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Chemical Compound Review

trientine     N,N'-bis(2-aminoethyl)ethane- 1,2-diamine

Synonyms: Trientina, Trientinum, Tecza, Trien, TETA, ...
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Disease relevance of trientine


High impact information on trientine

  • A 20% reduction in sciatic nerve motor conduction velocity after 2 mo diabetes was 90% ameliorated by 2 wk of treatment with deferoxamine or trientine [6].
  • We investigated whether chronic treatment with deferoxamine and trientine, transition metal chelating agents which can prevent autoxidation, could correct nerve conduction and blood flow changes in streptozotocin-diabetic rats [6].
  • In most of the patients the toxic symptoms which forced a change of therapy were reversed on trien therapy; however, elastosis perforans did not seem to benefit, and two patients with penicillamine-induced systemic lupus erythematosus were not helped by the change [7].
  • In the long-term administration of trientine, the incidence of hepatic cell carcinoma (HCC) in the treated rats was 67 percent that of the untreated LEC rats, and the number of HCCs per rat in the treated group was 0.7 +/- 0.5, being significantly lower as compared with 4.7 +/- 3.5 in the untreated rats [8].
  • Trientine caused the Cu balance to become negative in diabetic subjects through elevated urinary Cu losses and suppressed elevated EC-SOD [3].

Chemical compound and disease context of trientine


Biological context of trientine

  • Kinetics of copper(II)--glycylglycyl-L-histidine reactions. Acid decomposition and proton-assisted nucleophilic displacement by triethylenetetramine [13].
  • These results suggested that Cu plays a pivotal role in tumor development and angiogenesis in the murine HCC cells, and Cu-chelators, especially trientine, could inhibit angiogenesis and enhance apoptosis in the tumor with consequent suppression of the tumor growth in vivo [5].
  • Trientine treatment resulted in a marked suppression of neovascularization and increase of apoptosis in the tumor, whereas tumor cell proliferation itself was not altered [5].
  • They were synthesized in nonaqueous media from triethylenetetramine (TT) by monoalkylation of a primary amino group, followed by exhaustive carboxymethylation of the remaining amino groups using ethyl bromoacetate and subsequent alkaline hydrolysis of the ester [14].
  • However, TETA and TEPA produced significant increases in the amount of UDS activity, and thus were considered positive in inducing primary DNA damage in this assay [15].

Anatomical context of trientine

  • In addition, with a myeloid leukemic cell line (HL-60), triethylenetetramine inhibited SOD without causing significant GSH oxidation [16].
  • Reversal treatment (4 weeks untreated diabetes, 4 weeks trientine) did not effect endothelium-dependent relaxation compared with aortas from rats with 4 weeks of diabetes, however, there was a 22.5 +/- 6.2% improvement compared with 8 weeks of diabetes [17].
  • Ca uptake in rat liver mitochondria is accelerated by various aminoglucoside antibiotics and, to a lesser degree, by triethylenetetramine and by protamine [18].
  • Treatment of the rat gastric fundus with the inhibitors of Cu/Zn SOD, diethyldithiocarbamate (DETC, 1 mM for 2 h) or triethylenetetramine (TETA, 100 microM for 2 h) had no effect on the relaxations to NANC nerve stimulation (1-8 Hz), NO (0.03-3 microM) or on those to ATP (10 microM) [19].
  • Here we describe a highly reproducible in vivo model, in which hepatocytes are induced in the pancreas of adult rats that were maintained on copper-deficient diet containing a relatively non-toxic copper-chelating agent, triethylenetetramine tetrahydrochloride (0.6% w/w) for 7-9 weeks and then returned to normal rat chow [20].

