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1. 5 Bromo 2' Deoxyuridine
2. 5 Bromodeoxyuridine
3. 5-bromodeoxyuridine
4. Brdu
5. Bromodeoxyuridine
6. Bromouracil Deoxyriboside
7. Broxuridine
8. Budr
9. Deoxyriboside, Bromouracil
10. Nsc-38297
1. 59-14-3
2. Broxuridine
3. Bromodeoxyuridine
4. 5-bromodeoxyuridine
5. 5-brdu
6. Brdu
7. Budr
8. 5-bromouracil Deoxyriboside
9. Bromouracil Deoxyriboside
10. 5-bromodesoxyuridine
11. 5-bdu
12. Broxuridinum
13. 5-bromo-2-deoxyuridine
14. Broxuridina
15. 5-bromouracil-2-deoxyriboside
16. Nsc-38297
17. Uridine, 5-bromo-2'-deoxy-
18. Chebi:472552
19. 5-bromo-2'-deoxy Uridine
20. Chembl222280
21. 5-bromo-1-(2-deoxy-beta-d-ribofuranosyl)uracil
22. G34n38r2n1
23. 5-bromo-2'-deoxyuridine (brdu)
24. 5-bromo-1-((2r,4s,5r)-4-hydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl)pyrimidine-2,4(1h,3h)-dione
25. Ncgc00090770-05
26. Mfcd00006529
27. 5-bromo-1-[(2r,4s,5r)-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidine-2,4-dione
28. Dsstox_cid_13105
29. Dsstox_rid_79051
30. Dsstox_gsid_33105
31. Broxuridine [inn]
32. C9h11brn2o5
33. Broxuridinum [inn-latin]
34. Bdu
35. Broxuridina [inn-spanish]
36. Cas-59-14-3
37. Smr001227189
38. Bromodeoxyuridine (brdu)
39. Ccris 818
40. Hsdb 7477
41. Broxuridine [inn:jan]
42. Einecs 200-415-9
43. (+)-5-bromo-2'-deoxyuridine
44. Brn 0030395
45. Unii-g34n38r2n1
46. 5-bromo-2'-deoxyuridine(brdu)
47. 5-bromo-1-[(2r,4s,5r)-4-hydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl]pyrimidine-2,4-dione
48. 5-bromo-durd
49. 5-brom-2'-desoxyuridin
50. Broxuridine (jan/inn)
51. Broxuridine [mi]
52. Maybridge4_003385
53. Broxuridine [jan]
54. Broxuridine [hsdb]
55. Epitope Id:138105
56. Cid_6035
57. Broxuridine [mart.]
58. Lopac0_000212
59. Schembl27755
60. Broxuridine [who-dd]
61. 4-24-00-01234 (beilstein Handbook Reference)
62. Mls001055406
63. Mls002153366
64. Dtxsid7033105
65. 5-bromo-2'-deoxyuridine, 97%
66. Hms1619b05
67. Hms3039g15
68. Hms3260l05
69. Bcp21681
70. Zinc1081243
71. 5-bromo-2''-deoxy Uridine
72. Tox21_111016
73. Tox21_200106
74. Tox21_500212
75. Bdbm50207303
76. Brdu (5-bromo-2?? -deoxyuridine)
77. Hg1160
78. Stl530083
79. Akos001715166
80. Akos016015753
81. Akos037495737
82. Tox21_111016_1
83. Ccg-204307
84. Db12028
85. Lp00212
86. Sdccgsbi-0050200.p002
87. Ncgc00090770-01
88. Ncgc00090770-02
89. Ncgc00090770-03
90. Ncgc00090770-04
91. Ncgc00090770-06
92. Ncgc00090770-07
93. Ncgc00090770-08
94. Ncgc00090770-09
95. Ncgc00090770-14
96. Ncgc00175901-01
97. Ncgc00257660-01
98. Ncgc00260897-01
99. 1-[(4s,2r,5r)-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]-5-bromo-1,3-dihydropyrim Idine-2,4-dione
100. As-11762
101. Hy-15910
102. 5-bromo-2'-deoxyuridine, >=99% (hplc)
103. Eu-0100212
104. 5-bromo-2'-deoxyuridine, Bioultra, >=99%
105. 5-bromo-2'-deoxyuridine, >=99.0% (hplc)
106. B 5002
107. D01763
108. 5- Br-2 Inverted Exclamation Mark -deoxyuridine
109. 006b529
110. Q419861
111. Sr-01000075718
112. J-700086
113. Sr-01000075718-1
114. Br-du; 5-bromo-1-(2-deoxy-beta-d-ribofuranosyl)uracil
115. Carbobenzoxy-valyl-alanyl-aspartyl-[o-methyl]-fluoromethylketone
116. (+)-5-bromo-1-[(2r,4s,5r)-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]- Pyrimidine-2,4-dione
