8-bromo-Cyclic AMP
(Synonyms: 8-溴腺苷-3',5'-环单磷酸) 目录号 : GC42622A PKA activator
Cas No.:23583-48-4
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
8-bromo-Cyclic AMP is a brominated derivative of cAMP that remains long-acting due to its resistance to degradation by cAMP phosphodiesterase. It can activate cAMP-dependent protein kinase, inhibiting growth, decreasing proliferation, increasing differentiation, and inducing apoptosis of cancer cells.
| Cas No. | 23583-48-4 | SDF | |
| 别名 | 8-溴腺苷-3',5'-环单磷酸 | ||
| Canonical SMILES | OP1(OC[C@]2([H])[C@@]([C@@H](O)[C@H](N3C(N=CN=C4N)=C4N=C3Br)O2)([H])O1)=O | ||
| 分子式 | C10H11BrN5O6P | 分子量 | 408.1 |
| 溶解度 | PBS (pH 7.2): 3 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.4504 mL | 12.2519 mL | 24.5038 mL |
| 5 mM | 0.4901 mL | 2.4504 mL | 4.9008 mL |
| 10 mM | 0.245 mL | 1.2252 mL | 2.4504 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Cyclic AMP-mediated regulation of vascular smooth muscle cell cyclic AMP phosphodiesterase activity
Br J Pharmacol 1997 Sep;122(2):233-40.PMID:9313930DOI:10.1038/sj.bjp.0701376.
1. Rat cultured aortic vascular smooth muscle cells (VSMC) express both cyclic GMP-inhibited cyclic AMP phosphodiesterase (PDE3) and Ro 20-1724-inhibited cyclic AMP phosphodiesterase (PDE4) activities. By utilizing either cilostamide, a PDE3-selective inhibitor, or Ro 20-1724, a PDE4-selective inhibitor, PDE3 and PDE4 activities were shown to account for 15% and 55% of total VSMC cyclic AMP phosphodiesterase (PDE) activity. 2. Treatment of VSMC with either forskolin or 8-bromo-Cyclic AMP caused significant concentration- and time-dependent increases in total cellular cyclic AMP PDE activity. Using cilostamide or Ro 20-1724, we demonstrated that both PDE3 and PDE4 activities were increased following forskolin or 8-bromo-Cyclic AMP treatment, with a relatively larger effect observed on PDE3 activity. The increase in cyclic AMP PDE activity induced by forskolin or 8-bromo-Cyclic AMP was inhibited by actinomycin D or cycloheximide, demonstrating that new mRNA synthesis and protein synthesis were required. An analogue of forskolin which does not activate adenylyl cyclase (1,9-dideoxyforskolin) or an analogue of cyclic GMP (8-bromo-cyclic GMP) did not affect total cyclic AMP PDE activity. 3. Incubation of VSMC with 8-bromo-Cyclic AMP for 16 h caused a marked rightward shift in the concentration-response curves for both isoprenaline- and forskolin-mediated activation of adenylyl cyclase. A role for up-regulated cyclic AMP PDE activity in this reduced potency is supported by our observation that cyclic AMP PDE inhibitors (IBMX, cilostamide or Ro 20-1724) partially normalized the effects of isoprenaline or forskolin in treated cells to those in untreated cells. 4. We conclude that VSMC cyclic AMP PDE activity is increased following long-term elevation of cyclic AMP and that increases in PDE3 and PDE4 activities account for more than 70% of this effect. Furthermore, we conclude that increases in cyclic AMP PDE activity contribute to the reduced potency of isoprenaline or forskolin in treated VSMC. These results have implications for long-term use of cyclic AMP PDE inhibitors as therapeutic agents.
Phorbol myristate acetate and 8-bromo-cyclic AMP-induced phosphorylation of glial fibrillary acidic protein and vimentin in astrocytes: comparison of phosphorylation sites
J Neurochem 1991 May;56(5):1723-30.PMID:2013762DOI:10.1111/j.1471-4159.1991.tb02073.x.
Both the protein kinase C (PK-C) activator, phorbol 12-myristate 13-acetate (PMA), and the cyclic AMP-dependent protein kinase (PK-A) activator, 8-bromo-Cyclic AMP (8-BR), have been shown to increase 32P incorporation into glial fibrillary acidic protein (GFAP) and vimentin in cultured astrocytes. Also, treatment of astrocytes with PMA or 8-BR results in the morphological transformation of flat, polygonal-shaped cells into stellate, process-bearing cells, suggesting the possibility that signals mediated by these two kinase systems converge at the level of protein phosphorylation to elicit similar changes in cell morphology. Therefore, studies were conducted to determine whether treatment with PMA and 8-BR results in the phosphorylation of the same tryptic peptide fragments on GFAP and vimentin in astrocytes. Treatment with PMA increased 32P incorporation into all the peptide fragments that were phosphorylated by 8-BR on both vimentin and GFAP; however, PMA also stimulated phosphorylation of additional fragments of both proteins. The phosphorylation of vimentin and GFAP resulting from PMA or 8-BR treatment was restricted to serine residues in the N-terminal domain of these proteins. Studies were also conducted to compare the two-dimensional tryptic phosphopeptide maps of GFAP and vimentin from intact cells treated with PMA and 8-BR with those produced when the proteins were phosphorylated with purified PK-C or PK-A. PK-C phosphorylated the same fragments of GFAP and vimentin that were phosphorylated by PMA treatment. Additionally, PK-C phosphorylated some tryptic peptide fragments of these proteins that were not observed with PMA treatment in intact cells.(ABSTRACT TRUNCATED AT 250 WORDS)
One-day treatment of small molecule 8-bromo-Cyclic AMP analogue induces cell-based VEGF production for in vitro angiogenesis and osteoblastic differentiation
J Tissue Eng Regen Med 2016 Oct;10(10):867-875.PMID:24493289DOI:10.1002/term.1839.
