H-89 free base|CAS 127243-85-0|DC Chemicals

Cas No.:	127243-85-0
Chemical Name:	H89
Synonyms:	5-Isoquinolinesulfonamide,N-[2-[[3-(4-bromophenyl)-2-propen-1-yl]amino]ethyl]-;H-89 dihydrochloride;H 89 dihydrochloride;H-89;H89 diHCl;N-(2-((3-(4-Bromophenyl)allyl)amino)ethyl)isoquinoline-5-sulfonamide dihydrochloride;N-[2-(p-Bromocinnamylamino)ethyl]-5-Isoquinoline Sulfonamide;H 89;H 89 dihydrochloride,N-[2-[[3-(4-Bromophenyl)-2-propenyl]amino]ethyl]-5-isoquinolinesulfonamidedihydrochloride;Protein kinase inhibitor H-89;N-[2-[[3-(4-Bromophenyl)-2-propen-1-yl]amino]ethyl]-5-isoquinolinesulfonamide;H-89 hcl;H-89 ＆ H-89 2HCl;H-89 HYDROCHLORIDE;N-[2-[P-BROMOCINNAMYLAMINO]-ETHYL]-5-ISOQUINOLINESULFONMIDE;N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide;H-89 dihydrochloride,98%;H-89, Dihydrochloride Salt >99%;N-(2-(4-Bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide;N-[2-[[(E)-3-(4-bromophenyl)prop-2-enyl]amino]ethyl]isoquinoline-5-sulfonamide;N-(2-{[3-(4-bromophenyl)prop-2-en-1-yl]amino}ethyl)isoquinoline-5-sulfonamide;N-(2-{[(2E)-3-(4-bromophenyl)prop-2-en-1-yl]amino}ethyl)isoquinoline-5-sulfonamide;H89;M876330O56;5-Isoquinolinesulfonamide, N-(2-((3-(4-bromophenyl)-2-propenyl)amino)ethy
SMILES:	BrC1C([H])=C([H])C(=C([H])C=1[H])/C(/[H])=C(\[H])/C([H])([H])N([H])C([H])([H])C([H])([H])N([H])S(C1=C([H])C([H])=C([H])C2C([H])=NC([H])=C([H])C1=2)(=O)=O
Formula:	C₂₀H₂₀BrN₃O₂S
M.Wt:	446.3607
Purity:	98%
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Description:	H-89 is a potent 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.
Target:	IC50: 48 nM (protein kinase A)
In Vivo:	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[3].
In Vitro:	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[1]. 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[2].
Kinase Assay:	Kinase activities are assayed at 30°C for 2-5 min by measuring the transfer of 32P from [γ-32P]ATP to substrates. The reaction is terminated by adding 1 mL of 20% trichloroacetic acid, following the addition of 100 μg of bovine serum albumin as a carrier protein. The sample is centrifuged at 3000 rpm for 10 min, the pellet is resuspended in 5% trichloroacetic acid solution, the final pellet is dissolved in 1 mL of 1 N NaOH and the radioactivity is measured in a liquid scintillation counter.
Cell Assay:	After 48 h in culture, PCl2D cells are cultured in test medium containing 30 μM H-89 for 1 h and then exposed to fresh medium that contained both 10 μM forskolin and 30 μM H-89. Cells are scraped off with a rubber policeman and sonicated in the presence of 0.5 mL of 6% trichloroacetic acid. To extract trichloroacetic acid, 2 mL of petroleum ether is added, the preparation mixed and centrifuged at 3000 rpm for 10 min. After aspiration of the upper layer, the residue sample solution is used for determination.
Animal Administration:	Male albino mice weighing 20-25 g are obtained. Pentoxifylline (25, 50, 100 mg/kg), bucladesine (50, 100, 300 nM/mouse) and H-89 (0.05, 0.1, 0.2 mg/100 g) are administered intraperitoneally (i.p.) 30 min before intravenous (i.v.) infusion of PTZ. In combination groups, the first and second components are injected 45 and 30 min before PTZ infusion. In all groups, the respective control animalsreceive an appropriate volume of vehicle. For the i.v. infusion, the needle is inserted into the lateral tail vein, fixed to the tail vein by a narrow piece of adhesive tape, and the animal is allowed to move freely. PTZ solution is infused at a concentration rate of 1 mL/min.
