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| 10 mM * 1 mL in DMSO |
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Purity: ≥98%
8-Bromo-cAMP sodium is a potent and cell permeable cyclic AMP (cAMP) analog and a PKA activator. 8-Bromo-cAMP increased the cellular content of mRNA encoding the hCG a- and β-subunits and prevented the increase in fibronectin mRNA. This is determined by blot hybridization analysis using specific cDNA probes. 8-Bromo-cAMP also induced phosphorylation of Erk1,2 in AML193 cells. 8-Bromo-cAMP is an agent in AML193 cells and activates Erk1,2 , this condition happens does not accompanied by the involvement of Shc phosphorylation.
| Targets |
PKA/protein kinase A
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|---|---|
| ln Vitro |
8-Bromo-cAMP sodium salt is a brominated derivative of cyclic AMP that enhances cell reprogramming. 8-Bromo-cAMP sodium salt increases the reprogramming effectiveness of human newborn foreskin fibroblasts (HFF1). 8-Bromo-cAMP sodium salt reduces the proliferation, differentiation, and death of malignant glioma cell lines (A-172) and esophageal cancer cell lines (Eca-109) [1].
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| ln Vivo |
Researcher discovered that treatment with 8-Br-cAMP significantly reduced tumor number compared to control mice after the 7th, 14th, and 28th days of treatment. VM was evaluated by periodic acid-schiff (PAS)-CD31 staining, and we found that VM was inhibited by 8-Br-cAMP treatment in vivo. Immunohistochemistry confirmed the inhibition of vascular endothelial growth factor (VEGF) and cAMP and the activation of PKA by 8-Br-cAMP; quantitative real-time-PCR (qRT-PCR) demonstrated that 8-Br-cAMP regulated the expression of vascular endothelial (VE)-cadherin, matrix metalloproteinase 2 (MMP2), ephrin type-A receptor 2 (EphA2), and VEGF in vivo[4].
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| Enzyme Assay |
Human endometrium decidualization, a differentiation process involving biochemical and morphological changes, is a prerequisite for embryo implantation and successful pregnancy. Here, we show that the mammalian target of rapamycin (mTOR) is a crucial regulator of 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP )-induced decidualization in human endometrial stromal cells. The level of mSin1 in mTOR complex 2 (mTORC2) and DEPTOR in mTOR complex 1 (mTORC1) decreases during 8-Br-cAMP -induced decidualization, resulting in decreased mTORC2 activity and increased mTORC1 activity. Notably, DEPTOR displacement increases the association between raptor and insulin receptor substrate-1 (IRS-1), facilitating IRS-1 phosphorylation at serine 636/639. Finally, both S473 and T308 phosphorylation of Akt are reduced during decidualization, followed by a decrease in forkhead box O1 (FOXO1) phosphorylation and an increase in the mRNA levels of the decidualization markers prolactin (PRL) and insulin-like growth factor-binding protein-1 (IGFBP-1). Taken together, our findings reveal a critical role for mTOR in decidualization, involving the differential regulation of mTORC1 and mTORC2[3].
