rp-8-cpt-camps

Rp-8-CPT-cAMPS is a powerful and competitive antagonist of cAMP-induced activation of cAMP-dependent protein kinase (PKA) I and II. Acting as a potent cAMP analog, Rp-8-CPT-cAMPS exhibits a preference for site A of RI over site A of RII. Additionally, it favors site B of RII over site B of RI. This compound effectively inhibits cAMP-dependent PKA activation and demonstrates selectivity in binding to specific sites within the protein kinase.

Rp-8-CPT-cAMP is a structural combination of the lipophilic and non-hydrolyzable cAMP analogs, 8-CPT-cyclic AMP and Rp-cyclic AMPS .[1] It functions as a site-selective inhibitor of protein kinase A (PKA) type I and II, with preference towards site A of type I and site B of type II.2 By occupying cAMP binding sites at the regulatory subunit of PKA, Rp-8-CPT-cAMP prevents the kinase holoenzyme from dissociative activation.[2],[3]

Rp-cAMPS triethylammonium salt is an analog of cAMP.It acts as a potent, competitive and cell-permeable antagonist of cAMP-induced activation of cAMP-dependent PKA I and II with Kis of 6.05 µM and 9.75 µM, respectively.

Rp-8-bromo-Cyclic AMPS (Rp-8-bromo-cAMPS) is a cell-permeable cAMP analog that combines an exocyclic sulfur substitution in the equatorial position of the cyclophosphate ring with a bromine substitution in the adenine base of cAMP. It acts as an antagonist of cAMP-dependent protein kinases (PKAs) and is resistant to hydrolysis by cyclic nucleotide phosphodiesterases. Rp-8-bromo-cAMPS more effectively antagonizes cAMP-dependent activation of purified PKA type I from rabbit muscle than PKA type II from bovine heart.

cGMP-dependent protein kinase (PKG) inhibitor

Rp-cAMPS competitively inhibits the cAMP-induced activation of cAMP-dependent protein kinase (PKA).

8-CPT-2Me-cAMP sodium is a sodium salt compound that selectively activates exchange proteins activated by cAMP (Epac), which are cAMP-sensitive guanine nucleotide exchange factors (GEFs) responsible for activating small GTPases Rap1 and Rap2. It specifically activates Epac1 with an EC50 value of 2.2 μM, while showing no activation of PKA with an EC50 value greater than 10 μM [1]. Additionally, 8-CPT-2Me-cAMP sodium stimulates the Epac-mediated release of calcium ions (Ca2+) in vitro in pancreatic β-cells [2].

Rp-cAMPS sodium is a phosphorothioate analog of cAMP, a protein kinase A inhibitor and a membrane-permeable cAMP antagonist that inhibits cAMP-dependent protein kinases by blocking cAMP-induced conformational transitions, and can be used in the study of cardiovascular diseases.

Sp-8-CPT-cAMPS is a powerful and specific cAMP analog that activates cAMP-dependent protein kinase A (PKA I and PKA II) selectively and effectively. It exhibits a 153-fold preference for site A of RI over site A of RII, and a 59-fold preference for site B of RII over site B of RI.

8-CPT-Cyclic AMP (8-CPT-cAMP) sodium is a selective activator of cyclic AMP-dependent protein kinase (PKA) and a potent inhibitor of cyclic GMP-specific phosphodiesterase (PDE VA) with an inhibitory concentration (IC50) of 0.9 μM. It also inhibits PDE III and PDE IV while significantly activating Epac, demonstrating diverse pharmacological activities [1] [2].