Sp-5,6-DCl-cBIMPS is a potent and specific cAMP-dependent protein kinases (cAMP-PK) activator. Sp-5,6-DCl-cBIMPS stimulates insulin release. Sp-5,6-DCl-cBIMPS inhibits U46619-induced activation of Rho, Gq and G12/G13 in platelets.

4′-Demethylnobiletin is a bioactive metabolite that activates the PKA/ERK/CREB signaling pathway, enhances CRE-mediated transcription in hippocampal neurons, and reverses memory impairment associated with NMDA receptor antagonism by stimulating ERK signaling.

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

PKI(5-22)amide is the active inhibitory fragment of the inhibitor of the cyclic AMP-dependent protein kinase (PKA). PKI(5-22)amide inhibits PKA activation, but fails to attenuate homologous desensitization of CRF1 receptors.

DS89002333 is an orally active and potent PRKACA inhibitor, with an IC50 of 0.3 nM. DS89002333 shows good anti-tumor activity in an FL-HCC patient-derived xenograft model (expressing the DNAJB1-PRKACA fusion gene). DS89002333 can be used in study of fibrolamellar hepatocellular carcinoma (FL-HCC).

8-pCPT-2'-O-Me-cAMP-AM is a cyclic AMP analogue, selectively activates Epac-Rap signaling pathway. 8-pCPT-2'-O-Me-cAMP-AM protects renal function by activating Epac from ischemia injury. 8-pCPT-2'-O-Me-cAMP-AM also stimulates insulin secretion by interaction with PKA pathway.

6-Bnz-cAMP sodium salt is a cell-permeable cAMP analog. 6-Bnz-cAMP selectively activates cAMP-dependent PKA but not Epac signaling pathways.

8-CPT-Cyclic AMP (8-CPT-cAMP) sodium is a selective activator of cyclic AMP-dependent protein kinase (PKA). 8-CPT-Cyclic AMP sodium is also a potent inhibitor of the cyclic GMP-specific phosphodiesterase (PDE VA) with an IC50 of 0.9 μM. 8-CPT-Cyclic AMP sodium also inhibits PDE III and PDE IV with IC50Epac and is a potent Epac activator.

PKA-IN-1 is a potent and selective cyclic AMP-dependent protein kinase (PKA) catalytic subunit (cAK) inhibitor with an IC50 of 0.03 μM.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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-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.

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.

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.

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.

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.