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Bromodeoxyuridine (BrdU)

Alias: 5-BROMO-2'-DEOXYURIDINE; 59-14-3; Broxuridine; Bromodeoxyuridine; 5-Bromodeoxyuridine; 5-BrdU; BRDU; BrdU; Broxuridine; 5-Bromo-2''-deoxyuridine; BUdR
Cat No.:V1431 Purity: ≥98%
Bromodeoxyuridine (BrdU; Broxuridine; 5-Bromo-2-deoxyuridine; BUdR) is a nucleoside analog with potential anticancer activity.
Bromodeoxyuridine (BrdU)
Bromodeoxyuridine (BrdU) Chemical Structure CAS No.: 59-14-3
Product category: DNA(RNA) Synthesis
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Purity: ≥98%

Product Description

Bromodeoxyuridine (BrdU; Broxuridine; 5-Bromo-2'-deoxyuridine; BUdR) is a nucleoside analog with potential anticancer activity. It has been used in the detection of proliferating cells and functions as an antimetabolite anticancer agent by competing with thymidine for incorporation into DNA. Early on in the dedifferentiation process, the impact of 5-BrdU on the proliferation of grown Nicotiana glauca pith explants was investigated. Only when administered within the first 72 hours of culture did it turn out to be completely inhibitory; this inhibition could be overcome by simultaneously adding either thymidine or deoxyeytidine.

Biological Activity I Assay Protocols (From Reference)
Targets
DNA synthesis; antimetabolite
ln Vitro

Bromodeoxyuridine causes a dose-responsive, progressive suppression of cancer cell line and cancer stem cell population expansion in RG2 rat glioma cells. The cell cycle profile of BJ fibroblasts and H9 cells is changed by bromodeoxyuridine.[1]
BrdU is stably integrated into the DNA, making it suitable for use in evaluating other cell processes such as proliferation.[2]

