Fluorodeoxyuridine
 
Fluorodeoxyuridine (FUdR) is a mutagen and a potent inhibitor of thymidylate synthase (1), which leads to depletion of cellular pools of precursors to thymidine. The accuracy of both DNA replication and DNA repair is dependent upon a balanced supply of deoxyribonucleoside triphosphate (dNTP( precursors of DNA (2, 3), and perturbation of their relative levels has far-reaching effects. These include point mutation, chromosomal breakage, exchange or loss, as well as a stimulation of mitotic and meiotic recombination. Thus a large number of experimental systems and assays have responded positively to FUdR or its precursor 5-fluorouracil (summarized in Kunz et al. (3)), although they)unlike 5-bromo-, 5-iodo-, and 5-chlorodeoxyuridine) were not mutagenic for T4 bacteriophage in early studies (4). Unlike other nucleoside base analogues, such as 5-bromouracil or 2-aminopurine, FUdR does not directly affect base-pairing properties, but instead causes nucleotide pool imbalances through depleting dTTP and increasing dATP and dCTP pools (3).
 
References
1. S. S. Cohen, J. G. Flaks, H. D. Barner, M. R. Loeb, and J. Lichtenstein (1958) Proc. Natl. Acad. Sci. USA 44, 1004–1012. 
2. R. H. Haynes (1985) Basic Life Sci. 31, 1–23. 
3. B. A. Kunz, S. E. Kohalmi, T. A. Kunkel, C. K. Matthews, E. M. Mcintosh, and J. A. Reidy (1994) Mutat. Res. 318, 1–64. 
4. R. M. Litman and A. B. Pardee (1956) Nature 178, 529–531.