117. 5-bromo-1-(2-deoxy-beta-d-erythro-pentofuranosyl)-4-hydroxypyrimidin-2(1h)-one
118. 5-bromo-1-((2r,4s,5r)-4-hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)pyridine-2,4(1h,3h)-dione
119. 5-bromo-1-((2r,4s,5r)-4-hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)pyrimidine-2,4(1h,3h)-dione
| Molecular Weight | 307.10 g/mol |
|---|---|
| Molecular Formula | C9H11BrN2O5 |
| XLogP3 | -0.3 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 5 |
| Rotatable Bond Count | 2 |
| Exact Mass | 305.98513 g/mol |
| Monoisotopic Mass | 305.98513 g/mol |
| Topological Polar Surface Area | 99.1 Ų |
| Heavy Atom Count | 17 |
| Formal Charge | 0 |
| Complexity | 386 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 3 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Orphan Drug. Drug Trade name Broxine/Neomark. Used for radiation sensitivity in the treatment of primary brain tumors.
U.S. FDA; Orphan Drug List. (November 20, 2006)
The halogenated pyrimidine analogs, bromodeoxyuridine (BUdR) and iododeoxyuridine (IUdR) have been recognized as potential clinical radiosensitizers for over two decades. In vivo and in vitro experimental studies document that radiosensitization is directly dependent on the amount of thymidine replacement in DNA by these analogs. ...
PMID:6381432 Kinsella TJ et al; Int J Radiat Oncol Biol Phys 10 (8): 1399-406 (1984)
Carcinogenicity has not been demonstrated; in fact, it is a useful agent in the treatment of neoplasms because it sensitizes tumor cells to the lethal effects of X-rays to a greater degree than normal tissue cells.
NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
Antineoplastic adjunct (radiosensitizer); diagnostic aid (tumor cell label for cytokinetic analysis).
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 2006., p. 237
For more Therapeutic Uses (Complete) data for BROMODEOXYURIDINE (9 total), please visit the HSDB record page.
/The authors/ report here the results of a Phase I study conducted to determine the toxicity and serum levels that could be tolerated by patients receiving i.v. bromodeoxyuridine concomitantly with radiation therapy. Because of severe thrombocytopenia and leukopenia that was produced in three patients treated by a 96 hour infusion of bromodeoxyuridine at a dose of 1.5 g/sq m/24 hours, the dose was reduced to 0.8 g/sq m/24 hours in these patients and the remaining 9 patients in the study group. Even at this dosage, myelotoxicity was observed.
PMID:6480461 Phuphanich S et al; Int J Radiat Oncol Biol Phys 10 (9): 1769-72 (1984)
During a clinical Phase I study of bromodeoxyuridine (BUdR) as a radiation sensitizer ... the normal and malignant cells that incorporated the BUdR /were identified/. BUdR was infused for up to 14 days and the in vivo incorporation of BUdR into DNA was assessed using an immunohistochemical technique and a monoclonal antibody directed against BUdR. BUdR was identified in 50% of breast cancer cells and 10% of cells in a malignant melanoma. BUdR was also found in the basal layer of the normal epidermis and in 50% of cells in the marrow. The incorporation of BUdR into cells in the epidermis and marrow may produce the phototoxicity and myelosuppression observed in patients treated with BUdR. ...
