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Gene Review

CP20  -  Lymphocyte cytosolic protein, molecular...

Homo sapiens

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Disease relevance of CP20


High impact information on CP20

  • These studies have identified chelators such as 1,6-dimethyl-2-(N-4',N-propylsuccinamido)methyl-3-hydroxypyridin-4-one (CP358), which causes only a 10% inhibition of 5-LO after 24 h of incubation at 110 microm IBE (iron-binding equivalents) in comparison to simple dialkyl HPOs such as Deferiprone (CP20) which cause up to 70% inhibition [6].
  • The antioxidant activity of two iron chelators, pyoverdin (Pa) and hydroxypyrid-4-one derivative (CP20) was compared with that of desferrioxamine (DFO) on iron-loaded hepatocyte culture [7].
  • Moreover, the DFO and CP20 but not Pa showed protective effect on the leakage of the intracellular enzyme lactate dehydrogenase into the culture medium [7].
  • In rat and human hepatocytes cultured for 1 day in the presence of 1 microM 55Fe-50 microM iron citrate plus CP20, CP94 or desferrioxamine B, a decrease of iron uptake by the cells was observed [1].
  • Our results show that CP20 as well as deferoxamine inhibit HepG2 cell proliferation and block cell cycle in the S phase [8].

Chemical compound and disease context of CP20

  • The effects of 3-hydroxypyridin-4-one (HPO) iron chelators and desferrioxamine (DFO) on murine hemopoiesis in vivo and in vitro have been compared in order to investigate the mechanism by which leucopenia in mice and granulocytopenia in man occurs with 1,2-,dimethyl-HPO (CP20) [2].
  • CP20 (L1), the methyl derivative, has been given to humans, while at least two compounds with greater activity and relatively lower animal toxicity are close to being introduced [9].

Biological context of CP20

  • CP20, at the concentration of 50 or 100 microM, inhibited DNA synthesis after 48 hr of incubation and induced an accumulation of the cells in the S phase of the cell cycle [8].
  • Such conditioning-specific reductions of somatic K+ currents appear to depend on the phosphorylation of a 20-kDa G-protein (CP20) mediated by the Ca2+ and phospholipid-dependent kinase, protein kinase C (PKC) [10].
  • The orally active bidentate chelators CP502 and CP511, which also belong to the 3-hydroxypyridin-4-one family, but with higher affinities for iron than CP20, were monitored for their antiviral properties by checking for p24 antigen production and nuclear factor (NF)-kappaB activation, and their ability to induce apoptosis [3].

Anatomical context of CP20


Associations of CP20 with chemical compounds

  • Deferiprone (L1; CP20) is an orally absorbed bidentate hydroxypyridinone iron chelator that can induce urinary iron excretion, promote negative iron balance and reduce hepatic iron levels in some transfusion-dependent patients, particularly in those who are markedly iron overloaded and have not received regular deferoxamine therapy [12].
  • The urinary metabolic profiles of two novel orally active iron chelators, 1,2-dimethyl-3-hydroxypyridin-4-one (CP20 or L1) and 1,2-diethyl-3-hydroxypyridin-4-one (CP94), have been studied in rats [13].
  • The 3-O-methylated CP20 metabolite (metabolite I) accounted for 1% of the administered dose in both species, whereas the unmetabolized CP20 amounted to 10.5% and 4% of the dose administered in the rats and man, respectively [13].
  • The pursuit of orally available Fe(III) chelating agents has resulted in several clinical trials of 1,2-dimethyl-3-hydroxypyrid-4-one (CP20) [14].
  • By addition of Fe3+ (50 microM ferric ammonium citrate) to an acidified aqueous mobile phase, we have successfully separated a series of hydroxypyridones-including CP20-and the related pyrones maltol and ethylmaltol by HPLC on microBondapak C18 [14].

Other interactions of CP20

  • Iron chelation efficiency in the culture model was studied by analyzing the effect of CP20 on radioactive iron uptake, intracellular ferritin level, and transferrin receptor expression [8].

Analytical, diagnostic and therapeutic context of CP20

  • HepG2 cell cultures were maintained in the absence of fetal calf serum (FCS) and in the presence or not (control cultures) of CP20 at the concentrations of 50 or 100 microM; deferoxamine (DFO) was used as an iron chelator reference [8].


