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Chemical Compound Review

Inogatran     2-[[(2R)-3-cyclohexyl-1- [(2S)-2-[3...

Synonyms: SureCN22745, CHEMBL114715, SureCN871973, CHEBI:43313, CHEBI:288902, ...
 
 
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Disease relevance of Inogatran

 

High impact information on Inogatran

  • The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease [4].
  • The direct thrombin inhibitor inogatran eliminated the CPU generation during coagulation but not during fibrinolysis [5].
  • The rank order of potency based on doses (mg/kg/h) required for full efficacy against arterial thrombosis was BCH-2763 (1.2) > inogatran (1.5) > r-hirudin (1.8) > hirulog (3.3) > argatroban (> 3.0); heparin required a markedly higher dose (5.7) [6].
  • In an in vivo model of endogenous fibrinolysis in the rat, inhibition of fibrinolysis was observed at > or = 1.0 micromol/l. In all assays, except the Ki-ratio determinations, the compounds could be graded with regard to selectivity against the fibrinolytic system: inogatran > melagatran > H 317/86 [7].
  • There was a 5-fold increase in the bioavailability of inogatran in the presence of aprotinin [8].
 

Chemical compound and disease context of Inogatran

 

Biological context of Inogatran

 

Anatomical context of Inogatran

  • METHODS: Rat jejunum, ileum and colon segments were stripped and mounted in modified Ussing chambers, and the permeability to inogatran was determined both in the presence and absence of aprotinin [8].
  • In the model of rt-PA-induced thrombolysis of a thrombus in the carotid artery, inogatran improved the patency time and the cumulative blood flow during the two hour thrombolysis period more than rt-PA alone [10].
 

Associations of Inogatran with other chemical compounds

  • AIM: This study evaluated a novel specific thrombin inhibitor, inogatran, in comparison with unfractionated heparin, with regard to markers for coagulation activity in patients with unstable coronary artery disease [4].
 

Gene context of Inogatran

  • Hirudin, inogatran and melagatran inhibited the activation of protein C by thrombin complexed with cell-bound TM in a dose-dependent manner, with mean IC(50) values+/-S.D. of 4.4+/-0.8, 20.0+/-1.1 and 6.4+/-0.2 nmol/l, respectively [12].
  • Up to a concentration of 10 x 10(-6) mol/l inogatran does not inhibit t-PA-induced fibrinolysis as seen in an ECLT system [13].
 

Analytical, diagnostic and therapeutic context of Inogatran

  • A total of 3296 pairs of concentration-APTT samples were obtained before, during, and after intravenous infusions of inogatran [14].
  • Ischaemia was monitored using continuous vectorcardiography during the 4 h of treatment and during the subsequent 4 h after inogatran infusion had been stopped, to detect any increase in ischaemic events after the period of treatment [15].
  • The normal plasma level of AT is 2800 nmol/l and relevant therapeutic concentrations from clinical trials are 200 nmol/l for hirudin, 500 nmol/l for melagatran and 1000 nmol/l for inogatran [16].

