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Purity: ≥98%
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.
| Targets |
DNA synthesis; antimetabolite
DNA (as a thymidine analog incorporated into replicating DNA) [1][2] |
|---|---|
| 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] In human cancer cell lines (HeLa, MCF-7) and primary mouse fibroblasts, Bromodeoxyuridine (BrdU) was efficiently incorporated into DNA of S-phase cells at concentrations of 5-10 μM. The proportion of BrdU-positive cells was positively correlated with cell proliferation activity, detected by immunofluorescence or flow cytometry [1][2] - At high concentrations (>100 μM), Bromodeoxyuridine (BrdU) inhibited cell proliferation and induced DNA damage in HeLa cells, characterized by increased γ-H2AX expression and reduced colony formation efficiency [1] - Incubation with 10 μM Bromodeoxyuridine (BrdU) for 4-24 hours allowed specific labeling of proliferating cells, with a positive rate of 20-40% in exponentially growing cell populations [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]
In BALB/c nude mice bearing HeLa tumor xenografts, intraperitoneal administration of Bromodeoxyuridine (BrdU) at 50 mg/kg once daily for 3 days resulted in labeling of proliferating tumor cells. Immunohistochemical analysis showed 30-40% BrdU-positive cells in tumor tissues, mainly distributed in the proliferative zones [1] - In C57BL/6 mouse embryos (gestational day 12), intraperitoneal injection of 20 mg/kg Bromodeoxyuridine (BrdU) labeled proliferating cells in actively developing tissues (neuroepithelium, liver), with a positive rate of 40-60% detected by immunofluorescence staining [2] |
| 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/cm 2 , 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.
Immunofluorescence staining for cell proliferation [2] 1. Seed cells (HeLa/primary fibroblasts) on coverslips at 2×10⁴ cells/well and culture for 24 hours. 2. Treat cells with Bromodeoxyuridine (BrdU) at a final concentration of 5-10 μM and incubate for 4-6 hours. 3. Fix cells with 4% paraformaldehyde for 15 minutes at room temperature, then wash with PBS. 4. Denature DNA by incubating with 2 N HCl at 37°C for 30 minutes, followed by neutralization with Tris buffer. 5. Incubate with anti-BrdU primary antibody overnight at 4°C, then with fluorescent secondary antibody for 1 hour at room temperature. 6. Counterstain nuclei with DAPI, observe under a fluorescence microscope, and count the proportion of BrdU-positive cells [2] - Flow cytometry for cell cycle and proliferation analysis [2] 1. Culture MCF-7 cells to logarithmic phase, treat with 5 μM Bromodeoxyuridine (BrdU) for 2 hours. 2. Fix cells with 70% ice-cold ethanol overnight, then permeabilize with 0.2% Triton X-100 for 15 minutes. 3. Denature DNA with 2 N HCl for 20 minutes, neutralize, and wash with PBS. 4. Incubate with anti-BrdU antibody for 1 hour, then with fluorescent secondary antibody for 30 minutes. 5. Stain DNA with propidium iodide (PI), analyze BrdU-positive cells and cell cycle distribution by flow cytometry [2] - Immunohistochemical staining of cell [1] 1. Culture primary fibroblasts on coverslips for 48 hours, treat with 10 μM Bromodeoxyuridine (BrdU) for 6 hours. 2. Fix, denature, and neutralize cells as described above. 3. Incubate with peroxidase-conjugated anti-BrdU secondary antibody for 1 hour, develop with DAB substrate, and counterstain with hematoxylin. 4. Count BrdU-positive cells under a light microscope [1] |
| Animal Protocol |
300 mg/kg, i.p. or 0.8 mg/ml, p.o.
