artery thrombosis, complete arterial recanalization and good neurologic outcome were achieved with a treatment combining alteplase with tirofiban [22].
• Treatment of acute central retinal artery occlusionwith the platelet glycoprotein IIb/IIIa receptor inhibitor tirofiban [23].

Associations of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)- with other chemical compounds

• Randomized, double-blind, placebo-controlled dose-ranging study of tirofiban (MK-383) platelet IIb/IIIa blockade in high risk patients undergoing coronary angioplasty [24].
• In an open pilot study, the authors tested whether the nonpeptide glycoprotein (GP) IIb/IIIa antagonist tirofiban, a highly effective and selective blocker of platelet aggregation, prevents the transition of ischemic brain tissue into the infarct proper as defined by MRI (perfusion-weighted/T2-weighted) in patients with acute ischemic stroke [25].
• A similar pattern of benefit has emerged from clinical trials of such other GP IIb/IIIa inhibitors as eptifibatide, lamifiban, and tirofiban [26].
• Ticlopidine administration did not alter the pharmacokinetics of tirofiban [18].
• RESULTS: High-dose tirofiban completely prevents platelet loss during cardiopulmonary bypass. beta-Thromboglobulin release and sensitivity to adenosine diphosphate are significantly less than control at the end of bypass in all tirofiban groups [27].

Gene context of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• Platelet function was assessed before, during, and after tirofiban infusion using a panel of agonists for ADP receptors, PAR1 and PAR4 thrombin receptors, and collagen receptors [28].
• The aim of the present in-vitro-investigation was to elucidate the impact of ABO blood group dependent vWF concentrations on tirofiban mediated inhibition of GPIIb/IIIa function [29].
• Eptifibatide and 7E3, but not tirofiban, inhibit alpha(v)beta(3) integrin-mediated binding of smooth muscle cells to thrombospondin and prothrombin [30].
• Thus, the application of tirofiban together with hDAF improves the performance of pig hearts by reducing myocardial damage and intravascular thrombosis [31].
• In vitro testing of the GPIIb/IIIa blocking by a nonpeptidic analogue tirofiban and abciximab revealed a good correlation between the CPA test and the routine aggregometry [32].

Analytical, diagnostic and therapeutic context of L-Tyrosine, N-(butylsulfonyl)-O-(4-(4-piperidinyl)butyl)-

• CONCLUSIONS: Despite differences between women and men in baseline characteristics, the benefit of an early invasive strategy incorporating tirofiban and intracoronary stents was similar in women and men and was enhanced in women presenting with markers of increased risk [33].
• The volume of the platelet thrombi, which was 3,352 +/- 1,045 microm(3) before starting the second perfusion, was reduced to 778 +/- 102 microm(3), 812 +/- 122 microm(3), and 856 +/- 144 microm(3) after 6-min perfusion of blood containing abciximab, eptifibatide, and tirofiban, respectively [34].
• Patients with STEMI ineligible for reperfusion were randomized to enoxaparin, enoxaparin plus tirofiban, UFH, or UFH plus tirofiban [3].
• BACKGROUND: The use of HDB tirofiban in the catheterization laboratory is controversial [35].
• Flow cytometry revealed that the reduction in the monocyte-platelet interaction by abciximab, tirofiban and eptifibatide was not significantly different (20.0 +/- 21.9%, 23.8 +/- 18.2% and 21.0 +/- 19.8%, respectively; p = 0.87) [11].

References