The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

CHEMBL353187     1-(3,4-dihydroxyphenyl)-2- methyl-propan-1-one

Synonyms: AG-F-90460, SureCN8471397, NSC-27389, CHEBI:381335, AC1L2IQV, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of U 0521

 

High impact information on U 0521

  • The most active compounds were more than 1000 times more potent (IC50 = 3-6 nM) in vitro than the known COMT inhibitor, 3',4'-dihydroxy-2-methylpropiophenone (U 0521, IC50 = 6000 nM) [2].
  • The drug U-0521, which has been used as an inhibitor of catechol-O-methyltransferase (COMT), was also found to be an inhibitor of tyrosine hydroxylase [3].
  • Experiments were performed to determine the effect of pretreatment with 3',4'-dihydroxy-2-methyl-propiophenone (U-0521), a competitive inhibitor of COMT, on [18F]DOPA metabolism in the carbidopa-pretreated hooded rat [4].
  • Increased decarboxylation of [18F]DOPA in the striatum of U-0521-treated rats resulted in heightened radiocontrast between striatum and other cerebral tissues [4].
  • The effects of U-0521 and ascorbate on 2-OH-E2-stimulated progesterone production in vitro was also examined [5].
 

Biological context of U 0521

 

Anatomical context of U 0521

 

Associations of U 0521 with other chemical compounds

  • It is concluded that 3H-MPP+ is efficiently taken up by rat hepatocytes by a carrier-mediated mechanism sensitive to catecholamines, decynium22 and cyanane863, and to the enzyme inhibitors pargyline, Ro 01-2812 and U-0521 [13].
  • Cocaine (12 microM) enhanced the alpha-effect elicited by electrical stimulation 2.8 +/- 0.2 (n = 7) times but did not change the beta-effect, whereas U-0521 (50 microM) enhanced the beta-effect 3.4 +/- 0.2 (n = 8) times without changing the alpha-effect [14].
  • Catechol-O-methyltransferase inhibition by U-0521 increases striatal utilization of levodopa [15].
  • Segments of cat, rat or rabbit trachea, dog coronary artery or cat atria were incubated in isoprenaline, in the presence of U-0521 (100 mumol l-1) to inhibit catechol-O-methyltransferase [16].
  • Rabbit aortic strips (nerve-free, reserpine-pretreated or normal) whose noradrenaline-metabolizing enzymes were inhibited (by in vitro treatment with 0.5 mM pargyline for 30 min and by the presence of 0.1mM U-0521) were exposed to 1.18 muM labelled (-)- or (+)noradrenaline for 30 min [17].
 

Gene context of U 0521

  • In these experiments, 12 mumol/l cocaine (to inhibit uptake1), 41 mumol/l hydrocortisone (to reduce uptake2) and 50 mumol/l U-0521 (to inhibit COMT) were present during the perifusion [18].
  • Altered metabolism of [18F]-6-fluorodopa in the hooded rat following inhibition of catechol-O-methyltransferase with U-0521 [4].
  • U-0521, a potent COMT inhibitor, was shown, after i.p. injection, to effectively block the accumulation of OMD in the plasma and to enhance L-DOPA metabolism in rat brain [19].
 

Analytical, diagnostic and therapeutic context of U 0521

  • During electric stimulation, U-0521 markedly decreased the formation of NMN and OMDA and caused an increase in outflow of NE [6].
  • Denervation, reserpine and cortex-one blocked the accumulation of adrenaline, whereas U-0521 was the only drug to increase accumulation of adrenaline [20].

