aIn this study, the optimization of gemcitabine labeling with iodine-125 and its biological evaluation are described. Gemcitabine was labeled via direct electrophilic substitution using chloramine-T as an oxidizing agent. The optimum amounts of reactants were 75 mg gemcitabine, 75 mg chloramine-T and 18 MBq carrier-free Na 125 I. The labeled gemcitabine was stable for more than 20 h. Results of the in vivo evaluation revealed that the new tracer, [125 I] gemcitabine, tends to localize in tissues with high proliferation rate with preferential accumulation in cancerous tissues. Imaging should be carried at 2-h postinjection. The in vitro cell growth inhibition assay showed that the effect of [ 125 I] gemcitabine was stronger than the effect of tenfold cold gemcitabine, which strongly suggested that its cytotoxicity was mainly due to radiotoxicity rather than chemotherapeutic activity. The binding assay revealed that [125 I] gemcitabine uptake by the Ehrlich cells was high and that it bound well to DNA where the decay of the radionuclide introduced lethal irreversible double-strand breaks.

SUMMARYLong chain ~~~~I -l a b e l l e d fatty acids such as 16-I-hexadecanoic-, 17-I-heptadecanoic-, and 16-Ihexadec-9-enoic acid have been prepared without adding carrier by nucleOphilic in acetone, in the melt, and by use of phase transfer catalysts in non-polar solvents. While preparation in refluxing acetone required reaction times of more than 2 hours to reach saturation yields, halogen exchange in molten bromofatty acids at temperatures of about 150 C gave rise to yields of about 80% of radiochemically pure 1 7-1 231-heptadecanoic acid within only 5 minutes. Comparable yields were also obtained using Kryptofix 2 2 1 in refluxing toluene after 1 0 minutes, 231-for-Br exchange 0

aIn this study, the optimization of troxacitabine labeling with iodine-125 and its biological evaluation were described. Troxacitabine was labeled via direct electrophilic substitution using chloramine-T as oxidizing agent. The optimum amounts of reactants were: 50 lg troxacitabine, 75 lg Chloramine-T and $19 kBq carrier free Na 125 I. The labeled troxacitabine was stable for more than 24 h. Results of the in-vivo evaluation revealed that the new tracer, [ 125 I]troxacitabine, tends to localize in tissues with high proliferation rate with preferential accumulation in cancerous tissues. Imaging should be carried at 3 h postinjection. The in vitro cell growth inhibition assay showed that the effect of [ 125 I]troxacitabine was stronger than the effect of cold troxacitabine, which strongly suggested that its cytotoxicity was mainly due to radiotoxicity rather than chemotherapeutic activity. The binding assay revealed that [125 I]troxacitabine uptake by the Ehrlich and the ARAC8C cells was high and that it bounded well to DNA.

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