Small molecule-based regenerative engineering is emerging as a promising strategy for regenerating bone tissue. Small molecule cAMP analogues have been proposed as novel biofactors for bone repair and regeneration and, while promising, the effect that these small molecules have on angiogenesis, a critical requirement for successful bone regeneration, is still unclear. Our previous research demonstrated that the small molecule cAMP analogue 8-bromoadenosine-3',5'-cyclic monophosphate (8-Br-cAMP) was able to promote initial osteoblast adhesion on a polymeric scaffold via cAMP signalling cascades. Here, we report that 8-Br-cAMP is capable of inducing in vitro cell-based VEGF production for angiogenesis promotion. We first demonstrated that treating osteoblast-like MC3T3-E1 cells with 8-Br-cAMP for 1 day significantly increased VEGF production and secretion. We then demonstrated that 8-Br-cAMP-induced cell-secreted VEGF is biologically active and may promote angiogenesis, as evidenced by increased human umbilical vein endothelial cells (HUVECs) migration and tubule formation. In addition, treatment of MC3T3-E1 cells with 8-Br-cAMP for as short as a single day resulted in enhanced ALP activity as well as matrix mineralization, demonstrating in vitro osteoblastic differentiation. A short-term 8-Br-cAMP treatment also addresses the concern of non-specific cytotoxicity, as our data indicate that a 1-day 8-Br-cAMP treatment scheme supports cellular proliferation of MC3T3-E1 cells as well as HUVECs. While the major concern associated with small molecule drugs is the risk of non-specific cytotoxicity, the short exposure treatment outlined in this paper provides a very promising strategy to mitigate the risk associated with small molecules. Copyright © 2013 John Wiley & Sons, Ltd.
Effects of LH, prostaglandin E2, 8-bromo-Cyclic AMP and forskolin on progesterone secretion by pig luteal cells
J Reprod Fertil 1998 May;113(1):83-9.PMID:9713380DOI:10.1530/jrf.0.1130083.
The present study examined the effects of LH, prostaglandin E2 (PGE2), 8-bromo-Cyclic AMP (cAMP) and forskolin on progesterone secretion by small and large pig luteal cells. Corpora lutea were isolated from gilts (n > or = 3 per day) on days 9, 12 and 14 of the oestrous cycle and days 9, 12, 14 and 30 of pregnancy. After enzymatic dissociation of the corpora lutea, small and large luteal cells were obtained by elutriation. Culture plates (24-well) were then seeded with 150,000 small luteal cells or 30,000 large luteal cells per well in 1 ml M199 medium in the absence or presence of LH, PGE2, LH plus PGE2, 8-bromo-cAMP or forskolin. After 12 h of incubation, culture plates were centrifuged, and the supernatant collected and frozen for subsequent assay of progesterone. Differences within day were not detected between cyclic and pregnant gilts, and thus, results were combined for days 9, 12 and 14. Basal progesterone secretion by small luteal cells was less (P < 0.05) on days 14 and 30 than days 9 and 12. Treatment with LH, PGE2, 8-bromo-cAMP or forskolin increased (P < 0.05) progesterone secretion by small luteal cells on days 9 and 12; however, treatments had no effect on days 14 and 30. Basal progesterone production by large luteal cells was less (P < 0.05) on day 30 compared with other days. PGE2 stimulated (P < 0.001) progesterone production by large luteal cells at all days. In contrast, 8-bromo-cAMP and forskolin inhibited progesterone production by large luteal cells on day 12 (P < 0.05), and day 14 (P < 0.001). These data show that pregnancy status does not alter luteal cell response to the aforementioned secretagogues. However, regulation of progesterone secretion differs between small and large luteal cells, and the age of the corpora lutea. Also, it is unlikely that the stimulatory actions of PGE2 involve increased cAMP production in pig large luteal cells.
Differential effects of 8-bromo-Cyclic AMP on human chorionic gonadotropin (hCG), progesterone and estrogen production by term placental cells
Life Sci 1988;43(18):1451-8.PMID:2846979DOI:10.1016/0024-3205(88)90256-1.
The present study examined the effects of a cAMP analog on the output of hCG and progesterone (P) in human term trophoblast cells in culture, as well as the conversion of androstenedione and testosterone to estradiol--17 beta and estrone by these cells. The levels of hCG and P in the culture medium increased throughout the four-day culture period. Addition of 8-bromo-adenosine-3',5'-monophosphate (8-Br-cAMP), forskolin or cholera toxin (but not 8-Br-cGMP) stimulated hCG and P production by the cultivated placental cells. In contrast, the presence of 8-Br-cAMP for 2 days significantly decreased basal estradiol-17 beta output, as well as conversion of androstenedione to estradiol-17 beta; the conversion of androstenedione to estrone was not affected. 8-Br-cAMP attenuated the conversion of testosterone to both estradiol-17 beta and estrone. These results further support the view that cAMP could have both stimulatory and inhibitory actions on placental hormonogenesis.