- Home
- Signaling Pathways
- MAPK Signaling
- cAMP
- Dibutyryl-cAMP, sodium salt
Dibutyryl-cAMP, sodium salt
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, S?rensen 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.
- 1. Claire S. Durrant, et al. "p-tau Ser356 is associated with Alzheimer's disease pathology and is lowered in brain slice cultures using the NUAK inhibitor WZ4003." Acta Neuropathol. 2024 Jan 4;147(1):7. PMID: 38175261
- 2. Binglin Zhu, Emily Fisher, et al. "PTBP2 attenuation facilitates fibroblast to neuron conversion by promoting alternative splicing of neuronal genes." Stem Cell Reports. 2023 Nov 14;18(11):2268-2282. PMID: 37832540
- 3. Lewis W. Taylor, Elizabeth M. Simzer, et al. "Tau phosphorylated at serine 356 is associated with Alzheimer’s disease pathology and can be lowered in mouse and human brain tissue using the NUAK inhibitor WZ4003." bioRxiv. August 29, 2023.
| 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 (4aR,6S,7R,7aR)-6-(6-butyramido-9H-purin-9-yl)-7-(butyryloxy)tetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-2-olate 2-oxide |
| SDF | Download SDF |
| Canonical SMILES | CCCC(NC1=NC=NC2=C1N=CN2[C@H]3O[C@H]4[C@@H](OP(OC4)([O-])=O)[C@H]3OC(CCC)=O)=O.[Na+] |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| 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. |
|
Quality Control & MSDS
- View current batch:
Chemical structure