References

  1. Impairment of the extraneuronal O-methylating system of isoproterenol by stop-flow ischemia in the perfused rat heart. Inoue, M., Hifumi, K., Kurahashi, K., Fujiwara, M. J. Pharmacol. Exp. Ther. (1987) [Pubmed]
  2. Synthesis of some novel potent and selective catechol O-methyltransferase inhibitors. Bäckström, R., Honkanen, E., Pippuri, A., Kairisalo, P., Pystynen, J., Heinola, K., Nissinen, E., Linden, I.B., Männistö, P.T., Kaakkola, S. J. Med. Chem. (1989) [Pubmed]
  3. A comparison of 2-hydroxyestradiol and U-0521 (3'4'-dihydroxy-2-methylpropiophenone, Upjohn) as in situ and in vitro inhibitors of tyrosine hydroxylase. Lloyd, T., Boyd, B., Walega, M.A., Ebersole, B.J., Weisz, J. J. Neurochem. (1982) [Pubmed]
  4. Altered metabolism of [18F]-6-fluorodopa in the hooded rat following inhibition of catechol-O-methyltransferase with U-0521. Cumming, P., Boyes, B.E., Martin, W.R., Adam, M., Ruth, T.J., McGeer, E.G. Biochem. Pharmacol. (1987) [Pubmed]
  5. Metabolism of [3H]2-hydroxyestradiol by cultured porcine granulosa cells: evidence for the presence of a catechol-O-methyltransferase pathway and a direct stimulatory effect of 2-methoxyestradiol on progesterone production. Spicer, L.J., Walega, M.A., Hammond, J.M. Biol. Reprod. (1987) [Pubmed]
  6. Inactivation of norepinephrine in an isolated vein. Brandao, F. J. Pharmacol. Exp. Ther. (1977) [Pubmed]
  7. The antihypertensive effect of U-0521 (3',4'-dihydroxy-2-methylpropiophenone). Lloyd, T., Waldman, C.D. Life Sci. (1982) [Pubmed]
  8. Extraneuronal uptake inhibitor U-0521 decreases contractile responses in rat vas deferens. Rice, P.J., Abraham, S.T., Huang, N.Y., Doman, R.J. Gen. Pharmacol. (1997) [Pubmed]
  9. Metabolism of [3H]-(+/-)-isoprenaline by isolated atria and coronary arteries of the kitten. Cornish, E.J., Goldie, R.G. Br. J. Pharmacol. (1980) [Pubmed]
  10. Effect of 3',4'-dihydroxy-2-methyl-propriophenone (U-0521) on catechol-O-methyltransferase activity and on DOPA accumulation in rat red blood cells and corpus striatum. Reches, A., Jiang, D., Fahn, S. Biochem. Pharmacol. (1982) [Pubmed]
  11. The outward transport of axoplasmic noradrenaline induced by a rise of the sodium concentration in the adrenergic nerve endings of the rat vas deferens. Stute, N., Trendelenburg, U. Naunyn Schmiedebergs Arch. Pharmacol. (1984) [Pubmed]
  12. Uptake, distribution and metabolism of isoprenaline in the dog saphenous vein. Azevedo, I., Osswald, W. Naunyn Schmiedebergs Arch. Pharmacol. (1976) [Pubmed]
  13. Inward transport of 3H-MPP+ in freshly isolated rat hepatocytes: evidence for interaction with catecholamines. Martel, F., Martins, M.J., Azevedo, I. Naunyn Schmiedebergs Arch. Pharmacol. (1996) [Pubmed]
  14. Two different biophases for adrenaline released by electrical stimulation or tyramine from the sympathetic nerve endings of the dog saphenous vein. Guimarães, S., Paiva, M.Q. Naunyn Schmiedebergs Arch. Pharmacol. (1981) [Pubmed]
  15. Catechol-O-methyltransferase inhibition by U-0521 increases striatal utilization of levodopa. Reches, A., Jiang, D., Fahn, S. Naunyn Schmiedebergs Arch. Pharmacol. (1982) [Pubmed]
  16. Kinetic constants of isoprenaline and corticosterone for extraneuronal uptake in different cell types from various tissues. O'Donnell, S.R., Reid, J.J. Naunyn Schmiedebergs Arch. Pharmacol. (1984) [Pubmed]
  17. Stereoselectivity of the distribution of labelled noradrenaline in rabbit aortic strips after inhibition of the noradrenaline-metabolizing enzymes. Eckert, E., Henseling, M., Gescher, A., Trendelenburg, U. Naunyn Schmiedebergs Arch. Pharmacol. (1976) [Pubmed]
  18. Release and disposition of 3H-noradrenaline in the saphenous vein of neonate and adult dogs. Moura, D., Vaz-da-Silva, M.J., Azevedo, I., Brandão, F., Guimarães, S. Naunyn Schmiedebergs Arch. Pharmacol. (1993) [Pubmed]
  19. Catechol-O-methyltransferase and Parkinson's disease. Reches, A., Fahn, S. Advances in neurology. (1984) [Pubmed]
  20. The effects of drugs and denervation on removal and accumulation of adrenaline in the perfused hind-limb of the dog. Teixeira, F. Archives internationales de pharmacodynamie et de thérapie. (1977) [Pubmed]
 
WikiGenes - Universities