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5-Iodotubercidin

现货
Catalog No.
A3125
腺苷激酶抑制剂
组合的产品项目
规格价格库存 数量
5mg
¥ 970.00
现货
50mg
¥ 5,990.00
现货

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Background

5-Iodotubercidin (Itu) is a purine derivative and hence an inhibitor of adenosine kinase with an IC50 value of 26 nM [1].

Adenosine kinase is important in regulating the intracellular and extracellular concentrations of adenosine and hence diverse physiological actions of adenosine [2].

In various cells such as cancer cells, persisted AMPK activation could result in apoptosis [4]. In nude mice with colon carcinoma xenograft, Itu at a dose of 2.5 mg/kg resulted in rapid tumor regression compared with the control group. At the dose of 0.625 mg/kg, Itu still inhibited tumor growth, but p53-/- tumors were resistant to Itu at this lowered dose [1].

In male Wistar rat hepatocytes, incubation with Itu resulted in concentrations of AMP and ATP at 0.39 ± 0.06 and 1.51 ± 0.10 μmol/g cell wet mass, respectively; while control incubation at 0.27 ± 0.05 and 2.25 ± 0.33 μmol/g cell wet mass, respectively. Addition of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) and Itu simultaneously resulted in almost the same effect of Itu alone. It was probable that Itu inhibited adenosine kinase and blocked the synthesis of 5-aminoimidazole-4-carboxamide ribonucleotide (ZMP) from AICAR. ZAM is a structural AMP analogue and hence mimics the effect of AMP on the AMP-activated protein kinase (AMPK) activation [3].

References:
[1].  Xin Zhang, Deyong Jia, Huijuan Liu, et al. Identification of 5-Iodotubercidin as a Genotoxic Drug with Anti-Cancer Potential. PLOS ONE, 2013, 8(5):e62527.
[2].  Jaoek Park and Radhey S. Gupta. Adenosine: A Key Link between Metabolism and Brain Activity: Adenosine Metabolism, Adenosine Kinase, and Evolution. New York: Springer Science+Business Media, 2013.
[3].  García-Villafranca J. and Castro J. Effects of 5-iodotubercidin on hepatic fatty acid metabolism mediated by the inhibition of acetyl-CoA carboxylase. Biochem. Pharmacol., 2002, 63(11):1997-2000.
[4].  Haiyan Chen, Ji-ping Wang, Richard J. Santen, et al. Adenosine monophosphate activated protein kinase (AMPK), a mediator of estradiol-induced apoptosis in long-term estrogen deprived breast cancer cells. Apoptosis, 2015, 20:821-830.

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
M.Wt392.15
Cas No.24386-93-4
FormulaC11H13IN4O4
SynonymsNSC 113939; 5-ITu
Solubility<0.78 mg/mL in DMSO, <2.91 mg/mL in EtOH, <2.28 mg/mL in H2O
Chemical Name(2R,3R,4S,5R)-2-(4-amino-5-iodopyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)oxolane-3,4-diol
SDFDownload SDF
Canonical SMILESC1=C(C2=C(N1C3C(C(C(O3)CO)O)O)N=CN=C2N)I
运输条件试用装:蓝冰运输。 其他可选规格:常温运输或根据您的要求用蓝冰运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。

试验操作

细胞实验 [1]:

细胞系

MEFs和HCT116细胞

制备方法

在DMSO中的溶解度大于10 mM。若配制更高浓度的溶液,一般步骤如下:请将试管置于37 °C加热10分钟和/或将其置于超声波浴中震荡一段时间。原液于-20 °C可放置数月。

反应条件

0 ~ 2.5 μM;8小时

实验结果

在MEFs和HCT116细胞中,5-Iodotubercidin上调p53表达。此外,剂量实验表明,5-Iodotubercidin在浓度低至0.25 μM时仍能上调p53表达。在敲除ADK的HCT116细胞中,ADK水平降低不会显著改变p53蛋白水平。上述结果表明5-Iodotubercidin不是通过直接抑制ADK来诱导p53上调。

动物实验 [1]:

动物模型

携带HCT116细胞的裸鼠

给药剂量

0.625或2.5 mg/kg;腹腔注射

实验结果

在携带HCT116细胞的裸鼠中,2.5 mg/kg 5-Iodotubercidin诱导快速的肿瘤消退。然而,5-Iodotubercidin治疗也降低了小鼠的体重(治疗结束时,减轻了6%)。此外,5-Iodotubercidin也对p53-/- HCT116引发的肿瘤显示抑制作用。在0.625 mg/kg的较低剂量下,5-Iodotubercidin仍然具有肿瘤生长抑制作用,但p53-/- HCT116肿瘤对5-Iodotubercidin出现抗性。

注意事项

请于室内测试所有化合物的溶解度。虽然化合物的实际溶解度可能与其理论值略有不同,但仍处于实验系统误差的允许范围内。

References:

[1]. Xin Zhang, Deyong Jia, Huijuan Liu, et al. Identification of 5-Iodotubercidin as a Genotoxic Drug with Anti-Cancer Potential. PLOS ONE, 2013, 8(5):e62527.

生物活性

描述 5-Iodotubercidin是一种有效的腺苷激酶抑制剂。
靶点 adenosine kinase uridine formycin B      
IC50 26 nM 7 μM 15 μM      

质量控制