PMID:6469767 Morstyn G et al; Int J Radiat Oncol Biol Phys 10 (8): 1441-5 (1984)
Twelve patients were treated with continuous intravenous (24-hour) infusions of bromodeoxyuridine (BUdR) at 650 or 1,000 mg/sq m/d for up to two weeks. Myelosuppression, especially thrombocytopenia, was the major systemic toxicity and limited the infusion period to nine to 14 days. However, bone marrow recovery occurred within seven to ten days, allowing for a second infusion in most patients. Local toxicity (within the radiation field) was minimal, with the exception of one of four patients, who underwent abdominal irradiation. Pharmacology studies revealed a steady-state arterial plasma level of 6 X 10-7 mol/L and 1 X 10-6 mol/L during infusion of 650 and 1,000 mg/sq m/d, respectively. In vivo BUdR uptake into normal bone marrow was evaluated in two patients by comparison of preinfusion and postinfusion in vitro radiation survival curves of marrow CFUc with enhancement ratios (D0-pre/D0-post) of 1.8 (with 650 mg/sq m/d) and 2.5 (with 1,000 mg/sq m/d). In vivo BUdR incorporation into normal skin and tumor cells using an anti-BUdR monoclonal antibody and immunohistochemistry was demonstrated in biopsies from three patients revealing substantially less cellular incorporation into normal skin (less than 10%) compared with tumor (up to 50% to 70%). We conclude that local and systemic toxicity of continuous infusion of BUdR at 1,000 mg/sq m/d for approximately two weeks is tolerable. The observed normal tissue toxicity is comparable with our previous clinical experience with intermittent (12 hours every day for two weeks) infusions of BUdR. Theoretically, a constant infusion should allow for greater incorporation of BUdR into cycling tumor cells and thus, for further enhancement of radiosensitization.
PMID:6092551 Kinsella TJ et al; J Clin Oncol 2 (10): 1144-50 (1984)
... 12 hours of BUdR at a dose of 800-1,000 mg/sq m for five days a week was given to 23 patients with primary and secondary malignant brain tumors during radiation therapy. Radiation therapy was planned at a weekly dose of 10 Gy for five to six weeks. Fifteen patients received 1,000 mg/sq m of BUdR; six of them tolerated more than three weeks of treatment. In eight patients given doses of 800 mg/sq m, five patients tolerated more than three weeks. The most remarkable toxic effects were myelosuppression and stomatitis, which were major obstacles to maintaining the schedule.
PMID:3045898 Matsutani M et al; Radiat Med 6 (1): 33-9 (1988)
It is cytotoxic, strongly teratogenic, and mutagenic in some test systems.
NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
In man, the highest tolerated intravenous infusion dose is 700 mg/sq m/day when given over a period of 12 hr/day.
NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
Antimetabolites
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033) (See all compounds classified as Antimetabolites.)
Antiviral Agents
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. (See all compounds classified as Antiviral Agents.)
Radiation-Sensitizing Agents
Drugs used to potentiate the effectiveness of radiation therapy in destroying unwanted cells. (See all compounds classified as Radiation-Sensitizing Agents.)
Antimetabolites, Antineoplastic
Antimetabolites that are useful in cancer chemotherapy. (See all compounds classified as Antimetabolites, Antineoplastic.)
Twelve patients were treated with continuous intravenous (24-hour) infusions of bromodeoxyuridine (BUdR) at 650 or 1,000 mg/sq m/d for up to two weeks. ... Pharmacology studies revealed a steady-state arterial plasma level of 6 X 10-7 mol/L and 1 X 10-6 mol/L during infusion of 650 and 1,000 mg/sq m/d, respectively. In vivo BUdR uptake into normal bone marrow was evaluated in two patients by comparison of preinfusion and postinfusion in vitro radiation survival curves of marrow CFUc with enhancement ratios (D0-pre/D0-post) of 1.8 (with 650 mg/sq m/d) and 2.5 (with 1,000 mg/sq m/d). In vivo BUdR incorporation into normal skin and tumor cells using an anti-BUdR monoclonal antibody and immunohistochemistry was demonstrated in biopsies from three patients revealing substantially less cellular incorporation into normal skin (less than 10%) compared with tumor (up to 50% to 70%).
PMID:6092551 Kinsella TJ et al; J Clin Oncol 2 (10): 1144-50 (1984)
BrdU is absorbed from the gastrointestinal tract following parenteral injection and is presumably absorbed transplacentally (because of its teratogenic effects).
NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
Distribution and pharmacokinetics: Intra-arterial injection of BrdU into rodents results in extensive degradation... . Most of the portion which is not so degraded is incorporated into DNA of various tissues, particularly the colon, stomach, bone marrow, and spleen. The label of intraperitoneally injected deuterated BrdU in pregnant mice is also found in the liver of both mothers and embryos.
NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
BrdU tablets were implanted subcutaneously in rats, and BrdU concentrations were determined in the serum. Within 5 hr peak concentrations of 10 ug BrdU/mL blood were reached. ... With the use of agar-coated tablets, BrdU concentrations in the blood were reduced by half, and no peak concentration was found. ...
