KS‐133/KS‐487 Nanoparticles Exhibit Potent Antitumor Effects through Synergistic LRP1 Targeting and VIPR2 Inhibition: Therapeutic Nanoarchitectonics for Solid Tumors

Author:

Sakamoto Kotaro1,Nishiyama Taisei2,Miyako Eijiro2ORCID

Affiliation:

1. Research & Development Department Ichimaru Pharcos Company Limited 318‐1 Asagi Motosu Gifu 501‐0475 Japan

2. Graduate School of Advanced Science and Technology Japan Advanced Institute of Science and Technology 1‐1 Asahidai Nomi Ishikawa 923–1292 Japan

Abstract

AbstractVIPR2 is associated with psychiatric disorders, breast cancer metastasis, and cancer immunostimulation. The VIPR2 antagonist KS‐133 changes the polarity of macrophages to the M1 type, and nanoparticles (NPs) releasing KS‐133 exhibit antitumor effects against mouse colon cancer cells (CT26) in vivo. To enhance the antitumor effect of KS‐133 NPs, KS‐133 NPs are combined with the peptide KS‐487 targeting LRP1, which is expressed on CT26 cells. Subcutaneous injection of NPs containing indocyanine green (ICG) fluorescent dye and presenting KS‐487 in CT26 subcutaneous tumor‐bearing mice resulted in significant accumulation of ICG in the CT26 tumor compared to administration of NPs without KS‐487. NPs containing KS‐133 and presenting KS‐487 (KS‐133/KS‐487 NPs) exhibited dose‐dependent antitumor effects in CT26 subcutaneous tumor‐bearing mice; the antitumor effects are more potent than the effects of KS‐133 NPs without KS‐487. In addition, CD8‐positive T cells and macrophages significantly infiltrated into CT26 tumors after injection of KS‐133/KS‐487 NPs. Thus, KS‐133/KS‐487 NPs efficiently deliver KS‐133 to CT26 tumors via LRP1‐targeting and activate immune system cells such as CD8 positive T cells and macrophages via KS‐133 inhibition of VIPR2 signaling, resulting in antitumor effects. These results demonstrate the potential of KS‐133/KS‐487 NPs as a therapeutic candidate for treating solid tumors.

Publisher

Wiley

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