ln Vivo
Bromodeoxyuridine (300 mg/kg, i.p. or 0.8 mg/ml, p.o.) markedly slows the progression of the tumor in the rat glioma RG2 tumor model.[1]
Enzyme Assay
Telomere Length[1]
To determine whether the effects of BrdU are related to changes in telomere length, we performed a TeloTAGGG assay. Briefly, genomic DNA was isolated and digested with Hinf1 and Rsa1 enzymes. After digestion, the DNA fragments were separated by gel electrophoresis and transferred to a nylon membrane for Southern blot analysis. The blotted DNA fragments were hybridized to a digoxigenin (DIG)-labeled probe specific for telomeric repeats and incubated with a DIG-specific antibody covalently coupled to alkaline phosphatase. Finally, the immobilized telomere probe was visualized by virtue of alkaline phosphatase-metabolizing CDP-Star, a highly sensitive chemiluminescence substrate.
Telomerase Activity[1]
We used the TRAPeze ELISA kit assay to determine levels of telomerase activity in our control and BrdU-treated cells. Briefly, the sample cells' telomerase adds a number of telomeric repeats (GGTTAG) onto the 3′ end of the biotinylated telomerase substrate oligonucleotide (b-TS), and the extended products are then amplified by polymerase chain reaction. The extension/amplification was performed with biotinylated primer andDNP-labeled dCTP. Thus, the telomeric repeat amplification protocol (TRAP) products are tagged with biotin and DNP residues, and the labeled products can be immobilized onto streptavidin-coated microtiter plates through biotin-streptavidin interaction, and then detected by anti-DNP antibody conjugated to horseradish peroxidase (HRP). The amount of TRAP products was determined by means of the HRP activity using substrate TMB and subsequent color development.
Cell Assay
Initially plated at 2000 cells/cm2, cultures are measured using a Z2 Coulter Counter. After treating RG2 rat glioma cells once for 24 hours with 0, 1, 10, or 50 µM BrdU, cumulative growth curves were measured over a period of 18 days. After five, twelve, and eighteen days of treatment, control and treated cells are counted and replated at equal densities.
Animal Protocol
Subcutaneous Tumors and In Vivo BrdU Administration[1]
A bolus of either untreated or pretreated RG2 glioma cells (1 x 106 cells in 250 µl of PBS) was injected subcutaneously between the scapulae of anesthetized adult male Fisher 344 rats as previously described. Pretreated RG2 cells were treated with 50 µM BrdU for 24 hours before implantation. Tumors were measured every other day in two dimensions with digital calipers, and tumor volume was calculated [(π/6) x W2 x L (W = shortest dimension and L = longest dimension)]. The experimental end point was defined as a tumor volume ≥3000 mm3. At end point, euthanasia was performed by transcardial perfusion with 200 ml of 4% paraformaldehyde in PBS under deep sodium pentobarbital anesthesia (150 mg/kg, i.p.).[1]
BrdU administration, i.p. Untreated RG2 cells were implanted into 10 animals as described previously. The BrdU regimen was initiated when palpable tumors had reached a volume of 200 mm3. Half of the animals received three i.p. injections of BrdU (300 mg/kg) per day for 2 days, whereas the other half served as controls and received an equal number and volume of sterile saline injections.[1]
BrdU administration, oral. Again, untreated RG2 cells were implanted subcutaneously into 20 animals as described. Immediately after implantation, half of the animals were provided with drinking water containing BrdU (0.8 mg/ml), and half received normal drinking water. All animals were provided with freshly prepared water (either with or without BrdU) each day for 7 days, ad libitum. On the eighth day after implantation, all animals were placed on normal drinking water for the duration of the experiment.[1]
A dose of 300 mg/kg corresponds to a clinical dose of 1800 mg/m2. The rats received three of these doses per day for 2 days, thus receiving a total of 10,800 mg/m2. The drinking water dose (based on the standard 20-ml/day consumption by adult rats) is 640 mg/m2 per day for 7 days, or a total of 4480 mg/m2. By way of comparison, previous clinical trials (e.g., Kinsella et al.) included BrdU as a radiosensitizer as part of a multimodal therapy-treated patients with 350 mg/m2 for continuous 12-hour infusions every day for 14 days or 4900 mg/m2 total. Thus, the treatment range in our study is generally in accord with previous human clinical applications, because, although our injected BrdU was theoretically approximately twice what humans received, it is known that BrdU is active in plasma only for approximately 2 hours. Therefore, the continuous infusion used in the human trials likely resulted in more widespread BrdU incorporation than our injection paradigm.[1]
300 mg/kg, i.p. or 0.8 mg/ml, p.o.
Rat glioma RG2 tumor model
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
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%).
BrdU is absorbed from the gastrointestinal tract following parenteral injection and is presumably absorbed transplacentally (because of its teratogenic effects).