Rat glioma RG2 tumor model 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] Tumor xenograft proliferation labeling model [1] 1. Establish HeLa tumor xenografts in 6-8-week-old BALB/c nude mice by subcutaneous inoculation of 5×10⁶ cells. 2. When tumors reach 100 mm³, dissolve Bromodeoxyuridine (BrdU) in sterile saline and administer intraperitoneally at 50 mg/kg once daily for 3 days. 3. Euthanize mice 2 hours after the last dose, dissect tumor tissues, and fix in 4% paraformaldehyde for 24 hours. 4. Embed tumor tissues in paraffin, cut into 5 μm sections, and perform immunohistochemical staining to detect BrdU-positive cells [1] - Embryonic cell proliferation labeling model [2] 1. Treat C57BL/6 mice at gestational day 12 with intraperitoneal injection of 20 mg/kg Bromodeoxyuridine (BrdU) (dissolved in sterile saline). 2. Euthanize female mice 2 hours after administration, isolate embryos, and fix in 4% paraformaldehyde overnight. 3. Dehydrate embryos gradiently, embed in paraffin, cut into 6 μm serial sections, and perform immunofluorescence staining to label proliferating cells [2] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Twelve patients received continuous intravenous infusion (24 hours) of bromodeoxyuridine (BUdR) at doses of 650 or 1000 mg/m²/day for a maximum duration of two weeks. …Pharmacological studies showed that the steady-state concentrations of BUdR in arterial plasma were 6 × 10⁻⁷ mol/L and 1 × 10⁻⁶ mol/L during infusions at doses of 650 and 1000 mg/m²/day, respectively. In vivo uptake of BUdR in normal bone marrow was assessed by comparing the in vitro radiation survival curves of bone marrow CFUc before and after infusion in the two patients, with enhancement ratios (D0-pre/D0-post) of 1.8 (650 mg/m²/day) and 2.5 (1000 mg/m²/day), respectively. Using anti-BUdR monoclonal antibodies and immunohistochemistry, in vivo incorporation of BrdU into normal skin and tumor cells was confirmed in biopsy samples from three patients. The results showed that the incorporation rate in normal skin cells (less than 10%) was significantly lower than that in tumor cells (50% to 70%). Following parenteral injection, BrdU can be absorbed through the gastrointestinal tract, and due to its teratogenic effects, it is presumed that it can also be absorbed through the placenta. Distribution and pharmacokinetics: Intra-arterial injection of BrdU in rodents leads to its extensive degradation… Most of the undegraded BrdU is incorporated into the DNA of various tissues, particularly the colon, stomach, bone marrow, and spleen. Following intraperitoneal injection of deuterated BrdU in pregnant mice, BrdU labeling was detected in the livers of both mothers and embryos. Subcutaneous implantation of BrdU tablets into rats and measurement of serum BrdU concentrations were conducted. The peak serum BrdU concentration of 10 μg/mL was reached within 5 hours. ...After using agar-coated tablets, the concentration of BrdU in the blood was reduced by half, and no peak concentration was detected. ... Metabolism/Metabolites BrdU is degraded relatively rapidly after injection in mice and rats, through at least two metabolic pathways: one is glycosidic bond hydrolysis, producing bromouracil and 2-deoxyribose, the latter of which may be further metabolized; the other is debromination, manifested as the release of bromide ions. The subsequent fate of the remaining molecule has not been studied. 5-Bromodeoxyuridine is phosphorylated by thymidine kinase to produce 5-bromodeoxyuridine phosphate (L626). Absorption: Bromodeoxyuridine (BrdU) is rapidly absorbed after intraperitoneal injection, reaching peak plasma concentrations within 15-30 minutes. Oral bioavailability is approximately 40-50% [1]. - Distribution: Widely distributed in tissues, it can penetrate the blood-brain barrier and placental barrier. Concentrations are high in proliferating tissues (tumors, bone marrow, embryonic tissues) [1][2] - Metabolism: Intracellularly phosphorylated by thymidine kinase to form BrdU triphosphate, which is incorporated into replicating DNA as a substrate of DNA polymerase [1] - Excretion: Primarily excreted via the kidneys, with a plasma elimination half-life of 2-4 hours [1] |
| Toxicity/Toxicokinetics |
Toxicity Summary
5-Bromodeoxyuridine acts on DNA. It induces random point mutations in DNA through base substitution. After several replication cycles, the base pair changes from AT to GC, or from GC to AT. As a thymine analog, 5-bromodeoxyuridine typically pairs with adenine. Health Effects 5-Bromodeoxyuridine is a mutagen (causing mutations), cytotoxic, teratogenic, and weak carcinogen. Major harmful effects include gene mutation, anemia, reproductive disorders (fetal death or malformation), cataracts, and skin irritation. Inhalation can cause respiratory irritation, skin contact can cause skin irritation, and eye contact can cause eye irritation. As a reproductive toxin, BrDU should be considered an “Extremely Hazardous Substance” according to the laboratory standards of the U.S. Occupational Safety and Health Administration (OSHA). Interactions> Studies have found that 5-bromo-2'-deoxyuridine (BrdUrd) enhances the cytotoxicity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cisplatin on human glioma cells. At constant concentrations of BrdUrd and BCNU, cell loss was most significant in exponentially growing cells. As cell growth approached the plateau phase, cytotoxicity decreased, resulting in increased cell viability. Under different growth conditions, the percentage of thymine replaced by bromouracil in DNA decreased as the culture approached maximum density, as determined by gas chromatography/mass spectrometry. These data suggest that BrdUrd must be incorporated into DNA to observe the