Rp-cAMPS triethylammonium salt is an analog of cAMP which acts as a potent, competitive and cell-permeable antagonist of cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 6.05 µM and 9.75 µM, respectively). Rp-cAMPS triethylammonium salt is resistant to hydrolysis by phosphodiesterases.

Rp-cAMPS, a cAMP analog, is a potent, competitive cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 12.5 μM and 4.5 μM, respectively) antagonist. Rp-cAMPS is resistant to hydrolysis by phosphodiesterases.

Sp-cAMPS, a cAMP analog, is potent activator of cAMP-dependent PKA I 和 PKA II. Sp-cAMPS is also a potent, competitive phosphodiesterase (PDE3A) inhibitor with a Ki of 47.6 μM. Sp-cAMPS binds the PDE10 GAF domain with an EC50 of 40 μM.

Sp-cAMPS sodium salt, a cAMP analog, is potent activator of cAMP-dependent PKA I 和 PKA II. Sp-cAMPS sodium salt is also a potent, competitive phosphodiesterase (PDE3A) inhibitor with a Ki of 47.6 μM. Sp-cAMPS sodium salt binds the PDE10 GAF domain with an EC50 of 40 μM.

Rp-cAMPS sodium salt, a cAMP analog, is a potent, competitive cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 12.5 μM and 4.5 μM, respectively) antagonist. Rp-cAMPS sodium salt is resistant to hydrolysis by phosphodiesterases.

Rp-8-CPT-cAMPS sodium, a cAMP analog, is a potent and competitive antagonist of cAMP-induced activation of cAMP-dependent PKA I and II. Rp-8-CPT-cAMPS sodium preferentially selects site A of RI compares to site A of RII and site B of RII compares to site B of RI.

Rp-8-CPT-cAMPS, a cAMP analog, is a potent and competitive antagonist of cAMP-induced activation of cAMP-dependent PKA I and II. Rp-8-CPT-cAMPS preferentially selects site A of RI compares to site A of RII and site B of RII compares to site B of RI.

Sp-8-CPT-cAMPS, a cAMP analog, is a potent and selective activator of the cAMP-dependent protein kinas A (PKA I and PKA II). Sp-8-CPT-cAMPS selects site A of RI compares to site A of RII by 153-fold and site B of RII compares to site B of RI by 59-fold.

PKI(5-24) is a potent, competitive, and synthetic peptide inhibitor of PKA (cAMP-dependent protein kinase), with a Ki of 2.3 nM. PKI(5-24) corresponds to residues 5-24 in the naturally occurring heat-stable protein kinase inhibitor.

PKI(5-24) TFA is a potent, competitive, and synthetic peptide inhibitor of PKA (cAMP-dependent protein kinase), with a Ki of 2.3 nM. PKI(5-24) TFA corresponds to residues 5-24 in the naturally occurring heat-stable protein kinase inhibitor.

PKA Inhibitor Fragment (6-22) amide is an inhibitor of cAMP-dependent protein kinase A (PKA), with a Ki of 2.8 nM. PKA Inhibitor Fragment (6-22) amide can significantly reverse low-level morphine antinociceptive tolerance in mice.

PKA Inhibitor Fragment (6-22) amide TFA is an inhibitor of cAMP-dependent protein kinase A (PKA), with a Ki of 2.8 nM. PKA Inhibitor Fragment (6-22) amide TFA can significantly reverse low-level morphine antinociceptive tolerance in mice.

PKI 14-22 amide,myristoylated is a potent cAMP-dependent PKA inhibitor. PKI 14-22 amide,myristoylated reduces the IgG-mediated phagocytic response and also inhibits neutrophil adhesion.

PKI 14-22 amide,myristoylated TFA is a potent cAMP-dependent PKA inhibitor. PKI 14-22 amide,myristoylated TFA reduces the IgG-mediated phagocytic response and also inhibits neutrophil adhesion.

Malantide TFA is a synthetic dodecapeptide derived from the site phosphorylated by cAMP-dependent protein kinase (PKA) on the β-subunit of phosphorylase kinase. Malantide TFA is a highly specific substrate for PKA with a Km of 15 μM and shows protein inhibitor (PKI) inhibition >90% substrate phosphorylation in various rat tissue extracts. Malantide TFA is also an efficient substrate for PKC with a Km of 16 μM.