The animalswere cared for in line with the directions for the use and treatment of laboratory animals of the University of Shizuoka. Information was statistically analyzed by Students t test used by F test, and p 0. 0-5 was regarded as important. To analyze whether angiogenic boat qualified liposomes is useful for distribution of angiogenesis inhibitors,we first prepared liposomalSU1498, an GW0742 inhibitor ofVEGFR2tyrosine kinase. The chemical composition of SU1498 acrylonitrile] is shown in Fig. 1. We reviewed liposomal arrangement for successful entrapment of SU1498 into liposomes and established the essential fat part as follows; DPPC:POPC:DPPG:cholesterol: SU1498 dhge 10:10:2:2:1. Then, the efficiency of SU1498 in-to PEG or APRPG PEG modified liposomes was measured. About 75-80 of SU1498 was detected in liposome fractions but not detected in other fractions. In-addition, each size and page1=39 potential after extrusion was ?3mV and about 160nm, respectively. Next, to examine the antiangiogenic exercise of liposomal SU1498, cell proliferation assay of VEGF activated HUVECs was conducted. APRPG PEG Lip SU1498 highly suppressed endothelial cell proliferation induced by the therapy with VEGF, while PEG Lip SU1498 suppressed partly as well as free SU1498. On the other hand, APRPG PEG Lip SU1498, PEG Lip SU1498, and free SU1498 didn’t control the proliferation of Colon26 NL 17 carcinoma Infectious causes of cancer cells. These results suggest that liposomalization of SU1498 does not alter the inhibitory activity of it against VEGF signaling, and APRPG peptide modification of liposomes increases the effect of SU1498 maybe through the upsurge in option of the drug to HUVECs. Since liposomal SU1498 showed activity in vitro, we further examined the effect of angiogenic vessel targeted liposomal SU1498 in vivo. Antiangiogenic activity of APRPGPEG Lip SU1498 was analyzed in solid tumor bearing mice. We performed immunohistochemical staining for CD31, which can be an cell marker, and analyzed microvessel density in tumors of Colon26 NL 17 bearing mice following the treatment of APRPG PEG Lip SU1498. The procedure with APRPG PEG Lip SU1498 reduced microvessel density in-the tumors in comparison to control and to that with PEG Lip ALK inhibitor SU1498. The data suggest that targeted delivery of angiogenesis inhibitors to tumor endothelial cells permits to enhance the activity in tumor bearing rats. Since inhibition of angiogenesis could suppress cyst growth and metastasis, the result of liposomal SU1498 around the survival time of Colon26 NL 1-7 bearing mice was analyzed. as schedule of the procedure with VEGF RTK inhibitors the tumorbearing micewere administeredwith each trial by two different times as described above: schedule A is often used in liposomal reports, schedule T has been used.