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.
Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)
|Body Surface Area (m2)
|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.
Customer Product Validations & Biological Datas
||J Appl Oral Sci (2018). Figure 5. H-89
||CaCl2-induced ERK1/2 phosphorylation was not inhibited in the presence H-89.