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Chemical Compound Review

Lopac-A-8762     N-[2-(3,4-dihydroxyphenyl) ethyl]ethanamide

Synonyms: CHEMBL137743, SureCN328568, AG-E-75018, LS-9248, CCG-204188, ...
 
 
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Disease relevance of NSC 314644

 

High impact information on NSC 314644

  • One hour after a dose of 400 mg N-acetyldopamine/kg, dThd incorporation was completely suppressed by both P388 and L1210 tumor cells with minimal effects on bone marrow or gastrointestinal mucosa cells [2].
  • Similarly, N-acetyldopamine oxidized with one equivalent of sodium periodate causes a concentration-dependent inactivation of TPH as well [3].
  • Experiments with N-substituted dihydric phenol substrates (N-methyldopamine, N-acetyldopamine) demonstrate that oxygen consumption is retarded in the N-acetyl substituted material due to a diminished rate of cyclization [4].
  • It exhibited a pH optimum of 6.0 and readily converted chemically synthesized as well as enzymatically generated quinones derived from N-acetyldopamine, N-beta-alanyldopamine, and 3,4-dihydroxyphenethyl alcohol to highly unstable 2-hydroxy-p-quinone methides [5].
  • Quinone derivatives of DOPA, dopamine, and N-acetyldopamine inactivate tyrosine hydroxylase, the initial and rate-limiting enzyme in the biosynthesis of the catecholamine neurotransmitters [6].
 

Biological context of NSC 314644

 

Anatomical context of NSC 314644

 

Associations of NSC 314644 with other chemical compounds

 

Gene context of NSC 314644

 

Analytical, diagnostic and therapeutic context of NSC 314644

  • A simple method for the determination of N-acetyldopamine (NADA) (both free and conjugated) in children's urine by high-performance liquid chromatography with electrochemical detection has been developed [19].

References

  1. Sensitivity and specificity of urinary N-acetyldopamine as a marker for neuroblastomas: comparison with traditional urinary catecholamine metabolites. Muskiet, F.A., Kema, I.P. J. Chromatogr. (1992) [Pubmed]
  2. Synthesis and biologic evaluation of the dopamine analog N-acetyldopamine in experimental leukemia in mice. Wick, M.M., Mui, A. J. Natl. Cancer Inst. (1981) [Pubmed]
  3. Dopamine inactivates tryptophan hydroxylase and forms a redox-cycling quinoprotein: possible endogenous toxin to serotonin neurons. Kuhn, D.M., Arthur, R. J. Neurosci. (1998) [Pubmed]
  4. Evidence of the indirect formation of the catecholic intermediate substrate responsible for the autoactivation kinetics of tyrosinase. Cooksey, C.J., Garratt, P.J., Land, E.J., Pavel, S., Ramsden, C.A., Riley, P.A., Smit, N.P. J. Biol. Chem. (1997) [Pubmed]
  5. 4-alkyl-o-quinone/2-hydroxy-p-quinone methide isomerase from the larval hemolymph of Sarcophaga bullata. I. Purification and characterization of enzyme-catalyzed reaction. Saul, S.J., Sugumaran, M. J. Biol. Chem. (1990) [Pubmed]
  6. Tyrosine hydroxylase is inactivated by catechol-quinones and converted to a redox-cycling quinoprotein: possible relevance to Parkinson's disease. Kuhn, D.M., Arthur, R.E., Thomas, D.M., Elferink, L.A. J. Neurochem. (1999) [Pubmed]
  7. Biosynthesis of dehydro-N-acetyldopamine by a soluble enzyme preparation from the larval cuticle of Sarcophaga bullata involves intermediary formation of N-acetyldopamine quinone and N-acetyldopamine quinone methide. Saul, S.J., Sugumaran, M. Arch. Insect Biochem. Physiol. (1990) [Pubmed]
  8. N-acetyldopamine inhibits rat brain lipid peroxidation induced by lipopolysaccharide. Oxenkrug, G.F., Requintina, P.J. Ann. N. Y. Acad. Sci. (2005) [Pubmed]
  9. Biosynthesis of N-acetyldopamine and N-acetyloctopamine by Schistocerca gregaria nervous tissue. Mir, A.K., Vaughan, P.F. J. Neurochem. (1981) [Pubmed]
  10. Demonstration of N-acetyldopamine in human kidney and urine. Elchisak, M.A., Hausner, E.A. Life Sci. (1984) [Pubmed]
  11. Catecholamines and related o-diphenols in cockroach hemolymph and cuticle during sclerotization and melanization: comparative studies on the order Dictyoptera. Czapla, T.H., Hopkins, T.L., Kramer, K.J. J. Comp. Physiol. B, Biochem. Syst. Environ. Physiol. (1990) [Pubmed]
  12. Immune response in insects: the role of phenoloxidase in defense reactions in relation to melanization and sclerotization. Marmaras, V.J., Charalambidis, N.D., Zervas, C.G. Arch. Insect Biochem. Physiol. (1996) [Pubmed]
  13. A diphenol oxidase gene is part of a cluster of genes involved in catecholamine metabolism and sclerotization in drosophila. I. Identification of the biochemical defect in Dox-A2 [l(2)37Bf] mutants. Pentz, E.S., Black, B.C., Wright, T.R. Genetics (1986) [Pubmed]
  14. Biosynthesis of PAPS in vitro by human liver. Measurement by two independent assay procedures. Wong, K.P., Khoo, B.Y., Sit, K.H. Biochem. Pharmacol. (1991) [Pubmed]
  15. Methenyltetrahydrofolate synthetase is a high-affinity catecholamine-binding protein. Anguera, M.C., Stover, P.J. Arch. Biochem. Biophys. (2006) [Pubmed]
  16. The effects of lindane poisoning on N-acetyldopamine and N-acetyl 5-hydroxytryptamine concentrations in the brain of Locusta migratoria L. Moreteau, B., Chaminade, N. Ecotoxicol. Environ. Saf. (1990) [Pubmed]
  17. Immune-modulating effects of melatonin, N-acetylserotonin, and N-acetyldopamine. Perianayagam, M.C., Oxenkrug, G.F., Jaber, B.L. Ann. N. Y. Acad. Sci. (2005) [Pubmed]
  18. Model sclerotization studies. 4. Generation of N-acetylmethionyl catechol adducts during tyrosinase-catalyzed oxidation of catechols in the presence of N-acetylmethionine. Sugumaran, M., Nelson, E. Arch. Insect Biochem. Physiol. (1998) [Pubmed]
  19. Determination by high-performance liquid chromatography with electrochemical detection of free and conjugated N-acetyldopamine excretion in urine of children with neuroblastoma and nephroblastoma. Jouve, J., Herault, J., Tournade, H., Muh, J.P. J. Chromatogr. (1992) [Pubmed]
 
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