6-Bnz-cAMP sodium salt 

6-Bnz-cAMP sodium, a derivative of cyclic adenosine monophosphate (cAMP), is a selective PKA activator with inhibitory activity against the bTREK-1 K⁺ channel. 6-Bnz-cAMP sodium does not activate the Epac signaling pathway. It inhibits the bTREK-1 K⁺ channel via a voltage-independent, ATP-dependent mechanism that is independent of the PKA/Epac/calmodulin kinase/MAP kinase pathway. 6-Bnz-cAMP sodium activates CREB phosphorylation to regulate osteoblast-specific gene expression, induces osteoblast differentiation, promotes extracellular matrix mineralization, supports osteoblast proliferation, and shows no cytotoxicity toward osteoblasts. It can be used in studies related to bone tissue repair and regeneration^[1][2][3].

6-Bnz-cAMP (100 μM) sodium induces 44.9% relaxation of α-toxin-permeabilized human detrusor smooth muscle strips contracted by 1 μM [Ca²⁺]ᵢ, with a potency comparable to cAMP^[1].
6-Bnz-cAMP (<0.2-100 μM; 1-20 min) sodium potently inhibits bTREK-1 K⁺ channels in primary bovine AZF cells via an ATP-dependent, voltage-independent, PKA- and Epac-independent mechanism, with an IC₅₀ of less than 0.2 μM when applied intracellularly^[2].
6-Bnz-cAMP (100 µM; 7-21 days) sodium supports proliferation of osteoblast-like MC3T3-E1 cells and maintains >90% cell viability over 21 days without inducing cytotoxicity^[3].
6-Bnz-cAMP (100 µM; 7 days) sodium induces Runx2 protein expression in osteoblast-like MC3T3-E1 cells after 7 days of incubation^[3].
6-Bnz-cAMP (100 µM; 7-14 days) sodium significantly enhances ALP activity in osteoblast-like MC3T3-E1 cells at 7 and 14 days of incubation^[3].
6-Bnz-cAMP (100 µM; 18 days) sodium promotes production of extracellular OCN and OPN proteins in osteoblast-like MC3T3-E1 cells after 18 days of incubation^[3].
6-Bnz-cAMP (100 µM; 21 days) sodium significantly enhances extracellular matrix calcium deposition (mineralization) in osteoblast-like MC3T3-E1 cells after 21 days of incubation in mineralization medium^[3].
6-Bnz-cAMP (100 µM; 1-7 days) sodium activates phosphorylation of CREB in osteoblast-like MC3T3-E1 cells at 1 and 7 days of incubation, while inducing osteoblastic differentiation independent of Erk phosphorylation^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

455.29

C₁₇H₁₅N₅NaO₇P

1135306-29-4

Solid

White to off-white

O[C@@H]1[C@H](OP2(O[Na])=O)[C@@H](CO2)O[C@H]1N3C=NC4=C3N=CN=C4NC(C5=CC=CC=C5)=O

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Hayashi M, et al. Actions of cAMP on calcium sensitization in human detrusor smooth muscle contraction. BJU Int. 2016;117(1):179-191.

  [2]. Liu H, et al. N6-substituted cAMP analogs inhibit bTREK-1 K+ channels and stimulate cortisol secretion by a protein kinase A-independent mechanism. Mol Pharmacol. 2009;76(6):1290-1301.  [Content Brief]

  [3]. Lo KW, et al. The small molecule PKA-specific cyclic AMP analogue as an inducer of osteoblast-like cells differentiation and mineralization. J Tissue Eng Regen Med. 2012;6(1):40-48.