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Chemical Compound Review

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

Synonyms: AG-F-90460, SureCN8471397, NSC-27389, CHEBI:381335, AC1L2IQV, ...
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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].


  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]
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