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Chemical Compound Review

Comtess     (E)-2-cyano-3-(3,4-dihydroxy- 5-nitro...

Synonyms: Entacom, Comtan, ENTACAPONE, Entacapona, Entacaponum, ...
 
 
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Disease relevance of OR-611

 

High impact information on OR-611

  • Pretreatment with entacapone (OR-611), a peripheral catechol O-methyl-transferase (COMT) inhibitor, greatly reduces the plasma 3OMFD fraction and provides an ideal situation to evaluate the contribution of the plasma 3OMFD fraction in several kinetic models of FDOPA uptake [1].
  • We conclude that OR-611 prolongs the circulation time of FDOPA in the plasma but does not alter rate constants for striatal FDOPA uptake or decarboxylation [1].
  • A dose of 10 mg/kg i.p. of Ro 40-7592 alone, in contrast to the same dose of OR-611, decreased the dialysate level of HVA and increased that of DOPAC; this dose was thus used to differentiate between the effects of central and peripheral COMT inhibition [2].
  • Four monkeys each underwent two PET scans in the baseline condition, one PET scan after treatment with OR-462 (15 mg/kg, i.v.), and one PET scan after treatment with OR-611 (15 mg/kg, i.v.). Pharmacokinetic analysis of FDOPA metabolism in plasma indicated that these compounds blocked peripheral COMT activity by 80% for at least 60 minutes [3].
  • FDOPA/PET scans were performed in one rhesus monkey to study the influence of three catechol-O-methyltransferase (COMT) inhibitors (CGP 28014, OR-611 and Ro 40-7592) on FDOPA pharmacokinetics [4].
 

Chemical compound and disease context of OR-611

 

Biological context of OR-611

 

Associations of OR-611 with other chemical compounds

 

Gene context of OR-611

References

  1. Fluorodopa positron emission tomography with an inhibitor of catechol-O-methyltransferase: effect of the plasma 3-O-methyldopa fraction on data analysis. Ishikawa, T., Dhawan, V., Chaly, T., Robeson, W., Belakhlef, A., Mandel, F., Dahl, R., Margouleff, C., Eidelberg, D. J. Cereb. Blood Flow Metab. (1996) [Pubmed]
  2. Effects of catechol-O-methyltransferase inhibitors and L-3,4-dihydroxyphenylalanine with or without carbidopa on extracellular dopamine in rat striatum. Kaakkola, S., Wurtman, R.J. J. Neurochem. (1993) [Pubmed]
  3. Effect of catechol-O-methyltransferase inhibition on brain uptake of [18F]fluorodopa: implications for compartmental modelling and clinical usefulness. Léger, G., Gjedde, A., Kuwabara, H., Guttman, M., Cumming, P. Synapse (1998) [Pubmed]
  4. Cerebral 6-[18F]fluoro-L-DOPA uptake in rhesus monkey: pharmacological influence of aromatic amino acid decarboxylase (AAAD) and catechol-O-methyltransferase (COMT) inhibition. Psylla, M., Günther, I., Antonini, A., Vontobel, P., Reist, H.W., Zollinger, A., Leenders, K.L. Brain Res. (1997) [Pubmed]
  5. The effect of entacapone (OR-611) on brain [18F]-6-L-fluorodopa metabolism: implications for levodopa therapy of Parkinson's disease. Sawle, G.V., Burn, D.J., Morrish, P.K., Lammertsma, A.A., Snow, B.J., Luthra, S., Osman, S., Brooks, D.J. Neurology (1994) [Pubmed]
  6. Effect of entacapone, a peripherally acting catechol-O-methyltransferase inhibitor, on the motor response to acute treatment with levodopa in patients with Parkinson's disease. Merello, M., Lees, A.J., Webster, R., Bovingdon, M., Gordin, A. J. Neurol. Neurosurg. Psychiatr. (1994) [Pubmed]
  7. L-dopa as substrate for human duodenal catechol-O-methyltransferase and aromatic L-amino acid decarboxylase. Schultz, E. Biomed. Chromatogr. (1990) [Pubmed]
  8. Acute toxicity of three new selective COMT inhibitors in mice with special emphasis on interactions with drugs increasing catecholaminergic neurotransmission. Törnwall, M., Männistö, P.T. Pharmacol. Toxicol. (1991) [Pubmed]
  9. Reduction of circulating 3-O-methyldopa by inhibition of catechol-O-methyltransferase with OR-611 and OR-462 in cynomolgus monkeys: implications for the treatment of Parkinson's disease. Cedarbaum, J.M., Leger, G., Guttman, M. Clinical neuropharmacology. (1991) [Pubmed]
  10. Catechol-O-methyltransferase and aromatic L-amino acid decarboxylase activities in human gastrointestinal tissues. Schultz, E. Life Sci. (1991) [Pubmed]
 
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