正电子放射性药物18F-FAMT已被开发为一种肿瘤特异性的PET显像剂，18F-FAMT在研究中已成功应用于各种恶性肿瘤的诊断，具有极佳的临床应用前景。但是，18F-FAMT在显像中呈现较高的肾脏生理学背景，该缺陷限制了它在肾癌症诊断中的应用。我们前期体外研究表明FAMT肾脏背景吸收机制与有机阴离子转运体（OAT），特别是OAT1介导的跨膜转运有关，由于体外实验无法直接反应体内的情况，所以本项目拟采用小鼠动物模型考察OAT抑制剂对FAMT肾脏排泄和分布的影响，明确OAT1是否为介导FAMT肾脏背景吸收最关键的分子机制，并通过基因敲除小鼠进行确证。此外，该研究还探讨了导致FAMT肾脏背景吸收的关键结构基团。该结果将有助于临床开发肿瘤显像中减少肾脏生理学背景吸收的方法，并为今后设计高肿瘤特异性低生理学背景的PET显像剂提供理论基础。

3-18F-L-α-methyl-tyrosine (18F-FAMT) has been developed as a cancer-specific PET molecular probe for tumor imaging. 18F-FAMT PET has been proved useful in clinical studies for the prediction of prognosis, the assessment of therapy response and the differentiation of malignant tumors from inflammation and benign lesions. However, in 18F-FAMT PET, kidney is the only organ that shows high physiological background, limiting its usefulness in renal cancer diagnosis. Previously we have demonstrated that the renal background of FAMT are due to transporter-mediated process, in particularly relating to organic anion transporter (OAT)1. However, there has been no in vivo evidence that OAT1 is involved in renal accumulation of FAMT. Here, we will elucidate the OAT-medicated transport mechanism causing FAMT renal accumulation by in vivo mouse model treated with OAT inhibitors as well as the gene knockout mouse model. In addition, we will determine the critical structural features of FAMT responsible for its renal background. This study could aid in development of treatments to reduce renal background and enhance tumor uptake as well as to designing PET tracers with less renal accumulation.