5-Iminodaunorubicin
(Synonyms: 5-亚氨基柔红霉素) 目录号 : GC62389
5-Iminodaunorubicin 是一种醌改性蒽环类药物，具有抗肿瘤活性。5-Iminodaunorubicin 在癌细胞中可诱导 DNA 链断裂。
Cas No.:72983-78-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
5-Iminodaunorubicin is a quinone-modified anthracycline that retains antitumor activity[1]. 5-Iminodaunorubicin produces protein-concealed DNA strand breaks in cancer cells[2].
In mouse leukemia L1210 cells, 5-Iminodaunorubicin produces protein-concealed DNA strand breaks. Many of the 5-iminodaunorubicin breaks may arise from apposed single-strand breaks (i.e., double-strand breaks)[2].
In rat, 5-Iminodaunorubicin (5-ID; 1-16 mg/kg) treatment produces widening of the QRS complex, increased R- and S-wave voltage, and prolonged the Q alpha T interval. And the quinone redox cycling is suppressed in 5-Iminodaunorubicin. 5-Iminodaunorubicin shows lower cardiotoxic[1].
[1]. R A Jensen, et al. Electrocardiographic and transmembrane potential effects of 5-iminodaunorubicin in the rat. Cancer Res. 1984 Sep;44(9):4030-9.
[2]. L A Zwelling, et al. Cytotoxicity and DNA strand breaks by 5-iminodaunorubicin in mouse leukemia L1210 cells: comparison with adriamycin and 4’-(9-acridinylamino)methanesulfon-m-anisidide. Cancer Res. 1982 Jul;42(7):2687-91.
| Cas No. | 72983-78-9 | SDF | |
| 别名 | 5-亚氨基柔红霉素 | ||
| 分子式 | C27H30N2O9 | 分子量 | 526.54 |
| 溶解度 | 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 | 1.8992 mL | 9.496 mL | 18.9919 mL |
| 5 mM | 0.3798 mL | 1.8992 mL | 3.7984 mL |
| 10 mM | 0.1899 mL | 0.9496 mL | 1.8992 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-Iminodaunorubicin. Reduced cardiotoxic properties in an antitumor anthracycline
J Med Chem 1979 Jan;22(1):36-9.PMID:423181DOI:10.1021/jm00187a009.
Treatment of daunorubicin with methanolic ammonia affords 5-Iminodaunorubicin, the first quinone-modified analogue of either daunorubicin or adriamycin. This product retains antileukemic activity in mice, is less cardiotoxic by electrocardiographic measurements in rats, and is nonmutagenic in Salmonella typhimurium (Ames test).
Electrocardiographic and transmembrane potential effects of 5-Iminodaunorubicin in the rat
Cancer Res 1984 Sep;44(9):4030-9.PMID:6744318doi
5-Iminodaunorubicin (5-ID) is a quinone-modified anthracycline that retains antitumor activity but lacks the usual redox-cycling effects of quinoid agents. As a test for decreased cardiotoxicity, we have compared the dose- and time-dependent effects of multiple doses of 5-ID and doxorubicin (DXR) on the rat electrocardiogram (ECG) using a signal-averaging process and have related the ECG changes induced by 5-ID to transmembrane potential alterations in myocardial preparations isolated from treated rats. 5-ID was studied at dose levels of 16, 4, and 1 mg/kg, while DXR was given at 4, 2, and 1 mg/kg. At the high- and medium-dose levels, both agents produced widening of the QRS complex, increased R- and S-wave voltage, and prolonged the Q alpha T interval. The QRS widening reversed in all surviving rats, whereas Q alpha T prolongation was reversible with 5-ID but irreversible with DXR. At the lowest dose, 5-ID had no effect on the ECG until the end of treatment. Microelectrode studies on single cells showed that QRS widening occurring with 5-ID treatment was related to a decrease in the maximum rate of depolarization (Vmax) and that Q alpha T prolongation resulted from an increase in the duration of the action potential. Electron microscopic examination showed that although these toxic changes could not be related to specific morphological alterations, in general, the more severe the electrophysiological change, the greater the ultrastructural change. The most consistent ECG change was Q alpha T prolongation. Using this parameter as a marker for cardiotoxicity, 5-ID was about 4 to 5 times less cardiotoxic than was DXR at high- and medium-dose levels and was noncardiotoxic (i.e., below a threshold for cardiotoxicity) compared with DXR at 1 mg/kg over 20 (DXR) to 35 (5-ID) treatments. The decrease in cardiotoxicity relative to DXR is consistent with previous findings that quinone redox cycling is suppressed in 5-ID. However, the ECG and transmembrane potential effects that we identified at elevated doses of 5-ID can be associated with toxic changes in cardiac cell membranes. Therefore, membrane changes other than those due to quinone redox cycling and, presumably, lipid peroxidation must underlie the electrophysiological changes and structural modifications observed with 5-ID in this study. We believe that 5-ID is a useful mechanistic probe in anthracycline cardiotoxicity studies as well as being of obvious interest for clinical trials.