enhancing effect. In exponentially growing cells, the sensitizing effect depends on the concentrations of BrdUrd and the alkylating agent. Regression analysis (95% confidence interval) revealed a relationship between bromouracil levels in DNA and the degree of enhanced cytotoxicity at both BCNU concentrations (r² = 0.99, 0.96). Although bifunctional alkylating agents are known to exert cytotoxic effects by forming crosslinks between cDNA strands, no increased crosslink formation was observed in BrdUrd-substituted DNA as determined by alkaline elution. The data suggest that DNA damage induced by halopyrimidines may not involve interstrand crosslinks, and that these drugs may be used in combination with alkylating agents for the treatment of glioma. Toxicity Data Rat (oral): LD50: 8400 mg/kg Rat (intraperitoneal): LD50: 1500 mg/kg Toxicity Data Rat (oral): LD50: 8400 mg/kg Rat (intraperitoneal): LD50: 1500 mg/kg Rat (subcutaneous): LD50: 3900 mg/kg Rat (intravenous): LD50: 2320 mg/kg Mouse (oral): LD50: 9100 mg/kg Mouse (intraperitoneal): LD50: 3050 mg/kg Mouse (subcutaneous): LD50: 3500 mg/kg Mouse (intravenous): LD50: 2500 mg/kg LD50: 2500 mg/kg (intravenous, mouse) (T14) LD50: 3500 mg/kg (subcutaneous injection, mice) (T14) LD50: 3050 mg/kg (intraperitoneal injection, mice) (T14) LD50: 9100 mg/kg (oral administration, mice) (T14) Interactions5-Bromo-2'-deoxyuridine (BrdUrd) enhances the cytotoxicity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and cisplatin on human glioma cells. At constant BrdUrd and BCNU concentrations, cell loss was most significant in exponentially growing cells. As cell growth approached the plateau phase, cytotoxicity decreased, manifested as increased cell viability. Under different growth conditions, the percentage of thymine replaced by bromouracil in DNA decreased as the culture approached maximum density, as determined by gas chromatography/mass spectrometry. These data suggest that BrdUrd must be incorporated into DNA to observe the enhancing effect. In exponentially growing cells, the sensitizing effect depends on the concentrations of BrdUrd and the alkylating agent. Regression analysis (95% confidence interval) revealed a relationship between bromouracil levels in DNA and the degree of enhanced cytotoxicity at both BCNU concentrations (r² = 0.99, 0.96). Although bifunctional alkylating agents are known to exert cytotoxic effects by forming crosslinks between cDNA strands, no increased crosslink formation was observed in BrdUrd-substituted DNA as determined by alkaline elution. The data suggest that DNA damage induced by halopyrimidines may not involve interstrand crosslinks, and that these drugs may be used in combination with alkylating agents for the treatment of gliomas. Non-human toxicity values Mice intravenous LD50 2500 mg/kg Mice subcutaneous LD50 3500 mg/kg Mice intraperitoneal LD50 3050 mg/kg Mice oral LD50 9100 mg/kg For more complete non-human toxicity data for bromodeoxyuridines (8 in total), please visit the HSDB record page. In vitro toxicity: No significant cytotoxicity was observed at concentrations ≤50 μM; high concentrations (>100 μM) could inhibit cancer cell proliferation, induce DNA damage, and trigger cancer cell apoptosis [1] -In vivo toxicity: At experimental doses (20-100 mg/kg), no significant hepatotoxicity or nephrotoxicity was observed in mice, and serum transaminase and creatinine levels were normal [1] -Mutogenicity: Due to DNA incorporation, there may be a risk of mutagenicity; if used in pregnant animals, it may affect embryonic development [1][2] |
| References | |
| Additional Infomation |
Therapeutic Uses
Orphan drug. Brand name: Broxine/Neomark. Used to treat primary brain tumors to enhance radiosensitivity. Halogenated pyrimidine analogs, bromodeoxyuridine (BUdR) and iododeoxyuridine (IUdR), have been considered potential clinical radiosensitizers for over two decades. In vivo and in vitro studies have shown that radiosensitization directly depends on the amount of thymidine substitution in DNA by these analogs. … Carcinogenicity has not been confirmed; in fact, it is an effective cancer treatment because it makes tumor cells more sensitive to the lethal effects of X-rays than normal tissue cells. Adjuvant antitumor drug (radiosensitizer); diagnostic aid (tumor cell marker for cell kinetic analysis). For more complete data on the therapeutic uses of bromodeoxyuridine (9 in total), please visit the HSDB record page. Drug Warning /Author/This report presents the results of a Phase I study designed to determine tolerable toxicities and serum concentrations in patients receiving intravenous bromodeoxyuridine in combination with radiotherapy. Due to severe thrombocytopenia and leukopenia in three patients following a 96-hour infusion of bromodeoxyuridine (1.5 g/m²/24 h), the dose was reduced to 0.8 g/m²/24 h in these patients, as well as the remaining nine patients in the study group. Even at this dose, myelotoxicity was observed. In a Phase I clinical study of bromodeoxyuridine (BUdR) as a radiosensitizer… researchers identified normal and malignant cells incorporating BUdR. BUdR was infused for up to 14 days, and the in vivo incorporation of BUdR into DNA was assessed using immunohistochemistry and a monoclonal antibody against BUdR. BUdR was detected in 50% of breast cancer cells and 10% of malignant melanoma cells. BUdR was also found in the basal layer of normal epidermis and in 50% of bone marrow cells. Incorporation of BUdR into epidermal and bone marrow cells may lead to phototoxicity and bone marrow suppression in patients treated with BUdR. … Twelve patients received continuous intravenous (24-hour) infusions of bromodeoxyuridine (BUdR) at doses of 650 or 1000 mg/m²/day, with a maximum duration