These results were confirmed by biodistribution studies demonstrating that, as early as 1 h post-injection, the tumor to blood concentration ratio was 7.5 and increased to 27 at 4 h.
Biodistribution studies demonstrated that DC-CHOL formulations prepared with DSPE-PEG2000 accumulathreefoldfold higher in s.c. HT29 tumors than its PEG-free counterpart.
Biodistribution studies demonstrated that [131I]IPMBA cleared rapidly from normal tissues and exhibited thyroid levels < or =0.1% injected dose, consistent with a low degree of dehalogenation.
Biodistribution studies demonstrate that the extent and duration of tumour exposure to vincristine is dramatically improved when the drug is administered i.v. in liposomal form.
An in vivo biodistribution study demonstrated the superior tumor targetability of CC-HAMs to that of non-crosslinked HAMs, primarily ascribed to robust stability of CC-HAMs in the bloodstream.
The biodistribution study demonstrated high tumor-to-blood ratios (6.2 ± 0.9 and 6.9 ± 1.0, for DU-145 and MCF-7, respectively, at 4 h after injection).
Biodistribution studies demonstrated tumour localisation for both A33 IgG and TFM with low bone, liver and kidney levels.
In vivo biodistribution studies and confocal studies demonstrated that even though both aptamer and control micelles showed tumor accumulation, only the aptamer micelles internalized into fractalkine-expressing cancer cells, thus demonstrating the potential of the approach and showing that fractalkine may serve as a specific target for nanoparticle delivery to cancer cells.
The high specific therapy, as we have seen, was more efficient than the low specific, which is in accordance with the biodistribution studies which demonstrate that the uptake in GRPR-expressing tissues is highest for the lower peptide dose and is reduced with the higher peptide dose.