PMID:6617599 Maier P et al; Environ Mutagen 5 (5): 695-703 (1983)
BrdU is degraded at a fairly rapid rate in mice and rats upon injection, in at least two metabolic pathways; one is hydrolysis at the glycosyl bond to yield bromouracil and 2-deoxyribose which is presumably then further metabolized. The other is debromination which is evidenced by liberation of bromide ion. The further fate of the remainder of the molecule has not been investigated
Kriss JP, Revesz L; Cancer Res 22: 254-65 (1962) as cited in NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
The principal effects of BrdU in the animal body result from its incorporation into tissue DNA in place of thymidine (the 5-methyl analog of BrdU). Since chromosomal proteins have a greater affinity for BrdU-substituted DNA than for unsubstituted DNA, this results in a variety of chromosomal aberrations including chromosome lengthening, chromatid breakage, and effects on sister chromatid exchange frequency. Effects on meiosis as well as on mitosis have been reported.
NIH Division of Occupational Health and Safety; Safety Data Sheet for 5-Bromo-2'-deoxyuridine. Accessed through a query of https://www.niehs.nih.gov/odhsb/datasheets/home.htm as of February 20, 2007
5-Bromodeoxyuridine induces a senescence-like phenomenon in mammalian cells. This effect was dramatically potentiated by AT-binding ligands such as distamycin A, netropsin, and Hoechst 33258. The genes most remarkably affected by these ligands include the widely used senescence-associated genes and were located on or nearby Giemsa-dark bands of human chromosomes. /The authors/ hypothesize that AT-rich scaffold/nuclear matrix attachment region sequences are involved in this phenomenon. In fact, upon substitution of thymine with 5-bromouracil, a rat S/MAR sequence reduced its degree of bending and became insensitive to cancellation of the bending by distamycin A. The S/MAR sequence containing 5-bromouracil also bound more tightly to nuclear scaffold proteins in vitro and this binding was not inhibited by distamycin A. Under the same conditions, the S/MAR sequence containing thymine easily dissociated from the nuclear scaffold proteins. Taken together, the synergistic induction of the genes may be explained not only by opening of condensed chromatin by distamycin A but also by increase in the binding of 5-bromouracil-containing S/MAR sequences to the nuclear scaffolds.
PMID:12027447 Suzuki T et al; Exp Cell Res 276 (2): 174-84 (2002)
An ectopic gene integrated in the host genome is occasionally silenced due to a position effect of its adjacent chromatin structure. /The authors/ found that 5-bromodeoxyuridine clearly activated such a transgene in HeLa cells. The transgene was also activated to various degrees by inhibitors of histone deacetylase, DNA topoisomerases, or DNA methyltransferase. The peptide antibiotic distamycin A potentiated markedly the effect of 5-bromodeoxyuridine. Transient expression of an artificial AT-hook protein termed MATH20 also potentiated its effect although significantly activated the transgene alone. Since distamycin A and MATH20 are able to displace histone H1 and other DNA-binding proteins bound to specific AT-rich sequences by a dominant, mutually exclusive fashion, these results suggest that 5-bromodeoxyuridine targets such an AT-rich sequence located adjacent to the silenced transgene, resulting in chromatin accessibility.
PMID:11339824 Suzuki T et al; Exp Cell Res 266 (1): 53-63 (2001)
5-Bromodeoxyuridine (BrdU) universally induces a senescence-like phenomenon in mammalian cells. To assess this phenomenon at the level of gene expression, /the authors/ constructed a PCR-based subtractive cDNA library enriched for mRNA species that immediately increase by administration of BrdU to HeLa cells. Candidate cDNA clones were isolated by differential colony hybridization, and then positive clones were identified by Northern blot analysis. Sequencing analysis revealed that the identified cDNA species were classified into three groups: widely used senescence-markers, known species whose relevance to senescence is yet to be reported, and known or novel ESTs. As expected, the majority of them showed an increase in expression in senescent human diploid fibroblasts. These results suggest that similar mechanisms operate in the regulation of BrdU-induced genes and senescence-associated genes.
PMID:11250118 Suzuki T et al; Exp Gerontol 36 (3): 465-74 (2001)
For more Mechanism of Action (Complete) data for BROMODEOXYURIDINE (7 total), please visit the HSDB record page.
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