Associations of trientine with other chemical compounds


Gene context of trientine


Analytical, diagnostic and therapeutic context of trientine


  1. The use of trientine in preventing the effects of interrupting penicillamine therapy in Wilson's disease. Scheinberg, I.H., Jaffe, M.E., Sternlieb, I. N. Engl. J. Med. (1987) [Pubmed]
  2. Triethylene tetramine dihydrochloride toxicity in primary biliary cirrhosis. Epstein, O., Sherlock, S. Gastroenterology (1980) [Pubmed]
  3. Demonstration of a hyperglycemia-driven pathogenic abnormality of copper homeostasis in diabetes and its reversibility by selective chelation: quantitative comparisons between the biology of copper and eight other nutritionally essential elements in normal and diabetic individuals. Cooper, G.J., Chan, Y.K., Dissanayake, A.M., Leahy, F.E., Keogh, G.F., Frampton, C.M., Gamble, G.D., Brunton, D.H., Baker, J.R., Poppitt, S.D. Diabetes (2005) [Pubmed]
  4. Wilson disease and canine copper toxicosis. Brewer, G.J. Am. J. Clin. Nutr. (1998) [Pubmed]
  5. The copper-chelating agent, trientine, suppresses tumor development and angiogenesis in the murine hepatocellular carcinoma cells. Yoshii, J., Yoshiji, H., Kuriyama, S., Ikenaka, Y., Noguchi, R., Okuda, H., Tsujinoue, H., Nakatani, T., Kishida, H., Nakae, D., Gomez, D.E., De Lorenzo, M.S., Tejera, A.M., Fukui, H. Int. J. Cancer (2001) [Pubmed]
  6. Neurovascular dysfunction in diabetic rats. Potential contribution of autoxidation and free radicals examined using transition metal chelating agents. Cameron, N.E., Cotter, M.A. J. Clin. Invest. (1995) [Pubmed]
  7. Treatment of Wilson's disease with trientine (triethylene tetramine) dihydrochloride. Walshe, J.M. Lancet (1982) [Pubmed]
  8. Inhibition of hereditary hepatitis and liver tumor development in Long-Evans cinnamon rats by the copper-chelating agent trientine dihydrochloride. Sone, K., Maeda, M., Wakabayashi, K., Takeichi, N., Mori, M., Sugimura, T., Nagao, M. Hepatology (1996) [Pubmed]
  9. Prolonged copper depletion induces expression of antioxidants and triggers apoptosis in SH-SY5Y neuroblastoma cells. Lombardo, M.F., Ciriolo, M.R., Rotilio, G., Rossi, L. Cell. Mol. Life Sci. (2003) [Pubmed]
  10. Treatment of Wilson disease with ammonium tetrathiomolybdate: IV. Comparison of tetrathiomolybdate and trientine in a double-blind study of treatment of the neurologic presentation of Wilson disease. Brewer, G.J., Askari, F., Lorincz, M.T., Carlson, M., Schilsky, M., Kluin, K.J., Hedera, P., Moretti, P., Fink, J.K., Tankanow, R., Dick, R.B., Sitterly, J. Arch. Neurol. (2006) [Pubmed]
  11. The efficacy of trientine or ascorbate alone compared to that of the combined treatment with these two agents in familial amyotrophic lateral sclerosis model mice. Nagano, S., Fujii, Y., Yamamoto, T., Taniyama, M., Fukada, K., Yanagihara, T., Sakoda, S. Exp. Neurol. (2003) [Pubmed]
  12. Wilson disease. El-Youssef, M. Mayo Clin. Proc. (2003) [Pubmed]
  13. Kinetics of copper(II)--glycylglycyl-L-histidine reactions. Acid decomposition and proton-assisted nucleophilic displacement by triethylenetetramine. Wong, L.F., Cooper, J.C., Margerum, D.W. J. Am. Chem. Soc. (1976) [Pubmed]
  14. Decorporation of aged americium deposits by oral administration of lipophilic polyamino carboxylic acids. Bruenger, F.W., Kuswik-Rabiega, G., Miller, S.C. J. Med. Chem. (1992) [Pubmed]
  15. Evaluation of the genotoxic potential of alkyleneamines. Leung, H.W. Mutat. Res. (1994) [Pubmed]
  16. Inactivation of intracellular copper-zinc superoxide dismutase by copper chelating agents without glutathione depletion and methemoglobin formation. Kelner, M.J., Bagnell, R., Hale, B., Alexander, N.M. Free Radic. Biol. Med. (1989) [Pubmed]
