Receptor tyrosine kinase (RTK) c-Met is the only known cell surface receptor for hepatocyte growth factor (HGF). The RTK c-Met has become an interesting target in the field of oncolo-gy due to its overexpression in cancer cells; the degree of expression is often coinciding with disease progression. Overexpression is characteristic for cancer in epithelial cells and more often overexpressed in metastasis than in a primary tumour. The RTK c-Met is involved in the proliferation of cells, morphogenesis and protection from apoptosis; this contributes to the overall survival of the cancer cells. A variety of c-Met inhibitors have been developed over the last decade, leading to three classes of small molecular c-Met inhibitor. This includes the exquisitely selective class I c-Met inhibitor 1, developed by Pfizer. The field of nuclear pharmacy and the use of positron emission tomography (PET) makes 1 an interesting chemical structure to use as a base for the development of a new PET-tracer, [18F]2. The hydroxyl group in 1 is exchanged with an [18F]fluorine group. This is categorised as a bioisosteric replacement meaning that the replacement potentially can be done without making alterations to the affinity of the PET-tracer. The selective RTK c-Met PET tracer [18F]2 can result in a new novel PET imaging agent. This thesis aimed to synthesise a new PET tracer [18F]2 through the development of a synes-thetic strategy. This master thesis includes synthesis of the c-Met inhibitor 1, in a low scale suited for labora-tory work. Furthermore, it contains the synthetic efforts to perform a two-step radiosynthesis towards [18F]2 successfully. Ex vivo autoradiography of [18F]2 was performed to confirm binding of the new tracer to the c-MET receptor in tumours. The IC50 value of [18F]2 was de-termined via enzyme assay. Future studies are planned to evaluate the abilities of this new PET tracer further.