  1. Inhibition of iron toxicity in rat and human hepatocyte cultures by the hydroxypyridin-4-ones CP20 and CP94. Chenoufi, N., Hubert, N., Loréal, O., Morel, I., Pasdeloup, N., Cillard, J., Brissot, P., Lescoat, G. J. Hepatol. (1995) [Pubmed]
  2. In vivo and in vitro effects of 3-hydroxypyridin-4-one chelators on murine hemopoiesis. Hoyes, K.P., Jones, H.M., Abeysinghe, R.D., Hider, R.C., Porter, J.B. Exp. Hematol. (1993) [Pubmed]
  3. Human immunodeficiency virus type 1 replication inhibition by the bidentate iron chelators CP502 and CP511 is caused by proliferation inhibition and the onset of apoptosis. Georgiou, N.A., van der Bruggen, T., Oudshoorn, M., Hider, R.C., Marx, J.J., van Asbeck, B.S. Eur. J. Clin. Invest. (2002) [Pubmed]
  4. Assessment of the effect of the oral iron chelator deferiprone on asymptomatic Plasmodium falciparum parasitemia in humans. Thuma, P.E., Olivieri, N.F., Mabeza, G.F., Biemba, G., Parry, D., Zulu, S., Fassos, F.F., McClelland, R.A., Koren, G., Brittenham, G.M., Gordeuk, V.R. Am. J. Trop. Med. Hyg. (1998) [Pubmed]
  5. Deferiprone-associated myelotoxicity. al-Refaie, F.N., Wonke, B., Hoffbrand, A.V. Eur. J. Haematol. (1994) [Pubmed]
  6. Structure-function investigation of the interaction of 1- and 2-substituted 3-hydroxypyridin-4-ones with 5-lipoxygenase and ribonucleotide reductase. Kayyali, R., Porter, J.B., Liu, Z.D., Davies, N.A., Nugent, J.H., Cooper, C.E., Hider, R.C. J. Biol. Chem. (2001) [Pubmed]
  7. EPR study of antioxidant activity of the iron chelators pyoverdin and hydroxypyrid-4-one in iron-loaded hepatocyte culture: comparison with that of desferrioxamine. Morel, I., Sergent, O., Cogrel, P., Lescoat, G., Pasdeloup, N., Brissot, P., Cillard, P., Cillard, J. Free Radic. Biol. Med. (1995) [Pubmed]
  8. Antiproliferative effect of deferiprone on the Hep G2 cell line. Chenoufi, N., Drénou, B., Loréal, O., Pigeon, C., Brissot, P., Lescoat, G. Biochem. Pharmacol. (1998) [Pubmed]
  9. The development of iron chelating drugs. Porter, J.B., Huehns, E.R., Hider, R.C. Baillieres Clin. Haematol. (1989) [Pubmed]
  10. Outgrowths from Hermissenda photoreceptor somata are associated with activation of protein kinase C. Lederhendler, I.I., Etcheberrigaray, R., Yamoah, E.N., Matzel, L.D., Alkon, D.L. Brain Res. (1990) [Pubmed]
  11. Red blood cells participate in the metabolic clearance of catecholamines in the rat. Azoui, R., Schneider, J., Dong, W.X., Dabiré, H., Safar, M., Cuche, J.L. Life Sci. (1997) [Pubmed]
  12. A risk-benefit assessment of iron-chelation therapy. Porter, J.B. Drug safety : an international journal of medical toxicology and drug experience. (1997) [Pubmed]
  13. Urinary metabolic profiles in human and rat of 1,2-dimethyl- and 1,2-diethyl-substituted 3-hydroxypyridin-4-ones. Singh, S., Epemolu, R.O., Dobbin, P.S., Tilbrook, G.S., Ellis, B.L., Damani, L.A., Hider, R.C. Drug Metab. Dispos. (1992) [Pubmed]
  14. Reversed-phase high-performance liquid chromatography of non-transferrin-bound iron and some hydroxypyridone and hydroxypyrone chelators. el-Jammal, A., Templeton, D.M. J. Chromatogr. B, Biomed. Appl. (1994) [Pubmed]
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