Bucladesine calcium

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Chemical Structure| 938448-87-4 同义名 : Dibutyryl cAMP calcium salt;DBcAMP calcium salt
CAS号 : 938448-87-4
货号 : A722401
分子式 : C36H48CaN10O16P2
纯度 : 98+%
分子量 : 978.849
MDL号 : MFCD13152130
存储条件:

Pure form

In solvent -20°C:3-6个月-80°C:12个月

溶解度 :

DMSO: 105 mg/mL(107.27 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

H2O: 100 mg/mL(102.16 mM),配合低频超声助溶

动物实验配方:
生物活性
描述 PKA is a ubiquitous cellular kinase, also known as cAMP-dependent protein kinase (cAMP), and it is well-established that plays an important role in regulating several functions of cell processes, including regulation of glycogen, sugar, and lipid metabolism[1]. Bucladesine Calcium is a cell-permeable PKA activator that functions by preferentially activating endogenous cAMP. In vitro assays, Bucladesine Calcium was found to significantly suppress TNF-a production in a dose-dependent manner, with IC50 values of 247, 28.9, and 25.4 μM, respectively in RAW264.7 cells[2]. Additionally, Rat hepatocytes were cultured with cAMP agonists Bucladesine Calcium inhibits Nitric oxide synthesis and inducible nitric oxide synthase (iNOS) expression through effects on the iNOS promoter region and NF-kB-binding activity[3]. In hepatocytes, Bucladesine Calcium can prevent tumor necrosis factor α plus acti-nomycin D (TNFα/ActD)-induced apoptosis via a PKA-dependent mechanism[4]. In vivo model, Bucladesine Calcium shows a distinct anti-fibrotic effect via PKA/p-CREB/CBP signaling. Treatment of Bucladesine Calcium result in the decrease of the number and size of silicosis nodules, inhibition of myofibroblast differentiation, and extracellular matrix deposition[5]. Moreover, 4 days intra-peritoneal injections of Bucladesine Calcium (600 nM/mouse) significantly reversed zinc chloride- and lead acetate-induced avoidance memory retention alterations compared to control animals[6].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.05mL

0.41mL

0.20mL

10.24mL

2.05mL

1.02mL

20.47mL

4.09mL

2.05mL

参考文献

[1]Dolan S, Nolan AM. Biphasic modulation of nociceptive processing by the cyclic AMP-protein kinase A signalling pathway in sheep spinal cord. Neurosci Lett. 2001;309(3):157-60.

[2]Cho JY, Baik KU, et al. In vitro antiinflammatory effects of neolignan woorenosides from the rhizomes of Coptis japonica. J Nat Prod. 2000;63(9):1205-9.

[3]Harbrecht BG, Taylor BS, et al. cAMP inhibits inducible nitric oxide synthase expression and NF-kappaB-binding activity in cultured rat hepatocytes. J Surg Res. 2001 Aug;99(2):258-64.

[4]Wang Y, Kim PK, et al. Cyclic AMP and cyclic GMP suppress TNFalpha-induced hepatocyte apoptosis by inhibiting FADD up-regulation via a protein kinase A-dependent pathway. Apoptosis. 2006;11(3):441-51.

[5]Liu Y, Xu H, et al. Dibutyryl-cAMP attenuates pulmonary fibrosis by blocking myofibroblast differentiation via PKA/CREB/CBP signaling in rats with silicosis. Respir Res. 2017;18(1):38.

[6]Tabrizian K, Yazdani A, et al. Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice. Biol Trace Elem Res. 2016;169(1):106-13.