73210-73-8 Purity
98%
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To elucidate the potential efficacy of cyclic arginine-glycine-aspartic acid peptide (cRGD) in preventing atherogenesis in vivo, this work was performed in apolipoprotein E (ApoE)-deficient (-/-) mice fed a Western diet and treated with cRGD peptide for 2-4 weeks. In this experiment, cRAD peptide (cyclo-Arg-Ala-Asp- d -Phe-Val) was used as a negative control for cRGD peptide.
Bioassay of biological activity of long-term delivery of cRGD
· The biological efficacy of chronic cRGD treatment was verified by adding different concentrations of cRGD, cRAD or PBS to whole blood and measuring ADP-induced coagulation to examine whether the cRGD has an inhibitory effect on ADP-induced platelet aggregation.
· Aggregation was completely blocked in vitro with cRGD at a concentration of 10 μM. ADP-induced platelet aggregation was inhibited by about 50% even at concentrations as low as 10 nM. cRAD had a measurable but small effect on aggregation at a concentration of 10 μM.
· According to a series of individual results obtained in the blood of ApoE (-/-) mice chronically treated with cRAD, chronic infusion of the peptide did not affect ADP-induced platelet aggregation isolated from animals B11-B16. In contrast, 50% of the animals in the cRGD-treated group showed complete or significant inhibition of platelet aggregation.
· In addition, a mass-to-charge peak corresponding to the cRGD peptide was detectable in the sera of animals treated with the peptide, but not in serum samples from mice treated with PBS or the RAD peptide.