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Dibutyryl-cAMP, sodium salt

二丁酰环磷腺苷
Catalog No.
B9001
细胞渗透性cAMP类似物,激活cAMP依赖性蛋白激酶
组合的产品项目
规格价格库存 数量
50mg
¥ 618.00
Ship with 10-15 days
100mg
¥ 690.00
Ship with 10-15 days

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A

背景

Dibutyryl-cAMP sodium salt is a cell-permeable cAMP that activates cAMP-dependent protein kinase (PKA) and is a phosphodiesterase inhibitor. Because it mimics cAMP and induces normal physiological responses when added to cells under experimental conditions, dibutyryl-cAMP is widely used in a variety of research applications[1,2].

References:

[1]. Bartsch M, Zorn-Kruppa M, Kühl N, et al. Bioactivatable, membrane-permeant analogs of cyclic nucleotides as biological tools for growth control of C6 glioma cells. Biological Chemistry, 2003, 384(9): 1321-1326.

[2]. Rundfeldt C, Steckel H, Sörensen T, et al. The stable cyclic adenosine monophosphate analogue, dibutyryl cyclo-adenosine monophosphate (bucladesine), is active in a model of acute skin inflammation. Archives of Dermatological Research, 2012, 304(4): 313-317.

化学属性

Physical AppearanceA solid
StorageStore at -20°C
M.Wt491.37
Cas No.16980-89-5
FormulaC18H23N5NaO8P
Solubility≥49.1 mg/mL in H2O; ≥23.7 mg/mL in DMSO; ≥3.21 mg/mL in EtOH with gentle warming and ultrasonic
Chemical Namesodium (Z)-N-(9-((4aR,6R,7R,7aR)-7-(butyryloxy)-2-hydroxy-2-oxidotetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-6-yl)-9H-purin-6-yl)butyrimidate
SDFDownload SDF
Canonical SMILESCCC/C([O-])=N/C1=C(N=CN2[C@@]3([H])[C@@](OC(CCC)=O)([H])[C@@](O4)([H])[C@@](O3)([H])COP4(O)=O)C2=NC=N1.[Na+]
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试验操作

Cell experiment:[1]

Cell lines

Hippocampal neurons from 17E Sprague-Dawley rats

Reaction Conditions

0, 0.5, 1, 5, 10 and 50 μM dibutyryl cAMP for 1 h incubation

Applications

Dibutyryl cAMP significantly inhibited neuronal glucose uptake in a dose-dependent manner. Neurons exposed to 50 μM dibutyryl cAMP showed only 13% of glucose uptake by the control neurons.

Animal experiment:[2]

Animal models

Mice, 20 ~ 25 g

Dosage form

600 nM/mouse

Injected intraperitoneally for 4 days

Applications

Treatment with intraperitoneal injection of dibutyryl cAMP (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments in mice. Thus, dibutyryl cAMP could be used to explore the potential role of protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations.

Note

The technical data provided above is for reference only.

References:

1. Prapong T, Uemura E, Hsu WH. G protein and cAMP-dependent protein kinase mediate amyloid beta-peptide inhibition of neuronal glucose uptake. Experimental Neurology, 2001, 167(1): 59-64.

2. Tabrizian K, Yazdani A, Baheri B, et al. Zinc chloride and lead acetate-induced passive avoidance memory retention deficits reversed by nicotine and bucladesine in mice. Biological Trace Element Research, 2016, 169(1): 106-113.

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