%0 Journal Article %A Nobuto Hirai %A Tadashi Watabe %A Naoki Tani %A Tatsuya Sakai %A Yuwei Liu %A Sadahiro Naka %A Yasukazu Kanai %A Mitsuaki Tatsumi %A Eku Shimosegawa %A Jun Hatazawa %T Comparison between L and D-isomer of 18F-FBPA: PET evaluation using rat models of glioma and the inflammation. %D 2018 %J Journal of Nuclear Medicine %P 67-67 %V 59 %N supplement 1 %X 67Purpose: L-4-borono-2-18F-fluoro-phenylalanine (L-18F-FBPA) is focusing attention as a tumor specific tracer as a substrate of L-type amino acid transporter 1 (LAT1). This L-form optical isomer is usually used for PET studies, but little is known about D-isomer of 18F-FBPA (D-18F-FBPA). The purpose of this study was to evaluate the performance of D-18F-FBPA as a tumor specific probe by investigating the uptakes in tumor and inflammation tissue as well as comparing them with our previous study using L-18F-FBPA. [Method] PET studies were conducted in rat xenograft models of C6 glioma with LAT1 expression (n=6, body weight 196 ± 11.3g) and in rat models of turpentine oil-induced subcutaneous inflammation (n=6, body weight 186.5 ± 7.9 g). In both models, D-18F-FBPA was injected through the tail vein of the rat (C6 glioma models: 36.6 ± 5.9 MBq, inflammation models: 33.6 ± 3.9 MBq). Under isoflurane anesthesia, 70 min dynamic PET scan (n=2) and 10 min PET static scans (n=10, 60 min after injection) were performed. After the PET imaging, the rats were sacrificed to obtain tissue sections of tumor and inflammation for the histological analysis. Volumes of interest were placed on the tumor and the inflammatory lesion of PET images using PMOD (Ver 3.6). We estimated the concentration of D-18F-FBPA by measuring standardized uptake value (SUV) and compared the uptakes between the two lesions and to the previous result of L-18F-FBPA as well. [Results] The time-activity curve (TAC) obtained from dynamic PET analysis showed that there was no significant difference in the kinetics between the tumor and the inflammatory lesion. Similarly, static PET analysis based on SUVmax also showed that no significant difference was observed in the D-18F-FBPA accumulation between the tumor and the inflammatory lesion (SUVmax = 0.74 ± 0.05, 0.69 ± 0.19, respectively). Histological analysis revealed that proliferative dysplastic cells in the C6 glioma and layers of neutrophils and macrophages surrounded by granulation tissues in the inflammatory lesion. In comparison with our previous study using L-18F-FBPA, D-18F-FBPA showed significantly lower uptakes in the tumor and the inflammation throughout their kinetic process. In the SUVmax measurement of static PET analysis, D-18F-FBPA showed significantly lower accumulations both in the tumor and the inflammation lesion compared to L-18F-FBPA (SUVmax of L-18F-FBPA = 3.23 ± 0.40, 1.86 ± 0.19, respectively) (p<0.05 and p<0.05 by unpaired t-test, respectively). [Conclusion] This study showed that D-18F-FBPA failed to differentiate the tumor and the inflammation as a tumor-specific probe in the kinetics as well as the static uptakes. The LAT1 transport of D-18F-FBPA is considered to be quite different from that of L-18F-FBPA. Tumor selectivity as a PET tracer is superior in L-18F-FBPA compare to D-18F-FBPA. %U