Objective: To evaluate the relationship between the 18F-FDG and P-gp using Bcap37/MDR1 cells transected with hMDR 1 gene and Bcap37/MDR1 tumor-bearing mice models.Methods: The function of P-gp expressed in Bcap37/MDR1 cells was evaluated using Rhodamine123 (the classical substrate of P-gp) and verapamil or GF120918, the classical inhibiters of P-gp.Bcap37/MDR1 cells were divided into three groups: incubated with Rhodamine123 only, incubated with Rhodamine123 and verapamil or GF120918.After incubated in 1640 culture media for 60 min, the Fluorescence Units of Rhodamine123 in Bcap37/MDR1 cells were immediately analyzed.Bcap37/MDR1 cells were incubated in 1640 culture medium containing 18F-FDG for 60 min with or without the presence of verapamil or GF120918,respectively.18F-FDG accumulated in Bcap37/MDR1 cells was counted using γ-ray counter.Bald mice implanted with Bcap37/MDR1 cells were injected with 18F-FDG, 18F-FDG and verapamil by self-control.Micro PET images of Bcap37/MDR1 tumors in mice were performed 60 min after injection.Results: Verapamil and GF120918 can significantly increase the cellular accumulation of Rhodamine123 in Bcap37/MDR1 cells.The Rhodamine123 accumulated in cells were increased 1.64 and 1.80 times in the presence of verapamil and GF120918, respectively.It indicated that t Bcap37/MDR1 cells expressed the functionally P-gp.The cellular accumulation of 18F-FDG in Bcap37/MDR1 cells was also increased 1.69 and 1.67 times in the presence of verapamil and GF120918, respectively.SUVmean was increased 1.45 times after injected 18F-FDG with verapamil compared to the 18F-FDG.Conclusions: 18F-FDG was one of the substrates of P-gp.