AsiaChem | Chemistry in Japan | December 2021 Volume 2 Issue 1

www.asiachem.news December 2021 | 69 of non-glycosylated protein (HSA) was found to spread out the whole body. Since these are known substrates of receptors normally expressed on nonparenchymal liver cells, our histological studies could indeed confirm that mannose-terminated 1b was capturedbyKupper cells and/or macrophages through the interaction with C-type lectins. Meanwhile, glucosamine-terminated 1a and hybrid-type 1c mainly interacted with liver stellate cells and sinusoidal endothelial cells. As for galactose-terminated 1d, liver accumulation is consistent with being rapidly captured by certain receptors (asialoglycoprtein receptors, ASGPR) expressedonparenchymal hepatocytes. Intriguingly, dissection studies revealed an excretion pathway where 1d was found to be shuttled to the gall bladder and intestines from liver. On the other hand, sialylated-terminated 1f-g were Figure 5. (A) In vivo labeling of organ by the organ-targeting GArM-Au-1. I) Illustration of protein labeling on the surface of targeted cell by the GArM-Au-1 mediated reaction. II) Imaging data displayed that labeling of organs in mice were dependent on the identify of the linked N-glycan. (B) In vivo prevention of tumor onset and progression via SeCT therapy. I) Illustration of labeling target tumor cells with cRGD moieties in vivo to block integrin-based cell adhesion via the GArM-Au-1. II) A representative set of the tumor progression in mice after 4 weeks through IVIS imaging results. (C) In vivo inhibition of tumor growth using a therapeutic peptide via SeCT therapy. I) Illustration of labeling target tumor cells with a therapeutic peptide via (cRGD)ArM-Ru-2. II) Measurement of tumor size in mice over time. Comparison of mice survival rates under various treatment. (D) In vivo synthetic prodrug therapy against HeLa tumour growth in mice. I) Schematic depiction of HeLa targeted activation of prodrug using the GArM-Ru-1. II) Measurements of tumor size (mm3) in mice over time. Tumours were initially implanted in mice and developed over 4 days before therapy.

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