Interaction of 5-Iminodaunorubicin with Fe(III) and with cardiolipin-containing vesicles
Biochim Biophys Acta 1986 Mar 27;856(1):130-6.PMID:3955031DOI:10.1016/0005-2736(86)90019-2.
5-Iminodaunorubicin is an anthracycline derivative exhibiting promising antitumor activity. Using potentiometric and spectroscopic measurements we have shown that 5-Iminodaunorubicin forms with Fe(III) a complex in which three molecules of drug are bound to one Fe(III) ion. Each molecule is chelated through the C-12-carbonyl and the C-11-phenolate oxygen atoms. The stability constant is 1.6 X 10(34). Using circular dichroism measurements we have studied the interactions of 5-Iminodaunorubicin with cardiolipin-containing vesicles. We have shown that cardiolipin could bind one molecule of drug without penetration of the dihydroanthraquinone moiety into the bilayer.
Cytotoxicity and DNA strand breaks by 5-Iminodaunorubicin in mouse leukemia L1210 cells: comparison with adriamycin and 4'-(9-acridinylamino)methanesulfon-m-anisidide
Cancer Res 1982 Jul;42(7):2687-91.PMID:6896293doi
The effects upon cellular DNA and cytotoxicity produced by the anthracyclines 5-Iminodaunorubicin and Adriamycin were studied in mouse leukemia L1210 cells. 5-Iminodaunorubicin produced protein-concealed DNA strand breaks as measured by alkaline elution as had other intercalators including Adriamycin. 5-Iminodaunorubicin produced DNA breaks more efficiently than did Adriamycin despite a lower potency for free radical formation. Many of the 5-Iminodaunorubicin breaks measured in this assay may arise from apposed single-strand breaks (i.e., double-strand breaks). 5-Iminodaunorubicin produced breaks which disappeared within 1 to 2 hr following drug removal and were in this way similar to the breaks produced by the acridine intercalator 4'-(9-acridinylamino)methanesulfon-m-anisidide. Adriamycin produced more persistent breaks. Despite similarities in the kinetics of break disappearance, 5-Iminodaunorubicin produced greater cytotoxicity than did 4'-(9-acridinylamino)methanesulfon-m-anisidide when compared at doses producing equal single-strand or double-strand breaks. Differences in the ratio of single-strand breaks to double-strand breaks and the associated cytotoxicity for 5-Iminodaunorubicin and 4'-(9-acridinylamino)methanesulfon-m-anisidide indicate that a different mechanism is probably involved in the DNA break production by each agent. Differences between the cytotoxicity associated with the DNA break production by two agents with similar break disappearance kinetics indicate that intercalator-induced DNA breaks cannot be a uniformly lethal DNA lesion.
Low stimulation of NADH oxidation and oxygen consumption by 5-Iminodaunorubicin and its derivatives
Acta Biochim Pol 1990;37(2):251-9.PMID:2072983doi
NADH oxidation and oxygen consumption mediated by 5-Iminodaunorubicin and its derivatives have been studied. Experiments were carried out using two enzyme system: microsomes isolated from rat liver and cytochrome c-reductase. All 5-iminoanthracyclines examined were relatively poor electron transfer mediators. In addition, 5-imino-derivatives of daunorubicin modified at sugar moiety were less effective in stimulating NADH oxidation and oxygen radical production than 5-Iminodaunorubicin itself. This may be due to the additive effect of 5-imino structure and the presence of bulky substituents at sugar moiety, which might make the compounds poor enzyme substrates.