Edoxudine (EUDR)
(Synonyms: 乙去氧尿啶; EUDR) 目录号 : GC32148
Edoxudine (EUDR) 是一种抗病毒药物，是胸苷的类似物，对单纯疱疹病毒有效。
Cas No.:15176-29-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Edoxudine is an antiviral drug, is an analog of thymidine, shows effectiveness against herpes simplex virus.
| Cas No. | 15176-29-1 | SDF | |
| 别名 | 乙去氧尿啶; EUDR | ||
| Canonical SMILES | OC[C@@H]1[C@H](C[C@H](N2C(NC(C(CC)=C2)=O)=O)O1)O | ||
| 分子式 | C11H16N2O5 | 分子量 | 256.26 |
| 溶解度 | DMSO : ≥ 125 mg/mL (487.79 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.9023 mL | 19.5114 mL | 39.0229 mL |
| 5 mM | 0.7805 mL | 3.9023 mL | 7.8046 mL |
| 10 mM | 0.3902 mL | 1.9511 mL | 3.9023 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
5-Ethyl-2'-deoxyuridine: an explanation for its lack of cytotoxic action in vivo
Eur J Cancer Clin Oncol 1986 May;22(5):557-62.PMID:3770027DOI:10.1016/0277-5379(86)90043-x.
The aim of this study was to explain why 5-ethyldeoxyuridine (EUDR) showed cytotoxic activity against Ehrlich ascites tumour (EAT) cells in vitro but not in vivo. In vitro studies showed that EUDR was phosphorylated to nucleotides which inhibit thymidylate synthetase and DNA polymerase. Toxicity in tissue culture appeared to be related to the inhibition of one or both of these enzymes; and could be prevented/reversed by thymidine (TdR). In vivo EAT cells also formed active EUDR nucleotides at levels which in vitro would have been associated with cytotoxicity but these levels were not maintained. EUDR has been shown to compete with TdR for catabolism by pyrimidine nucleoside phosphorylases from mouse liver and gut. In the ascitic fluid it was found that the level of EUDR fell rapidly while that of TdR and 5-ethyl-uracil increased. It is proposed that competition for catabolism in vivo resulted in the rise in TdR which then compromised the antitumour effect of EUDR.
[Potentiation of 5-fluorouracil efficacy. Molecular mechanisms playing a role in the cytotoxic action of 5-fluorouracil and 5-ethyl-2'-deoxyuridine (EUDR) combination]
Magy Onkol 2004;48(3):243-51.PMID:15520875doi
Pharmacologic modulation of 5-fluorouracil (5-FU) metabolism provides a possibility for the enhancement of its clinical efficacy. Aim: The purpose of the present work was to study the effect of 5-ethyl-2'-deoxyuridine (EUDR), a potent 5-FU modulator, on different molecular mechanisms, influenced by 5-FU itself, and to obtain further data about the mode of action of the combination. Materials and methods: SW620 cell line was used for the experiments. Cytotoxicity was studied by MTT test, cell kinetic changes by FACStar flow cytometer, apoptosis by fluorescent microscope after staining the cells with acridine orange and ethydium bromide, DNA fragmentation by PAGE electrophoresis after RNase and proteinase-K digestion, thymidine incorporation with 3H-thymidine, p53 and PCNA protein expression by Western blotting. Results: The cytotoxicity of 5-FU was potentiated dose dependently by EUDR. One hundred muM concentration of EUDR resulted in a 40% decrease of the IC50 value of 5-FU. Cell cycle arrest in the G2/M transition phase was most pronounced after combined treatment with 5-FU+EUDR. EUDR potentiated the incorporation of 3Hthymidine into DNA. In addition to the increase of apoptosis rate, the expression of p53 protein, caused by 5-FU was further potentiated by UdR. Conclusion: This study demonstrated a potential novel approach to increase the efficacy of 5-FU by EUDR, which incorporated two complementary molecular actions, the selective modulation of TS inhibition and potentiation of the p53 protein expression, consequently leading to an increase in the apoptotic rate.
Modulation of 5-fluorouracil by 5-ethyl-2'-deoxyuridine on cell lines expressing different dihydropyrimidine dehydrogenase activities
Anticancer Drugs 1999 Jul;10(6):561-7.PMID:10885904DOI:10.1097/00001813-199907000-00008.
The purpose of the present study was to clarify the significance of the inhibition of dihydropyrimidine dehydrogenase (DPD) in the modulation of 5-fluorouracil (5-FU) action by 5-ethyl-2'-deoxyuridine (EUDR). Four human cell lines, which differed in their susceptibility to 5-FU and in their DPD activity, were selected as biological objects. Several other enzymes of pyrimidine metabolism, i.e. thymidylate synthase (TS), thymidine kinase (TK) and pyrimidine nucleoside phosphorylase (PNP), which might be involved in the 5-FU action were also studied to elucidate their potential role in the modulation of 5-FU cytotoxicity. Two out of the four cell lines, i.e. COLO1 and SW620, showed low (57 and 28 pmol/min/mg protein) and the other two cell lines, i.e. CAL51 and CAL33, showed high (235 and 184 pmol/min/mg protein) DPD activity, respectively. In our study, contrary to our expectation, no correlation between the DPD and TS activity of the cell lines and their 5-FU sensitivity could be observed. EUDR alone was cytotoxic only on CAL33 cells in a concentration below 1 mM (IC50=194 microM) which might be due to the high TK activity (857 pmol/min/mg protein) measured in this cell line, favoring the formation of the phosphorylated nucleotides EdUMP and EdUTP indispensable for the inhibition of TS and DNA polymerase, respectively. Surprisingly, although EUDR by metabolizing to EUra was able to reduce the high activity of DPD in CAL33 and CAL51 cells by 47 and 55%, respectively, no potentiation of the 5-FU action occurred on these cell lines. On the contrary, enhancement of the 5-FU cytotoxicity was demonstrated on COLO1 and SW620 cells with low DPD activity. Our findings suggest that the 5-FU modulatory action of EUDR may be directed on other molecular targets than DPD as well, i.e. the augmentation of TS inhibition by EdUMP as demonstrated on SW620 cells might be one of these mechanisms.
Potentiation of the antitumor action of 5-fluorouracil with 5-ethyl-2'-deoxyuridine in human colorectal tumor xenografts
Oncology 1984;41(3):155-8.PMID:6328393DOI:10.1159/000225813.
The tumor growth inhibitory effect of 5-ethyl-2'-deoxyuridine ( EUDR ) in combination with 5-fluorouracil (5-FU) has been studied on four human colorectal xenograft lines. In all lines the EUDR pretreatment potentiated the effect of 5-FU presumably due to the increased incorporation of 5-FU into RNA via elevated intracellular thymidine concentration and decreased rate of 5-FU catabolism.