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Chemical Compound Review

AC1L5AAB     2-[4-[4-(4- carbamimidoylphenyl)piperazin- 1...

Synonyms: MDDR 199187, GR144053, GR 144053, GR 144053F
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Disease relevance of 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid


High impact information on 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid

  • METHODS AND RESULTS: Three GP IIb/IIIa antagonists, eptifibatide, MK-0852, and GR144053, were compared in PRP (turbidimetry) and whole blood (platelet counting with an Ultra-Flo 100 Platelet Counter), with ADP and collagen used as agonists [3].
  • However, when GR144053 was injected in tPA -/- mice, the most significant changes were observed: that is the estimated ED50 was 14.8 times higher than the one in tPA +/+ mice [4].
  • Comparative antiplatelet effects of aspirin, vapiprost and GR144053, a GPIIb/IIIa antagonist, with a special reference to the role of platelet microaggregates [5].
  • Many more small aggregates were still formed when the highest dose of aspirin or vapiprost was used as compared with that of GR144053, although suppression of the platelet aggregation using the OD method, prolongation of the occlusion time and the bleeding time were quite similar [5].
  • When DX-9065a, a selective factor Xa inhibitor, or GR144053, a platelet glycoprotein (GP) complex IIb/IIIa antagonist was applied, the time required to occlusion was prolonged in a dose-dependent manner in all types of mice [6].

Chemical compound and disease context of 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid

  • The present study compared the antithrombotic properties of fractionated aurin tricarboxylic acid (ATA), an inhibitor of platelet glycoprotein (GP) Ib, and GR144053, a GPIIb/IIIa antagonist, in a hamster model of stenosis [1].

Biological context of 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid

  • 3. When the administration of GR144053 (1.0 mg kg-1 per hour) via an implanted osmotic pump was started 30 min before the injury and continued for the next 2 weeks, no suppression of neointima formation was observed, although platelet aggregation evoked ex vivo by adenosine diphosphate (ADP) at the end of treatment period was efficiently inhibited [7].
  • The bleeding time at the end of tPA infusion was significantly prolonged in the presence of the highest dose of GR144053 [2].
  • These findings suggest that GR144053 inhibits platelet activation on the injured artery and improves vascular patency after thrombolysis with tPA, which furthermore results in suppression of neointima formation [2].
  • In this study, SR 121566 exhibited a potent dose-dependent inhibition of adenosine diphosphate (ADP)-induced aggregation of rabbit platelets in vitro [median inhibitory concentration (IC50), 0.8 +/- 0.04 microM], whereas the GP IIb/IIIa antagonists SC 52012A and GR 144053F were devoid of antiplatelet activity [8].

Anatomical context of 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid


Associations of 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid with other chemical compounds

  • Compared with hirudin, citrate enhanced the potency of eptifibatide by up to 4-fold in both PRP and whole blood (P<0.0005), modestly enhanced MK-0852 potency (P=0.001), and had no effect on GR144053 [3].

Analytical, diagnostic and therapeutic context of 2-[4-[4-(4-carbamimidoylphenyl)piperazin-1-yl]-1-piperidyl]acetic acid

  • In conclusion, both inhibition of platelet activation by ATA or GR144053 prevent arterial thrombosis and enhance the thrombolytic effect of tPA, but GR144053 was more protective in its antithrombotic effect and more effective during thrombolytic therapy than ATA [1].
  • When GR144053 (0.3 and 1.0 mg/kg/h) was infused in addition to tPA, the incidence of reperfusion and the later patency of the reperfused artery were much improved as compared with tPA alone [2].


  1. Comparison of the antithrombotic effects and bleeding risk of fractionated aurin tricarboxylic acid and the GPIIb/IIIa antagonist GR144053 in a hamster model of stenosis. Ito, T., Matsuno, H., Kozawa, O., Niwa, M., Sakai, N., Uematsu, T. Thromb. Res. (1999) [Pubmed]
  2. Effect of GR144053, a fibrinogen-receptor antagonist, on thrombus formation and vascular patency after thrombolysis by tPA in the injured carotid artery of the hamster. Matsuno, H., Kozawa, O., Niwa, M., Ito, T., Tanabe, K., Nishida, M., Hayashi, H., Uematsu, T. J. Cardiovasc. Pharmacol. (1998) [Pubmed]
  3. Differential effects of glycoprotein IIb/IIIa antagonists on platelet microaggregate and macroaggregate formation and effect of anticoagulant on antagonist potency. Implications for assay methodology and comparison of different antagonists. Storey, R.F., Wilcox, R.G., Heptinstall, S. Circulation (1998) [Pubmed]
  4. Lack of tPA significantly affects antithrombotic therapy by a GPIIb/IIIa antagonist, but not by a thrombin inhibitor in mice. Matsuno, H., Kozawa, O., Ueshima, S., Matsuo, O., Collen, D., Uematsu, T. Thromb. Haemost. (2000) [Pubmed]
  5. Comparative antiplatelet effects of aspirin, vapiprost and GR144053, a GPIIb/IIIa antagonist, with a special reference to the role of platelet microaggregates. Matsuno, H., Kozawa, O., Nagashima, S., Kanamaru, M., Uematsu, T. Br. J. Pharmacol. (1999) [Pubmed]
  6. tPA, but not uPA, significantly affects antithrombotic therapy by a glycoprotein IIb/IIIa antagonist, but not by a factor Xa inhibitor. Nishida, M., Matsuno, H., Kozawa, O., Ueshima, S., Matsuo, O., Collen, D., Uematsu, T. J. Cardiovasc. Pharmacol. (2000) [Pubmed]
  7. GR144053, a fibrinogen receptor antagonist, enhances the suppression of neointima formation by losartan, an angiotensin II receptor antagonist, in the injured carotid artery of hamster. Matsuno, H., Kozawa, O., Niwa, M., Kaida, T., Hayashi, H., Uematsu, T. Br. J. Pharmacol. (1997) [Pubmed]
  8. Antiplatelet and antithrombotic efficacy of SR 121787, a nonpeptide orally active GP IIb/IIIa antagonist, in rabbits: comparison with clopidogrel and aspirin. Hoffmann, P., Bernat, A., Savi, P., Herbert, J.M. J. Cardiovasc. Pharmacol. (1997) [Pubmed]
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