5-Bromouracil induces A-type DNA, which messes with the placement of nucleosomes.

Metabolism / Metabolites
Eosinophils utilize eosinophil peroxidase, hydrogen peroxide (H₂O₂), and bromide ions (Br⁻) to generate hypobromoic acid (HOBr), a bromination intermediate. This strong oxidant may play a role in host defense against invading parasites and eosinophil-mediated tissue damage. In this study, the authors explored the possibility of HOBr generated by eosinophil peroxidase oxidizing nucleic acids. When uracil, uridine, or deoxyuridine was exposed to the reagent HOBr, each reaction mixture produced a major oxidation product that co-migrated with the corresponding standard bromopyrimidine in reversed-phase high-performance liquid chromatography (HPLC). The eosinophil peroxidase-H₂O₂-Br⁻ system also converted uracil to a major oxidation product in near-quantitative yields. Mass spectrometry, HPLC, UV-Vis spectroscopy, and NMR spectroscopy identified the product as 5-bromouracil. Eosinophil peroxidase requires H₂O₂ and Br⁻ to generate 5-bromouracil, indicating that HOBr is an intermediate in this reaction. Primary and secondary bromides can also bromate uracil, suggesting that long-lived bromides may also be physiologically relevant bromination intermediates. Human eosinophils utilize the eosinophil peroxidase-H₂O₂-Br⁻ system to oxidize uracil. Mass spectrometry, high-performance liquid chromatography, and UV-Vis spectroscopy identified the product as 5-bromouracil. In summary, these results indicate that HOBr produced by eosinophil peroxidase can oxidize uracil to 5-bromouracil. Thymidine phosphorylase, a pyrimidine salvage enzyme, can convert 5-bromouracil to 5-bromodeoxyuracil, a mutagenic analog of thymidine. These findings suggest that halogenated nucleobases produced by eosinophil peroxidase may exert cytotoxic and mutagenic effects at eosinophil-rich inflammatory sites. The authors used a sensitive and specific mass spectrometry method to detect two products of myeloperoxidase: 5-chlorouracil and 5-bromouracil in neutrophil-rich human inflammatory tissues. Since halogenated uracil is a specific product of the myeloperoxidase system in vitro, myeloperoxidase is likely the source of 5-chlorouracil in vivo. Conversely, previous studies have shown that both eosinophilic peroxidase and myeloperoxidase can generate 5-bromouracil, which preferentially brominates uracil under plasma halide concentrations and moderately acidic conditions. These observations suggest that the myeloperoxidase system promotes nucleobase halogenation in vivo. Given that 5-chlorouracil and 5-bromouracil can be incorporated into nuclear DNA, and that these thymine analogs are known mutagens, our observations suggest that phagocytic-initiated halogenation reactions may be one pathway for mutagenesis and cytotoxicity at the site of inflammation. 5-Bromouracil is metabolized to 5-bromodeoxyuridine by thymidine phosphorylase. (L626)

Toxicity Summary
Thymidine phosphorylase is a pyrimidine salvage enzyme that converts 5-bromouracil to 5-bromodeoxyuridine, a mutagenic analog of thymidine. Ultimately, 5-bromouracil acts on DNA, inducing random point mutations through base substitution. After several replication cycles, the base pair changes from AT to GC, or from GC to AT, depending on whether 5-bromouracil enters the DNA molecule internally or as a foreign base in an enolized or ionized form. 5-Bromouracil typically pairs with adenine. However, because the electronegativity of the bromine atom is stronger than that of the methyl group at the C-5 position, the proportion of 5-bromouracil enol tautomers is higher than that of thymine. Therefore, the incorporation of 5-bromouracil is particularly likely to lead to changes in base pairing during subsequent DNA replication.

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Toxicity Data
LD50: 1700 mg/kg (rat, intraperitoneal injection); LD50: 1400 mg/kg (mouse, intraperitoneal injection) (T14)Interactions
The addition of 5-bromouracil (BU) and 5-bromo-2-deoxyuridine (BUdR) to bacterial culture media resulted in a significant increase in bacterial susceptibility to ultraviolet radiation. Similar effects were observed with the nucleic acid base analog 8-azaadenine (8-AA), but less pronounced than with BU. This paper reports an experimental study investigating the effects of BU or BUdR in combination with 8-AA on Escherichia coli, Proteus mirabilis, Bacillus subtilis, and Bacillus cereus. The sensitization effect of BUdR was not enhanced by the additional addition of 8-AA during culture; on the contrary, it was reduced. This result may be due to the protective effect of the adenine derivative against ultraviolet radiation, provided that the derivative is present in the cell but not integrated into the DNA.
Cherenkov radiation and ionizing radiation cause cumulative damage to E. coli AB2487 recA, increasing its lethality rather than synergistically. Bromouracil substitution enhances the lethality of high-energy X-rays on E. coli AB2487 recA through mechanisms that increase radiosensitivity and photosensitivity.

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Non-human toxicity values
Intraperitoneal LD50 in mice: 1400 mg/kg
Intraperitoneal LD50 in rats: 1700 mg/kg

Therapeutic Uses

Antimetabolites
/Experimental Treatment/ This paper synthesizes ternary complexes of Mn(II), Co(II), Ni(II), Cu(II), Zn(II), and Cd(II) ions with 5-halouracil (i.e., 5-fluorouracil (5FU), 5-chlorouracil (5ClU), and 5-bromouracil (5BrU)) and the biologically significant ligand L-histidine (HISD). These complexes were characterized by elemental analysis, conductivity measurements, infrared spectroscopy, electronic spectroscopy, and room-temperature magnetic moment measurements. Based on these studies, the structures of these complexes are proposed. All of these ternary complexes were screened for anti-Dalton lymphoma activity in C3H/He mice. The study found that only the complexes of Mn(II)-5BrU-HISD, Co(II)-5BrU-HISD, Cu(II)-5ClU-HISD, Cu(II)-5BrU-HISD, Zn(II)-5FU-HISD, and Zn(II)-5BrU-HISD exhibited significant antitumor activity, with T/C values greater than 125% (where T and C represent the mean survival of mice in the treatment and control groups, respectively). The complexes of Mn(II)-5FU-HISD, Co(II)-5FU-HISD, Co(II)-5ClU-HISD, Ni(II)-5ClU-HISD, Ni(II)-5BrU-HISD, and Zn(II)-5ClU-HISD also showed effective antitumor activity, with T/C values greater than 115%. These complexes, which exhibited effective antitumor activity in vivo, were also found to inhibit the incorporation of 3H-thymidine (DNA replication) in Dalton lymphoma cells in vitro.

C4H3BRN2O2

190.98

189.937

51-20-7

5802

Prisms from water

2.0±0.1 g/cm3

384ºC

>300 °C(lit.)

1.590

-0.35

2

2

0

9

199

0

BrC1=C([H])N([H])C(N([H])C1=O)=O

LQLQRFGHAALLLE-UHFFFAOYSA-N

InChI=1S/C4H3BrN2O2/c5-2-1-6-4(9)7-3(2)8/h1H,(H2,6,7,8,9)

5-bromo-1H-pyrimidine-2,4-dione

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 100 mg/mL (523.62 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (13.09 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (13.09 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (13.09 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)