Dibutyryl-cAMP, sodium salt
mRNA synthesis
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Inhibitor Cocktails
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
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.
Physical Appearance | A solid |
Storage | Store at -20°C |
M.Wt | 491.37 |
Cas No. | 16980-89-5 |
Formula | C18H23N5NaO8P |
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 Name | sodium (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 |
SDF | Download SDF |
Canonical SMILES | CCC/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+] |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 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。溶液形式一般不宜长期储存,请尽快用完。 |
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. |
质量控制和MSDS
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