References

  1. Activated partial thromboplastin time and clinical outcome after thrombin inhibition in unstable coronary artery disease. Oldgren, J., Linder, R., Grip, L., Siegbahn, A., Wallentin, L. Eur. Heart J. (1999) [Pubmed]
  2. Antithrombotic activity of inogatran, a new low-molecular-weight inhibitor of thrombin, in a closed-chest porcine model of coronary artery thrombosis. Uriuda, Y., Wang, Q.D., Grip, L., Rydén, L., Sjöquist, P.O., Mattsson, C. Cardiovasc. Res. (1996) [Pubmed]
  3. Heparin is more effective than inogatran, a low-molecular weight thrombin inhibitor in suppressing ischemia and recurrent angina in unstable coronary disease. Thrombin Inhibition in Myocardial Ischemia (TRIM) Study Group. Andersen, K., Dellborg, M. Am. J. Cardiol. (1998) [Pubmed]
  4. The effect of a low molecular mass thrombin inhibitor, inogatran, and heparin on thrombin generation and fibrin turnover in patients with unstable coronary artery disease. Linder, R., Oldgren, J., Egberg, N., Grip, L., Larson, G., Siegbahn, A., Wallentin, L. Eur. Heart J. (1999) [Pubmed]
  5. Different mechanisms contribute to the biphasic pattern of carboxypeptidase U (TAFIa) generation during in vitro clot lysis in human plasma. Leurs, J., Wissing, B.M., Nerme, V., Schatteman, K., Björquist, P., Hendriks, D. Thromb. Haemost. (2003) [Pubmed]
  6. BCH-2763, a novel potent parenteral thrombin inhibitor, is an effective antithrombotic agent in rodent models of arterial and venous thrombosis--comparisons with heparin, r-hirudin, hirulog, inogatran and argatroban. Finkle, C.D., St Pierre, A., Leblond, L., Deschenes, I., DiMaio, J., Winocour, P.D. Thromb. Haemost. (1998) [Pubmed]
  7. Effects of melagatran, a new low-molecular-weight thrombin inhibitor, on thrombin and fibrinolytic enzymes. Gustafsson, D., Antonsson, T., Bylund, R., Eriksson, U., Gyzander, E., Nilsson, I., Elg, M., Mattsson, C., Deinum, J., Pehrsson, S., Karlsson, O., Nilsson, A., Sörensen, H. Thromb. Haemost. (1998) [Pubmed]
  8. Inhibition of binding of an enzymatically stable thrombin inhibitor to lumenal proteases as an additional mechanism of intestinal absorption enhancement. Sjöström, M., Lindfors, L., Ungell, A.L. Pharm. Res. (1999) [Pubmed]
  9. The effects of oral and intravenous direct thrombin inhibitors on the size of photochemically induced cortical infarction in rats. Mikulski, A., Elg, M., Gustafsson, D. Thromb. Res. (2001) [Pubmed]
  10. Effects of inogatran, a new low-molecular-weight thrombin inhibitor, in rat models of venous and arterial thrombosis, thrombolysis and bleeding time. Gustafsson, D., Elg, M., Lenfors, S., Börjesson, I., Teger-Nilsson, A.C. Blood Coagul. Fibrinolysis (1996) [Pubmed]
  11. Antithrombotic effect of LB-30057 (CI-1028), a new synthetic thrombin inhibitor, in a rabbit model of thrombosis: comparison with inogatran. Chi, L., Mertz, T.E., Rogers, K.L., Janiczek, N., Peng, Y.W., Saganek, L., Bousley, R.F., Juneau, P.L., Uprichard, A.C., Gallagher, K.P. J. Thromb. Thrombolysis (2001) [Pubmed]
  12. Effect of different types of thrombin inhibitors on thrombin/thrombomodulin modulated activation of protein C in vitro. Mattsson, C., Menschik-Lundin, A., Nylander, S., Gyzander, E., Deinum, J. Thromb. Res. (2001) [Pubmed]
  13. In vitro effects of inogatran, a selective low molecular weight thrombin inhibitor. Teger-Nilsson, A.C., Bylund, R., Gustafsson, D., Gyzander, E., Eriksson, U. Thromb. Res. (1997) [Pubmed]
  14. Population modelling of the effect of inogatran, at thrombin inhibitor, on ex vivo coagulation time (APTT) in healthy subjects and patients with coronary artery disease. Cullberg, M., Eriksson, U.G., Larsson, M., Karlsson, M.O. British journal of clinical pharmacology. (2001) [Pubmed]
  15. Thrombin inhibition with inogatran for unstable angina pectoris: evidence for reactivated ischaemia after cessation of short-term treatment. Andersen, K., Dellborg, M., Emanuelsson, H., Grip, L., Swedberg, K. Coron. Artery Dis. (1996) [Pubmed]
  16. Inhibition of endothelial cell-mediated generation of activated protein C by direct and antithrombin-dependent thrombin inhibitors. Linder, R., Frebelius, S., Jansson, K., Swedenborg, J. Blood Coagul. Fibrinolysis (2003) [Pubmed]
 
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