H-9 dihydrochloride - CAS 116700-36-8
Category: Inhibitor
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Molecular Weight:
H-9 dihydrochloride is a protein kinase inhibitor. It inhibits PKA (Ki = 1.9 μM), PKG (Ki = 0.9 μM), CaMK II (Ki = 60 μM), PKC (Ki = 18 μM), casein kinase I (Ki = 110 μ M) and casein kinase II (Ki > 300 μM). H-9 hydrochloride reduces the cAMP-mediated excitatory response to serotonin in C. elegans enteric neurons2 and inhibits PKA-mediated phosphorylation in a rat seizure model.
Brife Description:
protein kinase inhibitor
≥99% by HPLC
Related CAS:
84468-17-7 (free base)
N-(2-Aminoethyl)-5-isoquinolinesulfonamide dihydrochloride
Canonical SMILES:
1.Delay of iris flower senescence by cytokinins and jasmonates.
van Doorn WG;Çelikel FG;Pak C;Harkema H Physiol Plant. 2013 May;148(1):105-20. doi: 10.1111/j.1399-3054.2012.01690.x. Epub 2012 Oct 9.
It is not known whether tepal senescence in Iris flowers is regulated by hormones. We applied hormones and hormone inhibitors to cut flowers and isolated tepals of Iris × hollandica cv. Blue Magic. Treatments with ethylene or ethylene antagonists indicated lack of ethylene involvement. Auxins or auxin inhibitors also did not change the time to senescence. Abscisic acid (ABA) hastened senescence, but an inhibitor of ABA synthesis (norflurazon) had no effect. Gibberellic acid (GA3 ) slightly delayed senescence in some experiments, but in other experiments it was without effect, and gibberellin inhibitors [ancymidol or 4-hydroxy-5-isopropyl-2-methylphenyltrimethyl ammonium chloride-1-piperidine carboxylate (AMO-1618)] were ineffective as well. Salicylic acid (SA) also had no effect. Ethylene, auxins, GA3 and SA affected flower opening, therefore did reach the flower cells. Jasmonates delayed senescence by about 2.0 days. Similarly, cytokinins delayed senescence by about 1.5-2.0 days. Antagonists of the phosphatidylinositol signal transduction pathway (lithium), calcium channels (niguldipine and verapamil), calmodulin action [fluphenazine, trifluoroperazine, phenoxybenzamide and N-(6-aminohexyl)-5-chloro-1-naphtalenesulfonamide hydrochloride (W-7)] or protein kinase activity [1-(5-isoquinolinesulfonyl)-2-methylpiperazine hydrochloride (H-7), N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide hydrochloride (H-8) and N-(2-aminoethyl)-5-isoquinolinesulfonamide dihydrochloride (H-9)] had no effect on senescence, indicating no role of a few common signal transduction pathways relating to hormone effects on senescence.
2.Evidence for a role for cyclic AMP in modulating the action of 5-HT and an excitatory neuropeptide, FLP17A, in the pharyngeal muscle of Caenorhabditis elegans.
Papaioannou S;Holden-Dye L;Walker RJ Invert Neurosci. 2008 Jun;8(2):91-100. doi: 10.1007/s10158-008-0072-8. Epub 2008 May 8.
The feeding activity of the nematode Caenorhabditis elegans is regulated by an anatomically well-defined network of 20 enteric neurones that employs small molecule and neuropeptidergic signalling. Two of the most potent excitatory agents are 5-HT and the neuropeptide FLP17A. Here we have examined the role of cAMP in modulating their excitatory actions by pharmacological manipulation of the level of cAMP. Application of the membrane permeable cAMP analogue, dibutyryl-cAMP (1 microM), enhanced the excitatory response to both FLP17A and 5-HT. Furthermore, the adenylyl cyclase activator, forskolin (50 nM), significantly enhanced the excitatory response to both FLP17A and 5-HT. The phosphodiesterase inhibitor, ibudilast (10 microM), enhanced the excitatory response to FLP17A. The protein kinase inhibitor, H-9 dihydrochloride (10 microM) significantly reduced the excitatory response to 5-HT. H-9 dihydrochloride also had a direct effect on pharyngeal activity. The effect of FLP17A and 5-HT on two mutants, egl-8 (loss-of-function phospholipase-Cbeta) and egl-30 (loss-of-function Galphaq) was also investigated. Both these mutants have a lower pharyngeal pumping rate than wild-type which has to be considered when interpreting the effects of these mutations on the excitatory responses to FLP17A and 5HT.
3.Protein kinase activity, growth and differentiation of murine erythroleukemia cells.
Flickinger RA Cancer Lett. 1988 Feb;39(1):113-7.
The addition of type 2 cAMP-dependent protein kinase stimulates division of cultured Friend erythroleukemia cells. A synthetic peptide representing the inhibitory portion of the heat stable protein kinase inhibitor protein and an inhibitor of cAMP-dependent protein kinase (N-(2-aminoethyl)-5-isoquinolinesulfonamide dihydrochloride or H-9) inhibited cell division. The latter inhibitor (H-9) induced differentiation of the cells.
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CAS 116700-36-8 H-9 dihydrochloride

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