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• W2177111572 abstract "Tumour formation is dependent on nutrient and oxygen supply from adjacent blood vessels. Angiogenesis inhibitors can play a vital role in controlling blood vessel formation and consequently tumour progression by inhibiting endothelial cell proliferation, sprouting and migration. The primary aim of the present study was to design cyclic thrombospondin-1 (TSP-1) mimetics using disulfide-rich frameworks for anti-angiogenesis therapies and to determine whether these peptides have better potency than the linear parent peptide. A short anti-angiogenic heptapeptide fragment from TSP-1 (GVITRIR) was incorporated into two cyclic disulfide-rich frameworks, namely MCoTI-II (Momordica cochinchinensis trypsin inhibitor-II) and SFTI-1 (sunflower trypsin inhibitor-1). The cyclic peptides were chemically synthesized and folded in oxidation buffers, before being tested in a series of in vitro evaluations. Incorporation of the bioactive heptapeptide fragment into the cyclic frameworks resulted in peptides that inhibited microvascular endothelial cell migration, and had no toxicity against normal primary human endothelial cells or cancer cells. Importantly, all of the designed cyclic TSP-1 mimetics were far more stable than the linear heptapeptide in human serum. The present study has demonstrated a novel approach to stabilize the active region of TSP-1. The anti-angiogenic activity of the native TSP-1 active fragment was maintained in the new TSP-1 mimetics and the results provide a new chemical approach for the design of TSP-1 mimetics." @default.
• W2177111572 created "2016-06-24" @default.
• W2177111572 creator A5008575244 @default.
• W2177111572 creator A5079308758 @default.
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• W2177111572 date "2015-11-26" @default.
• W2177111572 modified "2023-09-25" @default.
• W2177111572 title "Cyclic thrombospondin-1 mimetics: grafting of a thrombospondin sequence into circular disulfide-rich frameworks to inhibit endothelial cell migration" @default.
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• W2177111572 doi "https://doi.org/10.1042/bsr20150210" @default.
• W2177111572 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4660582" @default.
• W2177111572 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26464514" @default.
• W2177111572 hasPublicationYear "2015" @default.
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