CAS NO: | 16980-89-5 |
包装 | 价格(元) |
50mg | 电议 |
100mg | 电议 |
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 |
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 | 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。溶液形式一般不宜长期储存,请尽快用完。 |
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, Sorensen 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.
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. |