Rapidly dividing cells, like cancer cells, consume dTMP at rapid rates for incorporation into DNA. Interfering with the thymidylate synthase reaction will decrease dTMP production, and this happens with 5-fluorodeoxyuridylate (FdUMP), which is an irreversible inhibitor of thymidylate synthase. Its inhibition occurs within the metabolic pathway, and so the enzyme is permanantly taken out of circulation (a "mechanism-based" inhibitor). Of course, such a therapeutic modality would also affect other normally rapidly dividing cells, like those in hair follicles, bone marrow, the immune system and intestinal mucosa, and hence the well-known side effects.
The dihydrofolate reductase step can also be blocked with competitive inhibiton of the enzyme by analogs of DHF, including aminopterin, methotrexate and trimethoprim. Not surprisingly, then, these type of drugs are known as "anti-folates". Trimethoprim turns out to be a good antibiotic, as it binds more strongly to bacterial, as opposed to mammalian, dihydrofolate reductases.