of two weeks. Bone marrow suppression, particularly thrombocytopenia, was the main systemic toxicity, leading to a shortened infusion time of 9 to 14 days. However, bone marrow function recovered within 7 to 10 days, and most patients were able to receive a second infusion. Local toxicity (within the radiation field) was minimal, with only 1 of 4 patients receiving abdominal radiation therapy experiencing local toxicity. Pharmacological studies showed that the steady-state concentrations of BUdR in arterial plasma were 6 × 10⁻⁷ mol/L and 1 × 10⁻⁶ mol/L during infusions at doses of 650 and 1000 mg/m²/day, respectively. Ibuprofen (BUdR) uptake in normal bone marrow from two patients was assessed by comparing in vitro radiation survival curves of bone marrow colony-forming units (CFUc) before and after infusion, with enhancement ratios (D0-pre/D0-post) of 1.8 (650 mg/m²/day) and 2.5 (1000 mg/m²/day), respectively. In vivo incorporation of ibuprofen in normal skin and tumor cells was confirmed in biopsy tissues from three patients using anti-ibuprofen monoclonal antibodies and immunohistochemistry. The results showed that the incorporation rate in normal skin cells (less than 10%) was significantly lower than that in tumor cells (up to 50% to 70%). We concluded that continuous infusion of ibuprofen at a dose of 1000 mg/m²/day for approximately two weeks was tolerable in both local and systemic toxicity. The observed normal tissue toxicity was comparable to our previous clinical experience with intermittent (12 hours daily for two weeks) BUdR infusions. Theoretically, continuous infusion should allow for greater incorporation of BUdR into proliferating tumor cells, thereby further enhancing radiosensitization. During radiotherapy, 23 patients with primary and secondary malignant brain tumors received BUdR infusions 5 days a week, 12 hours daily, at a dose of 800–1000 mg/m². The radiotherapy plan was a weekly dose of 10 Gy for 5–6 weeks. Fifteen patients received a 1000 mg/m² BUdR infusion; six of these tolerated the treatment for more than three weeks. Of the eight patients receiving an 800 mg/m² dose, five tolerated the treatment for more than three weeks. The most significant toxicities were myelosuppression and stomatitis, which severely hampered the implementation of the treatment regimen. It has cytotoxicity, strong teratogenicity and mutagenicity, and also exhibits mutagenicity in some testing systems. Bromideoxyuridine (BrdU) is a synthetic thymidine analog widely used as a molecular probe for detecting cell proliferation in scientific research[1][2]. -Mechanism of action: During the S phase of the cell cycle, BrdU replaces thymidine and is incorporated into the replicated DNA under the action of DNA polymerase. Anti-BrdU antibodies can specifically detect the presence of BrdU in DNA, thereby reflecting the cell proliferation status[1][2]. -Main applications: Used in cell biology, oncology, developmental biology and other fields to detect cell proliferation activity, analyze the cell cycle, label proliferating cell populations and assess tumor proliferation potential[1][2]. -Detection advantages: Simple operation, compatible with multiple detection methods (immunofluorescence, flow cytometry, immunohistochemistry), and high sensitivity[2]. -Precautions: DNA denaturation is required during the detection process to expose the incorporated BrdU antigen, in order to avoid false negative results[2]. |
| Molecular Formula |
C9H11BRN2O5
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| Molecular Weight |
307.1
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| Exact Mass |
305.985
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| Elemental Analysis |
C, 35.20; H, 3.61; Br, 26.02; N, 9.12; O, 26.05
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| CAS # |
59-14-3
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| Related CAS # |
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| PubChem CID |
6035
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| Appearance |
White to off-white solid powder
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| Density |
1.9±0.1 g/cm3
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| Melting Point |
191-194 °C (dec.)(lit.)
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| Index of Refraction |
1.652
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| LogP |
-0.81
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
17
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| Complexity |
386
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| Defined Atom Stereocenter Count |
3
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| 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
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| InChi Key |
WOVKYSAHUYNSMH-RRKCRQDMSA-N
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| 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
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| Chemical Name |
5-bromo-1-[(2R,4S,5R)-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidine-2,4-dione
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| 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. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| 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. View More
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. 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. |
| 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.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
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.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| 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 |
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