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.
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. ...
Metabolism / Metabolites
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
5-bromodeoxyuridine is phosphorylated by thymidine kinase to produce 5-bromodeoxyuridine-phosphate. (L626)
Toxicity/Toxicokinetics
Toxicity Summary
5-bromodeoxyuridine acts on DNA. It induces a random DNA point mutation via base substitution. The base pair will change from an A-T to a G-C or from a G-C to an A-T after a number of replication cycles. As a thymine analog, 5-bromodeoxyuridine normally pairs with adenine.
Toxicity Summary
5-bromodeoxyuridine acts on DNA. It induces a random DNA point mutation via base substitution. The base pair will change from an A-T to a G-C or from a G-C to an A-T after a number of replication cycles. As a thymine analog, 5-bromodeoxyuridine normally pairs with adenine.
Health Effects
5-bromodeoxyuridine is a mutagen (causes mutations), a cytotoxin, a teratogen and a weak carcinogen. The primary harmful effects are genetic mutation, anemia, reproductive disorders (fetal death or abnormality), cataracts, and skin irritation. It can cause respiratory tract irritation if inhaled, skin irritation if it contacts the skin and eye irritation if it contacts the eyes. As a reproductive toxin BrDU would be considered a “particularly hazardous substance” under the OSHA lab standard.
Interactions
5-Bromo-2'-deoxyuridine (BrdUrd) was found to increase the cytotoxicity induced by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cisplatin in human glioma cells. At a fixed concentration of BrdUrd and BCNU, the greatest cell loss was observed in exponentially growing cells. As cells approached plateau growth, cytotoxicity was reduced as indicated by greater cell viability. Under varying growth conditions the percentage of thymine replacement by bromouracil in DNA, as determined by gas chromatography/mass spectrometry analysis, declined as cultures approached maximum density. These data indicate BrdUrd must be incorporated into DNA for the enhanced effect to be observed. In exponentially growing cells, sensitization was dependent upon both the concentration of BrdUrd and alkylating agent. Using regression analysis (at 95% CL), a relationship between the level of bromouracil in DNA and the extent of enhanced cytotoxicity was observed at two concentrations of BCNU (r2 = 0.99, 0.96). Although it is known that bifunctional alkylating agents exert cytotoxicity by forming cross-links between cDNA strands, increased cross-link formation was not observed in BrdUrd substituted DNA as determined by alkaline elution. The data suggest that DNA damage induced by halogenated pyrimidines may not involve interstrand cross-links and that these agents may be useful in the treatment of glioma in combination with alkylating agents.
ToxicityData
Rat(po): LD50: 8400 mg/kg
Rat(ip): LD50: 1500 mg/kg
Toxicity Data
Rat(po): LD50: 8400 mg/kg
Rat(ip): LD50: 1500 mg/kg
Rat(sc): LD50: 3900 mg/kg
Rat(iv): LD50: 2320 mg/kg
Mouse(po): LD50: 9100 mg/kg
Mouse(ip): LD50: 3050 mg/kg
Mouse(sc): LD50: 3500 mg/kg
Mouse(iv): LD50: 2500 mg/kg
LD50: 2500 mg/kg (Intravenous, Mouse) (T14)
LD50: 3500 mg/kg (Subcutaneous, Mouse) (T14)
LD50: 3050 mg/kg (Intraperitoneal, Mouse) (T14)
LD50: 9100 mg/kg (Oral, Mouse) (T14)
Interactions
5-Bromo-2'-deoxyuridine (BrdUrd) was found to increase the cytotoxicity induced by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cisplatin in human glioma cells. At a fixed concentration of BrdUrd and BCNU, the greatest cell loss was observed in exponentially growing cells. As cells approached plateau growth, cytotoxicity was reduced as indicated by greater cell viability. Under varying growth conditions the percentage of thymine replacement by bromouracil in DNA, as determined by gas chromatography/mass spectrometry analysis, declined as cultures approached maximum density. These data indicate BrdUrd must be incorporated into DNA for the enhanced effect to be observed. In exponentially growing cells, sensitization was dependent upon both the concentration of BrdUrd and alkylating agent. Using regression analysis (at 95% CL), a relationship between the level of bromouracil in DNA and the extent of enhanced cytotoxicity was observed at two concentrations of BCNU (r2 = 0.99, 0.96). Although it is known that bifunctional alkylating agents exert cytotoxicity by forming cross-links between cDNA strands, increased cross-link formation was not observed in BrdUrd substituted DNA as determined by alkaline elution. The data suggest that DNA damage induced by halogenated pyrimidines may not involve interstrand cross-links and that these agents may be useful in the treatment of glioma in combination with alkylating agents.
Non-Human Toxicity Values
LD50 Mouse iv 2500 mg/kg
LD50 Mouse sc 3500 mg/kg
LD50 Mouse ip 3050 mg/kg
LD50 Mouse oral 9100 mg/kg
For more Non-Human Toxicity Values (Complete) data for BROMODEOXYURIDINE (8 total), please visit the HSDB record page.
References

