H-89 is a selective and potent protein kinase A inhibitor (IC50: 48 nM), a candidate cardioprotectant, induces spatial learning impairment in rats, and can be used to study myocardial infarction.

protein kinase A:48 nM

Pretreatment of PC12D cells with H-89 (30 μM) significantly inhibited cAMP-dependent histone IIb phosphorylation activity in cell lysates, but did not affect other protein phosphorylation activities [1]; in rat skin EDL fibers , H-89 (10 μM) only slightly inhibited the force response to depolarization; H-89 (1-2 μM) significantly slowed the re-excitation rate in rat skin EDL fibers, most likely because of its Deleteriously affects the T system potential; H-89 (10-100 μM) also inhibits the net uptake of Ca2+ by SR. [2]

b>METHODS: H-89 (0.05, 0.1, 0.2 mg/100 g, intraperitoneal injection) was used 30 minutes before the infusion of pentylene tetrazolium (PTZ) in mice to study the effect of H-89 on Bucladesine-induced epileptic activity in PTZ-treated mice.
RESULTS: H-89 (0.2 mg/100 g) significantly increased the seizure latency and threshold of PTZ-treated animals; H-89 (0.05, 0.2 mg/100 g) blocked the epileptogenic activity of Bucladesine and significantly increased the seizure latency and seizure threshold. [3]