6-Bnz-cAMP  (Synonyms: N6-Benzoyl-cAMP)

6-Bnz-cAMP, a derivative of cyclic adenosine monophosphate (cAMP), is a selective PKA activator with inhibitory activity against the bTREK-1 K⁺ channel. 6-Bnz-cAMP does not activate the Epac signaling pathway. 6-Bnz-cAMP 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 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. 6-Bnz-cAMP can be used in studies related to bone tissue repair and regeneration^[1][2][3].

6-Bnz-cAMP (100 μM) 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) 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) 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) induces Runx2 protein expression in osteoblast-like MC3T3-E1 cells after 7 days of incubation^[3].
6-Bnz-cAMP (100 µM; 7-14 days) 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) 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) 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) 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.

433.31

C₁₇H₁₆N₅O₇P

30275-80-0

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

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• [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[J]. Molecular pharmacology, 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.