CW 008, a derivative of pyrazole-pyridine, is a CREB or PKA pathway agonist. CW 008 also is a stem cell differentiating agent. CW 008 stimulates osteoblast differentiation of human MSCs and increases bone formation in ovariectomized mice. CW008 promotes osteogenesis by activating cAMP/PKA/CREB signaling pathway and inhibiting leptin secretion[1][2][3].
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[1].
H-89 is a potent inhibitor of cyclic AMP-dependent protein kinase (protein kinase A) with IC50 of 48 nM and has weak inhibition on PKG, PKC, Casein Kinase, and others kinases.
Hu7691 free base is an orally active, selective Akt inhibitor with IC50s of 4.0 nM, 97.5 nM, 28 nM for Akt1, Akt2 and Akt3, respectively. Hu7691 free base inhibits tumor growth and enables decrease of cutaneous toxicity in mice[1].
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[1][2].
BLU0588 is an orally active, potent and selective PRKACA (protein kinase cAMP-activated catalytic subunit alpha) kinase inhibitor, with an IC50 of 1 nM and dissociation constant (Kd) of 4 nM. BLU0588 can be used for fibrolamellar carcinoma (FLC) research[1].
KT5720 is a cell-permeable, potent, specific, reversible, ATP-competitive inhibitor of protein kinase A (PKA), with a Ki of 60 nM[1][2].
PKI (5-24),amide (IP20-amide) is a 20-residue peptide that corresponds to the active portion of the heat-stable inhibitor protein of cAMP-dependent protein kinase. PKI (5-24),amide is a potent cAMP-dependent protein kinase (PKA) (PKA) inhibitor with a Ki of 2.3 nM[1].
PF-4950834 is a potent, selective, orally bioavailable, ATP-competitive rho kinase inhibitor with IC50 values of 8.35 nM and 33.12 nM against ROCK2 and ROCK1, respectively. PF-4950834 inhibits neutrophil migration[1].
TX-1123 is a potent protein tyrosine kinase (PTK) inhibitor for Src, eEF2-K, and PKA, and EGFR-K/PKC. TX-1123 is a cyclo-oxygenase (COX) inhibitor with IC50 values of 1.16 μM and 15.7 μM for COX2 and COX1, respectively. TX-1123 has low mitochondrial toxicity. TX-1123 can be used in research of cancer[1][2].
H-8 (dihydrochloride) is a cell-permeable, reversible and ATP-competitive PKA inhibitor[1].
Metadoxine blocks adipocyte differentiation in association with inhibition of the protein kinase A-cAMP response element binding protein (PKA-CREB) pathway.
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[1][2].
Synaptamide is a potent mediator for neurogenic differentiation of NSCs acting through PKA/CREB activation.Target: in vitro: Synaptamide inhibits forskolin-mediated cAMP production (IC50 =6 μM) in CHO-HCR cells. Synaptamide decreases the viability of the LNCaP and PC3 prostate cancer cell lines (IC50=120-130 μM) grown in media containing 10% fetal bovine serum. [1] Synaptamide is an endogenous DHA metabolite with endocannabinoid-like structure, promotes neurite growth, synaptogenesis and synaptic function. Synaptamide potently induces neuronal differentiation of NSCs. Treatment of NSCs with Synaptamide at low nanomolar concentrations significantly increased the number of MAP2 and Tuj-1 positive neurons with concomitant induction of PKA/CREB phosphorylation. [2]
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[1][2][3].
PKI (14-24)amide TFA is a potent PKA inhibitor. PKI (14-24)amide strongly inhibited cyclic AMP-dependent protein kinase activity in the cell homogenate[1][2].
8-Bromo-cAMP sodium salt (8-Br-Camp sodium salt), a cyclic AMP analog, is an activator of cyclic AMP-dependent protein kinase (PKA)[1].
H-Arg-Gly-Tyr-Ala-Leu-Gly-OH is a competitive and CAMP dependent protein kinase inhibitor[1].
H-89 dihydrochloride is a potent inhibitor of protein kinase A (PKA) with an IC50 of 48 nM and has weak inhibition on PKG, PKC, Casein Kinase.
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[1][2].
Warangalone is an anti-malarial compound which can inhibit the growth of both strains of parasite 3D7 (chloroquine sensitive) and K1 (chloroquine resistant) with IC50s of 4.8 μg/mL and 3.7 μg/mL, respectively. Warangalone can also inhibit cyclic AMP-dependent protein kinase catalytic subunit (cAK) with an IC50 of 3.5 μM.
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[1][2][3].
K-252a, a staurosporine analog isolated from Nocardiopsis sp. soil fungi, inhibits protein kinase, with IC50 values of 470 nM, 140 nM, 270 nM, and 1.7 nM for PKC, PKA, Ca2+/calmodulin-dependent kinase type II, and phosphorylase kinase, respectively[1][2].
Akt1&PKA-IN-1 is a potent dual Akt/PKA inhibitor with IC50 values of 0.03 , 0.11 μM, and 9.8 μM for PKAa, Akt, and CDK2, respectively. Akt1&PKA-IN-1 is selective for cyclin-dependent kinase 2 (CDK2)[1].
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[1][2][3][4][5][6].
PKI (14-24)amide is a potent PKA inhibitor. PKI (14-24)amide strongly inhibited cyclic AMP-dependent protein kinase activity in the cell homogenate[1][2].
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[1][2][3].
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[1][2][3][4][5].
H-9 Dihydrochloride is a PKA (protein kinase) inhibitor. H-9 Dihydrochloride (10 μM) significantly reduces the excitatory response to 5-HT. H-9 Dihydrochloride also has a direct effect on pharyngeal activity. H-9 Dihydrochloride inhibits signal-transduction and cell growth in EGF (epidermal growth factor)-dependent epithelial cell lines[1][2][3].
Bucladesine calcium salt(DC2797 calcium salt) is a membrane permeable selective activator of PKA.Target: PKABucladesine (bilateral infusion of 10 mM or 100 mM) leads to a significant reduction in escape latency and travel distance (showing an improvement in spatial memory) compared to the control, as assesed by Morris water maze task in male rats. Bucladesine at 1 mM and 5 mM concentrations infused within minutes after 0.5 mg nicotine infusion improves spatial memory retention in male rats [1]. Bucladesine (10 mM/side) combined with Nicotine (0.5 mM/side) results in a significant increase in the ChAT and VAChT immunoreactivity in CA1 regions, and increase in the optical density and amount of ChAT and VAChT immunostaining correlates with the decrease in escape latency and traveled distance in rats treated with Nicotine and low dose of Bucladesine [2]. Bucladesine is absorbed very rapidly and almost completely when the aqueous solution is applied to the site where the skin has been excised. Bucladesine is absorbed rapidly but slower than in the full-thickness abrasion rat model in the case of stripped skin [3]. Bucladesine (single or multiple administration of an emulsion containing 1.5%) is capable of significantly reducing the inflammatory oedema in the arachidonic acid induced ear oedema model in mice [4].