6-Bnz-cAMP sodium salt

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.