References:	[1]. Chijiwa T, et al. Inhibition of forskolin-induced neurite outgrowth and protein phosphorylation by a newly synthesized selective inhibitor of cyclic AMP-dependent protein kinase, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), of PC12D [2]. Blazev R, et al. Effects of the PKA inhibitor H-89 on excitation-contraction coupling in skinned and intact skeletal muscle fibres. J Muscle Res Cell Motil. 2001;22(3):277-86. [3]. Hosseini-Zare MS, et al. Effects of pentoxifylline and H-89 on epileptogenic activity of bucladesine in pentylenetetrazol-treated mice. Eur J Pharmacol. 2011 Nov 30;670(2-3):464-70.

Cat. No.	Product name	Field of application
DC31079	Abarelix	Abarelix is a synthetic decapeptide and antagonist of naturally occurring gonadotropin-releasing hormone (GnRH). Abarelix directly and competitively binds to and blocks the gonadotropin releasing hormone receptor in the anterior pituitary gland, thereby inhibiting the secretion and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone. As a result, this may relieve symptoms associated with prostate hypertrophy or prostate cancer, since testosterone is required to sustain prostate growth.
DC31074	Isopropyl myristate	Isopropyl myristate is the ester of isopropyl alcohol and myristic acid.
DC79856	EVT0185	EVT0185 is an orally active ATP citrate lyase (ACLY) inhibitor. EVT0185 is converted to a CoA thioester in the liver by SLC27A2 and interacts with the CoA-binding site of ACLY. EVT0185-CoA inhibits ACLY activity with an IC50 of 2.5 μM. EVT0185 can phenocopy the immune and antitumour effects of genetic ACLY deletion. EVT0185 can increase tumour-infiltrating B cells and chemokine CXCL13 levels. EVT0185 can be used for the research of cancer, such as hepatocellular carcinoma (HCC).
DC79609	NCGC00685960	NCGC00685960 is a Nicotinamide N-methyltransferase (NNMT) inhibitor with an IC50 < 10  nM. NCGC00685960 has potent antitumor activity. NCGC00685960 increases H3K27 trimethylation levels in ovarian cancer cells and inhibits α-SMA expression in NNMT-expressing ovarian fibroblasts. NCGC00685960 reduces 1-MNA levels, reverses SAM and H3K27 hypomethylation and significantly impairs collagen contractility in cancer-associated fibroblasts (CAFs). NCGC00685960 can be used for cancers research.
DC79112	Simepdekinra	Simepdekinra (Compound 221) is a IL-17A modulator with IC50s ≤10  nM and 10-100 nM for IL-17A/A HEK-Blue and IL-17A/F HEK-Blue cells. Simepdekinra can be used for inflammatory diseases such as psoriasis, ankylosing spondylitis and psoriatic arthritis research.
DC78751	RSL3-NH2	RSL3-NH2 is a GPX4 inhibitor and Ferroptosis inducer. RSL3-NH2 can be used as a cytotoxic payload for synthesis of antibody-drug conjugates (ADCs).
DC77831	Vicadrostat	Vicadrostat (compound 29 A) is a potent and selective inhibitor of aldosterone synthase(CYP11B2) with an IC50 of 16 nM. It exhibits potential in renal disease, diabetic nephropathy, cardiovascular diseases and fibrotic disorder research.
DC77813	Zeltociclib	Zeltociclib is a cyclin-dependent kinase inhibitor with antitumor effects.
DC77784	UNC10013	UNC10013 is a SETDB1 allosteric modulator that forms a covalent bond with Cys385 in the 3TD domain, exhibiting negative allosteric regulatory activity. It has a kinact/KI value of 1.0 × 106 M-1*s-1. UNC10013 effectively disrupts SETDB1-mediated Akt methylation and holds potential value for research in cancer and neurodegenerative diseases.
DC77740	T0080	T0080 is a FPR-1 antagonist. T0080 reduces the cell apoptosis, inhibits ROS production and pro-inflammatory cytokines (TNF-α and IL-1β) from plaque macrophages, which attenuates atherosclerotic progression in ApoE−/− mice.