[1]. Neoplasia . 2008 Aug;10(8):804-16.

[2]. Curr Protoc Cytom . 2007 Apr:Chapter 7:Unit7.31.

Additional Infomation
Therapeutic Uses
Orphan Drug. Drug Trade name Broxine/Neomark. Used for radiation sensitivity in the treatment of primary brain tumors.
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. ...
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.
Antineoplastic adjunct (radiosensitizer); diagnostic aid (tumor cell label for cytokinetic analysis).
For more Therapeutic Uses (Complete) data for BROMODEOXYURIDINE (9 total), please visit the HSDB record page.
Drug Warnings
/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.
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. ...
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.
... 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.
It is cytotoxic, strongly teratogenic, and mutagenic in some test systems.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C9H11BRN2O5
Molecular Weight
307.1
Exact Mass
305.985
Elemental Analysis
C, 35.20; H, 3.61; Br, 26.02; N, 9.12; O, 26.05
CAS #
59-14-3
Related CAS #
59-14-3
PubChem CID
6035
Appearance
White to off-white solid powder
Density
1.9±0.1 g/cm3
Melting Point
191-194 °C (dec.)(lit.)
Index of Refraction
1.652
LogP
-0.81
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
2
Heavy Atom Count
17
Complexity
386
Defined Atom Stereocenter Count
3
SMILES
BrC1C(N([H])C(N(C=1[H])[C@@]1([H])C([H])([H])[C@@]([H])([C@@]([H])(C([H])([H])O[H])O1)O[H])=O)=O
InChi Key
WOVKYSAHUYNSMH-RRKCRQDMSA-N
InChi Code
InChI=1S/C9H11BrN2O5/c10-4-2-12(9(16)11-8(4)15)7-1-5(14)6(3-13)17-7/h2,5-7,13-14H,1,3H2,(H,11,15,16)/t5-,6+,7+/m0/s1
Chemical Name
5-bromo-1-[(2R,4S,5R)-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidine-2,4-dione
Synonyms
5-BROMO-2'-DEOXYURIDINE; 59-14-3; Broxuridine; Bromodeoxyuridine; 5-Bromodeoxyuridine; 5-BrdU; BRDU; BrdU; Broxuridine; 5-Bromo-2''-deoxyuridine; BUdR
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 61~250 mg/mL (198.6~814.1 mM)
Water: <1 mg/mL
Ethanol: ~3 mg/mL (~9.8 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (6.77 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 20.8 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.

Solubility in Formulation 2: ≥ 2.08 mg/mL (6.77 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 20.8 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: ≥ 2.08 mg/mL (6.77 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 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


Solubility in Formulation 4: 14.29 mg/mL (46.53 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 3.2563 mL 16.2813 mL 32.5627 mL
5 mM 0.6513 mL 3.2563 mL 6.5125 mL
10 mM 0.3256 mL 1.6281 mL 3.2563 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT00001650 Completed N/A Acquired Immunodeficiency Syndrome
HIV Infection
National Institute of Allergy
and Infectious Diseases
(NIAID)
May 13, 2011 N/A
NCT00003832 Completed Procedure: conventional surgery
Drug: bromodeoxyuridine
Stage I Prostate Cancer
Stage IIA Prostate Cancer
National Cancer Institute
(NCI)
July 1999 Phase 2
Biological Data
  • Proliferation suppression is common among all cancer cells examined and is independent of BrdU retention. Neoplasia . 2008 Aug;10(8):804-16.
  • BrdU induces a progressive, dose-responsive suppression of cancer cell line and cancer stem cell population expansion. Neoplasia . 2008 Aug;10(8):804-16.
  • BrdU does not lead to increased γH2A.X immunoreactivity. Neoplasia . 2008 Aug;10(8):804-16.
  • Transient, low-dose BrdU suppresses expansion rate. Neoplasia . 2008 Aug;10(8):804-16.
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