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| Cell Assay |
The cultured Eca-109 cells were divided into four groups: E1 group (co-cultured with 8-Br-cAMP for 24 h); E2 group (co-cultured with 8-Br-cAMP for 48 h); C1 group (treated without 8-Br-cAMP for 24 h); and C2 group (treated without 8-Br-cAMP for 48 h). The same concentration of cell suspension of each group was dropped separately onto the slides and nitrocellulose membranes (NCM). The biotin-labeled cDNA probes for c-myc, wild-type (wt) p53, bcl-2 and iNOS were prepared for in situ hybridization. The expressions of epidermal growth factor receptor (EGFR), p38 kinase, FAS, FasL and caspase-3 were detected using immunocytochemistry, and the NOS activity and the ratio of differentiated cells/proliferating cells were examined by cytochemistry. Immunocytochemistry, cytochemistry, and in situ hybridization were separately carried out on both slides and NCM specimens for each group. In addition, TUNEL was used to detect the cell apoptosis rate in each group.[2]
Results: The apoptotic rate of E2 group was significantly higher compared to E1 group, while there was no difference in the ratio of differentiated cells/proliferating cells between E1 and E2 groups. The signals of wt p53 and iNOS were markedly stronger, while the signals of c-myc and EGFR were obviously weaker in E1 group than those in C1 group (P<0.05). Moreover, the signals of wt p53, iNOS, p38 kinase, caspase-3 and NOS activity were significantly stronger, whereas, the signals of bcl-2, c-myc and Fas/FasL were markedly weaker in E2 group than those in C2 group (P<0.05).[2] Conclusion: The differentiation and apoptosis of human esophageal cancer cell Eca-109 can be induced after 24- and 48-h treatment with 8-Br-cAMP , respectively. Upregulation of wt p53, iNOS and downregulation of c-myc may be associated with differentiation and apoptosis of Eca-109 cells. Furthermore, upregulation of FasL, p38 kinase and caspase-3 as well as downregulation of bcl-2, and Fas may be involved in the apoptosis of Eca-109 cells.[2] |
| Animal Protocol |
Thirty-six mice received the implantation of CT26 carcinoma tissue in their cecum. After general anesthesia and sterilization, a 2 cm vertical incision was made at the right lower quadrant of the abdomen. The cecum was then pulled out of the abdomen. The serosa of the cecum that was exposed out was scratched, and a 2 mm diameter tumor tissue was attached with fibrin glue. Finally, the cecum was put back into place and the skin was sealed. After tumor implantation, mice were randomly divided into a control group and an experimental group. In the experimental group, the intraperitoneal injection of 8-Br-cAMP (60 mg/kg/day) was performed for 7 days, while control mice received injection of normal saline. Mice were sacrificed on the 7th, 14th, and 28th days, and tumor tissue was harvested for the evaluation of gene expression. However, due to a high mortality rate, the number of mice for sacrifice at each time point was adjusted in order to guarantee that mice were available for culling on the 28th day. [4]
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| References |
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| Additional Infomation |
A long-acting derivative of cyclic AMP. It is an activator of cyclic AMP-dependent protein kinase, but resistant to degradation by cyclic AMP phosphodiesterase.
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| Molecular Formula |
C10H10BRN5NAO6P
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|---|---|---|
| Molecular Weight |
430.08
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| Exact Mass |
428.944
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| Elemental Analysis |
C, 27.93; H, 2.34; Br, 18.58; N, 16.28; Na, 5.35; O, 22.32; P, 7.20
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| CAS # |
76939-46-3
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| Related CAS # |
8-Bromo-AMP;23567-96-6
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| PubChem CID |
23702958
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| Appearance |
White to off-white solid powder
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| LogP |
0.964
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
1
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| Heavy Atom Count |
24
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| Complexity |
538
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| Defined Atom Stereocenter Count |
4
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| SMILES |
C1[C@@H]2[C@H]([C@H]([C@@H](O2)N3C4=NC=NC(=C4N=C3Br)N)O)OP(=O)(O1)[O-].[Na+]
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| InChi Key |
DMRMZQATXPQOTP-GWTDSMLYSA-M
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| InChi Code |
InChI=1S/C10H11BrN5O6P.Na/c11-10-15-4-7(12)13-2-14-8(4)16(10)9-5(17)6-3(21-9)1-20-23(18,19)22-6;/h2-3,5-6,9,17H,1H2,(H,18,19)(H2,12,13,14);/q;+1/p-1/t3-,5-,6-,9-;/m1./s1
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| Chemical Name |
sodium (4aR,6R,7R,7aS)-6-(6-amino-8-bromo-9H-purin-9-yl)-7-hydroxytetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinin-2-olate 2-oxide
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.84 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (4.84 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (4.84 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (232.51 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.3251 mL | 11.6257 mL | 23.2515 mL | |
| 5 mM | 0.4650 mL | 2.3251 mL | 4.6503 mL | |
| 10 mM | 0.2325 mL | 1.1626 mL | 2.3251 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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