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Fludarabine phosphate (Synonyms: 磷酸氟达拉滨; NSC 118218 phosphate) 纯度: ≥98.0%
Fludarabine phosphate (NSC 118218 phosphate) 是一种腺苷和脱氧腺苷类似物,与 dATP 竞争,并入到 DNA,导致 DNA 合成受阻。
Fludarabine phosphate Chemical Structure
CAS No. : 75607-67-9
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Free Sample (0.1-0.5 mg) | Apply now | ||
10 mM * 1 mL in DMSO | ¥798 | In-stock | |
10 mg | ¥725 | In-stock | |
50 mg | ¥1953 | In-stock | |
100 mg | ¥2697 | In-stock | |
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500 mg | 询价 |
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生物活性 |
Fludarabine (phosphate) is an analogue of adenosine and deoxyadenosine, which is able to compete with dATP for incorporation into DNA and inhibit DNA synthesis. |
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体外研究 (In Vitro) |
Fludarabine phosphate significantly reduces the cell viability in a dose-dependent manner. Fludarabine phosphate exhibits no effect in all tested concentrations when combined with either PBS or control vector, ACE-GFP. Fludarabine phosphate causes a significant decrease in cell viability for 24 h after exposure to ACE-PNP when compared to PBS and ACE-GFP at concentrations of 2.5, 5 and 10 μg/mL[2]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
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体内研究 (In Vivo) |
F-araAMP (100 mg/kg given 15 times, 167 mg/kg given 9 times, or 250 mg/kg given 3 times, i.p.) leads to complete regressions of all tumors and cures of all mice. Parental D54 tumors (i.e. without E. coli PNP) are not sensitive to treatment with F-araAMP. Intratumoral injection of Ad/PNP followed by IT F-araAMP can elicit a substantial regressive effect on otherwise refractory solid tumors in a fashion substantially superior to viral PNP transduction followed by systemic prodrug administration[1]. The comparison of ACE-GFP/fludarabine phosphate with ACE-GFP/PBS demonstrats that fludarabine phosphate alone has no growth inhibitory activity on KU-19-19 tumors[2]. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
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Clinical Trial |
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分子量 |
365.21 |
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Formula |
C10H13FN5O7P |
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CAS 号 |
75607-67-9 |
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中文名称 |
磷酸氟达拉滨;2-氟阿糖腺苷酸;氟达拉宾碱;氟达那苷 |
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运输条件 |
Room temperature in continental US; may vary elsewhere. |
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储存方式 |
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溶解性数据 |
In Vitro:
DMSO : ≥ 100 mg/mL (273.82 mM) H2O : 5 mg/mL (13.69 mM; Need ultrasonic) * “≥” means soluble, but saturation unknown. 配制储备液
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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。 In Vivo:
请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用; 以下溶剂前显示的百
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参考文献 |
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Cell Assay [2] |
Briefly, 2×103 KU-19-19 cells are seeded in each well of 96-well plates and allowed to grow overnight. Cells are then exposed to PBS, ACE-GFP or ACE-PNP for 3 h. Twenty-four hours post-infection, the cells are treated with various concentrations of fludarabine phosphate. After the 24-h incubation, cytotoxicity is determined by using WST-1; 4-[3-(4-iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate. The absorbance value is determined at 450 nm by a microplate reader. 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
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Animal Administration [1] |
Mice: Parental and E. coli PNP expressing D54MG (human glioma) tumor cells (2×107 cells) are injected subcutaneously into the flanks of nude mice (nu/nu). D54 tumor cells stably transduced with E. coli PNP are prepared as described previously. Tumors are measured with calipers and an estimate of the weight calculated using the equation, (length × width2)/2=mm3, and converted to mg assuming unit density. Unless stated otherwise, therapeutic drugs and the adenoviral vector expressing E. coli PNP (Ad/PNP), or vehicle controls are injected into D54 tumors in 150 μL volumes by 8 separate injections of approximately 20 μL each in an effort to evenly distribute the administered agent. At least 6 mice are studied in each treatment group. Mice are monitored daily and body weights and tumor dimensions collected twice weekly. T-C (tumor growth delay) is determined as the difference in median days to 2 doublings (median days to 600 mg for the D54 and DU145 (human prostate cancer) analysis) between drug-treated and vehicle-treated groups. For the NIH-H322M (human non-small cell lung cancer) study, because of tumor proliferation characteristics, total growth inhibition (TGI) is used as the evaluation point. TGI is equal to the control group mean delta minus the treated group mean delta divided by the control group mean delta, where delta is the change in tumor weight for each animal between day 36 and day 59. The time to the evaluation point for each animal is used as the end point for the student’s t-test, Mann-Whitney rank sum test, or a life table analysis in order to statistically compare growth data between treatment groups. All key results are repeated under similar conditions and findings confirmed. Treatments are initiated when tumors are 250 to 300 mg (appr 1-1.5% of total animal weight). 上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only. |
参考文献 |
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