VTN and prostate carcinoma: These compounds were also assayed for their ability to inhibit the adhesion to vitronectin of both αVβ3-overexpressing and αVβ3-lacking cells (namely, αVβ3-positive endothelial progenitor cells EPCs and melanoma cells M21, as well as αVβ3-lacking human prostate carcinoma cells PC3 and human erythroleukemia cells K562); the results showed that conjugates 1–3 inhibited cell adhesion to vitronectin of αVβ3-overexpressing cells in the low micromolar range, while the c(AmpRGD) parent compound did not impact at all on cell adhesion to vitronectin in αVβ3-lacking cells [18,19].