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The functions and applications of A7R in anti-angiogenic therapy, imaging and drug delivery systems.


ABSTRACT: Vascular endothelial growth factor receptor 2 (VEGFR-2) and neuropilin-1 (NRP-1) are two prominent antiangiogenic targets. They are highly expressed on vascular endothelial cells and some tumor cells. Therefore, targeting VEGFR-2 and NRP-1 may be a potential antiangiogenic and antitumor strategy. A7R, a peptide with sequence of Ala-Thr-Trp-Leu-Pro-Pro-Arg that was found by phage display of peptide libraries, can preferentially target VEGFR-2 and NRP-1 and destroy the binding between vascular endothelial growth factor 165 (VEGF165) and VEGFR-2 or NRP-1. This peptide is a new potent inhibitor of tumor angiogenesis and a targeting ligand for cancer therapy. This review describes the discovery, function and mechanism of the action of A7R, and further introduces the applications of A7R in antitumor angiogenic treatments, tumor angiogenesis imaging and targeted drug delivery systems. In this review, strategies to deliver different drugs by A7R-modified liposomes and nanoparticles are highlighted. A7R, a new dual targeting ligand of VEGFR-2 and NRP-1, is expected to have efficient therapeutic or targeting roles in tumor drug delivery.

SUBMITTER: Lu L 

PROVIDER: S-EPMC7032227 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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The functions and applications of A7R in anti-angiogenic therapy, imaging and drug delivery systems.

Lu Lu L   Chen Hongyuan H   Hao Dake D   Zhang Xinke X   Wang Fengshan F  

Asian journal of pharmaceutical sciences 20190525 6


Vascular endothelial growth factor receptor 2 (VEGFR-2) and neuropilin-1 (NRP-1) are two prominent antiangiogenic targets. They are highly expressed on vascular endothelial cells and some tumor cells. Therefore, targeting VEGFR-2 and NRP-1 may be a potential antiangiogenic and antitumor strategy. A7R, a peptide with sequence of Ala-Thr-Trp-Leu-Pro-Pro-Arg that was found by phage display of peptide libraries, can preferentially target VEGFR-2 and NRP-1 and destroy the binding between vascular end  ...[more]

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