TK1 is synthesized by the cell during the S phase of cell division. After cell division is completed, TK1 is degraded intracellularly and does not pass to body fluids after normal cell division. There is a feed-back regulation of the action of thymidine kinase in the cell: thymidine triphosphate (TTP), the product of the further phosphorylation of thymidine, acts as an inhibitor to thymidine kinase. This serves to maintain a balanced amount of TTP available for nucleic acid synthesis, not oversaturating the system. 5'-Aminothymidine, a non-toxic analogue of thymidine, interferes with this regulatory mechanism and thereby increases the cytotoxicity of thymidine analogues used as antineoplastic drugs. The reaction kinetics of thymidine and thymidine analogues phosphorylation is complicated and only partly known. The overall phosphorylation of thymidine to thymidine triphosphate does not follow Michaelis-Menten kinetics, and the various phosphates of thymidine and uridine interfere with the phosphorylation of each other. The kinetics of TK from different species differ from each other's and also the different forms from a given species (monomer, dimer, tetramer and serum form) have different kinetic characteristics.