Abstract
A paired-label biodistribution was performed in athymic mice bearing SK-N-SH human neuroblastoma xenografts to compare the tissue uptake of meta-[ 211At]astatobenzylguanidine ([ 211At]MABG) and [ 131I]MIBG. Significantly higher ( p < 0.05) uptake of [ 211At]MABG was seen in tumor (3.8 ± 0.8% ID/g vs. 3.1 ± 0.7% ID/g at 8 h) compared to [ 131I]MIBG. Desipramine reduced tumor uptake of [ 211At] MABG by 43%, suggesting that its accumulation was related to the specific uptake-1 mechanism. Higher uptake of [ 211At]MABG was also seen in normal tissue targets such as heart (6.0 ± 0.9% ID/g vs. 4.5 ± 0.8% ID/g at 8 h; p < 0.05). Pretreatment of mice with unlabeled MIBG increased tumor uptake of [ 211At]MABG by 1.5-fold while reducing uptake in heart and several other normal tissues. The vesicular uptake inhibitor tetrabenazine reduced heart uptake by 30% without reducing the tumor uptake. These results suggest such strategies might be useful for improving [ 211At]MABG tumor-to-normal tissue ratios.
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