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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Metabolism of N-[2-(dimethylamino)ethyl]acridine-4-carboxamide in cancer patients undergoing a phase I clinical trial.

N-[2-(Dimethylamino)ethyl]acridine-4-carboxamide (DACA) is an experimental antitumour agent that has just completed phase I clinical trials in New Zealand and the United Kingdom. Urine (0-72 h) was analysed from 20 patients receiving DACA infused over 3 h (dose range 60-1000 mg/m2, the latter being the highest dose achieved in the trial). Aliquots were analysed for DACA and its metabolites by high-performance liquid chromatography (HPLC). Over 72 h, 44+/-5% (range 20-60%) of the dose was recovered in the urine, with 0.8+/-0.3% (range 0-3.1%) occurring as DACA. The major urinary metabolite was DACA-N-oxide-9(10H)acridone, accounting for 34+/-3% of the dose. Minor metabolites were identified as N-monomethyl-DACA-9(10H)acridone (2.0+/-0.5%), DACA-9(10H)acridone (3.3+/-0.5%), N-monomethyl-DACA (0.2+/-0.1%) and DACA-N-oxide (0.5+/-0.1%). No ring-hydroxylated metabolite was detected. The urinary excretion of metabolites was greatest over 0-6 h in most patients. The composition of urinary metabolites was also independent of the delivered dose. Plasma was sampled at intervals throughout the infusion and at time points up to 48 h post-administration. The major plasma metabolites observed were DACA-9(10H)acridone and DACA-N-oxide-9(10H)acridone. These results indicate that, based on urinary excreted metabolites, the major biotransformation reactions for DACA in humans involve N-oxidation of the tertiary amine side chain and acridone formation, both of which appear to be detoxication reactions.[1]


  1. Metabolism of N-[2-(dimethylamino)ethyl]acridine-4-carboxamide in cancer patients undergoing a phase I clinical trial. Schofield, P.C., Robertson, I.G., Paxton, J.W., McCrystal, M.R., Evans, B.D., Kestell, P., Baguley, B.C. Cancer Chemother. Pharmacol. (1999) [Pubmed]
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