Fig 1.
Synthetic scheme of c(RGDfK)-SH.
To introduce thiol into c(RGDfK), SATA was conjugated to c(RGDfK). Subsequently, the sulfhydryl group was deprotected using hydroxylamine.
Table 1.
Lipid composition of the liposomes.
Fig 2.
Particle size distribution curves of RGD-liposomes and NT-liposomes.
Fig 3.
Inhibition of 125I-echistatin binding to αvβ3 integrin on PANC-1 cells by RGD-, RKG-, and NT-liposomes (n = 3).
The x-axis represents the concentration of the liposomal membrane lipid. The RGD-liposomes dose-dependently inhibited the binding of 125I-echistatin to PANC-1 cells in a dose-dependent manner. However, no inhibition was observed with RKG- or NT-liposomes.
Fig 4.
Biodistribution of 111In-RGD-liposomes and 111In-NT-liposome in PANC-1 xenograft-bearing nude mice at 24 h post-injection (n = 3–4).
Results are expressed as the percentage of the ID/g tissue. The 111In-NT-liposome showed the highest accumulation in both tumor and blood. Among the 111In-RGD-liposomes, the 111In-H-RGD-liposome showed the lowest accumulation in these tissues. Accumulation in the spleen varied with the degree of RGD peptide modification on the liposomes.
Fig 5.
Tumor-to-blood, -pancreas, and -muscle ratios of 111In-RGD-liposomes and 111In-NT-liposomes in PANC-1 xenograft-bearing nude mice at 24 h post-injection (n = 4).
Tumor to normal tissue ratios were calculated from the biodistribution data.
Fig 6.
MR imaging (9.4 T) of PANC-1 xenograft-bearing scid mice.
(a) RARE T1 MR images after treatment with H-RGD-liposomes loaded with ferrioxamine B. Open arrowheads indicate enhanced areas. (b) RARE T1 MR images after treatment with RKG-liposomes loaded with ferrioxamine B. (c) Tumor-to-muscle signal (T/M) ratios for H-RGD- and RKG-liposomes loaded with ferrioxamine B (n = 3).