  17. Effects of chelator treatment on aorta and corpus cavernosum from diabetic rats. Keegan, A., Cotter, M.A., Cameron, N.E. Free Radic. Biol. Med. (1999) [Pubmed]
  18. Activation of calcium uptake in rat liver mitochondria by aminoglucoside antibiotics. Kröner, H. Biochem. Pharmacol. (1990) [Pubmed]
  19. Effect of thiol modulators and Cu/Zn superoxide dismutase inhibition on nitrergic relaxations in the rat gastric fundus. De Man, J.G., De Winter, B.Y., Boeckxstaens, G.E., Herman, A.G., Pelckmans, P.A. Br. J. Pharmacol. (1996) [Pubmed]
  20. Almost total conversion of pancreas to liver in the adult rat: a reliable model to study transdifferentiation. Rao, M.S., Dwivedi, R.S., Subbarao, V., Usman, M.I., Scarpelli, D.G., Nemali, M.R., Yeldandi, A., Thangada, S., Kumar, S., Reddy, J.K. Biochem. Biophys. Res. Commun. (1988) [Pubmed]
  21. Equilibrium studies on the binding of cadmium(II) to human serum transferrin. Harris, W.R., Madsen, L.J. Biochemistry (1988) [Pubmed]
  22. Polymerase chain reaction-directed DNA sequencing of bleomycin-induced "nondeletion"-type, 6-thioguanine-resistant mutants in Chinese hamster ovary cell derivative AS52: effects of an inhibitor and a mimic of superoxide dismutase. An, J., Hsie, A.W. Environ. Mol. Mutagen. (1994) [Pubmed]
  23. Separation of proteins on polymeric stationary phases grafted with various amine groups. Choi, S.H., Hwang, Y.M., Lee, K.P. Journal of chromatography. A. (2003) [Pubmed]
  24. Reducible poly(amido ethylenimine) directed to enhance RNA interference. Hoon Jeong, J., Christensen, L.V., Yockman, J.W., Zhong, Z., Engbersen, J.F., Jong Kim, W., Feijen, J., Wan Kim, S. Biomaterials (2007) [Pubmed]
  25. Influence of the "innocent" ligands on the MLCT excited-state behavior of mono(bipyridine)ruthenium(II) complexes: a comparison of X-ray structures and 77 K luminescence properties. Chen, Y.J., Xie, P., Heeg, M.J., Endicott, J.F. Inorganic chemistry. (2006) [Pubmed]
  26. Chelation and intercalation: complementary properties in a compound for the treatment of Alzheimer's disease. Cherny, R.A., Barnham, K.J., Lynch, T., Volitakis, I., Li, Q.X., McLean, C.A., Multhaup, G., Beyreuther, K., Tanzi, R.E., Masters, C.L., Bush, A.I. J. Struct. Biol. (2000) [Pubmed]
  27. Combination of copper-chelating agent, trientine, and methotrexate attenuates colorectal carcinoma development and angiogenesis in mice. Yoshiji, H., Yoshii, J., Kuriyama, S., Ikenaka, Y., Noguchi, R., Yanase, K., Namisaki, T., Kitade, M., Yamazaki, M., Fukui, H. Oncol. Rep. (2005) [Pubmed]
  28. The copper chelator trientine has an antiangiogenic effect against hepatocellular carcinoma, possibly through inhibition of interleukin-8 production. Moriguchi, M., Nakajima, T., Kimura, H., Watanabe, T., Takashima, H., Mitsumoto, Y., Katagishi, T., Okanoue, T., Kagawa, K. Int. J. Cancer (2002) [Pubmed]
  29. Anticopper therapy against cancer and diseases of inflammation and fibrosis. Brewer, G.J. Drug Discov. Today (2005) [Pubmed]
  30. Wilson disease: genetic basis of copper toxicity and natural history. Schilsky, M.L. Semin. Liver Dis. (1996) [Pubmed]
  31. Gallium-68 1,1,1-tris (5-methoxysalicylaldiminomethyl) ethane: a potential tracer for evaluation of regional myocardial blood flow. Green, M.A., Welch, M.J., Mathias, C.J., Fox, K.A., Knabb, R.M., Huffman, J.C. J. Nucl. Med. (1985) [Pubmed]
  32. Ferromagnetism in a dinuclear nickel(II) complex containing triethylenetetramine and tricyanomethanide. Boca, R., Gembický, M., Herchel, R., Haase, W., Jäger, L., Wagner, C., Ehrenberg, H., Fuess, H. Inorganic chemistry. (2003) [Pubmed]
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