H-89

Research use only, not for human use.

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.

H-89 is a potent and selective 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.

H-89 inhibits protein kinase A, in competitive fashion against ATP. H-89 causes a dose-dependent inhibition of the forskolin-induced protein phosphorylation, with no decrease in intracellular cyclic AMP levels in PC12D cells. H-89 significantly inhibits the forskolin-induced neurite outgrowth from PC12D cells. H-89 (30 μM) inhibits significantly cAMP-dependent histone IIb phosphorylation activity in PC12D cell lysates. H-89 (1-2 μM) significantly slows the repriming rate in rat skinned fibres, most likely due to it deleteriously affecting the T-system potential. H-89 (10-100 μM) inhibits net Ca2+ uptake by the SR and affectes the Ca32-sensitivity of the contractile apparatus in rat skinned fibres.

H-89 (0.2 mg/100g, i.p.) significantly increases seizure latency and threshold in PTZ-treated animals. H-89 (0.05, 0.2 mg/100 g, i.p.) prevents the epileptogenic activity of bucladesine (300 nM) with significant increase of seizure latency and seizure threshold.

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Apoptosis

PKA

PKA

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127243-85-0

446.36

C20H20BrN3O2S

>98% (HPLC)

In Vitro:?DMSO : 100 mg/mL (224.03 mM; Ultrasonic )

O=S(=O)(NCCNCC=CC1=CC=C(Br)C=C1)C2=CC=CC=3C=NC=CC32

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(-20℃)

With Ice Pack

≥ 2 years