H-89 is a potent and selective inhibitor of PKA, with an IC50 of about 50 nM. H-89 inhibits several other kinases with IC50 of 80, 120, 135, 270, 2600 and 2800 nM for S6K1, MSK1, PKA, ROCKII, PKBα and MAPKAP-K1b, respectively. H-89 also inhibits PKG and the µ isotype of PKC (at about 500 nM). In contrast, most other PKC isotypes are much more weakly inhibited, with IC50’s in the 32 µM range. Intraperitoneal administration of H-89 (0.2 mg/100g) significantly increased seizure latency and threshold in PTZ-treated animals. H-89 (0.05, 0.2 mg/100g) prevented the epileptogenic activity of bucladesine (300 nM) with significant increase of seizure latency and seizure threshold.
|Source||J Appl Oral Sci (2018). Figure 5. H-89|
|Cell Lines||mDP cells|
|Incubation Time||6 h|
|Results||CaCl2-induced ERK1/2 phosphorylation was not inhibited in the presence H-89.|
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Related PKA Products|
CCG215022 is a G protein-coupled receptor kinases (GRKs) inhibitor with IC50 values of 0.15±0.07 μM, 0.38±0.06 μM and 3.9±1 μM for GRK2, GRK5 and GRK1, respectively.
|Bucladesine Sodium Salt
Bucladesine, a membrane permeable selective activator of PKA, has a critical role in up-regulation of ChAT and VAChT gene expression in PC12 cells by activation of extracellular signal regulated kinase (ERK) in Ca2+- and PKA-dependent manner.
H-89 dihydrochloride is a selective inhibitor of protein kinase A (PKA) with an IC50 value of 135 nM.
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