Catalog number: 210538-75-3
Category: Main Product
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N-(1,2,3,4-tetrahydroisoquinolin-5-yl)methanesulfonamide; hydrochloride; N-(1,2,3,4-tetrahydroisoquinolin-5-yl)methanesulfonamidehydrochloride; 210538-75-3; T6496996; AC1Q3C61
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1.Involvement of tyrosine kinases on cyclooxygenase expression and prostaglandin E2 production in human gingival fibroblasts stimulated with interleukin-1beta and epidermal growth factor.
Yucel-Lindberg T1, Ahola H, Carlstedt-Duke J, Modéer T. Biochem Biophys Res Commun. 1999 Apr 13;257(2):528-32.
The purpose of the present study was to investigate the involvement of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and tyrosine kinase on prostaglandin E2 (PGE2) production in human gingival fibroblasts stimulated by interleukin-1beta (IL-1beta) and/or epidermal growth factor (EGF). The cytokine IL-1beta and to a lesser extent EGF, enhanced COX-2 mRNA levels in gingival fibroblasts. Simultaneous treatment with EGF and IL-1beta resulted in enhanced COX-2 mRNA levels accompanied by a synergistic stimulation of PGE2 biosynthesis compared to the cells treated with IL-1beta or EGF alone. Neither IL-1beta EGF nor the combination of IL-1beta and EGF enhanced COX-1 mRNA levels in gingival fibroblasts. The tyrosine kinase inhibitors, Herbimycin A and PD 153035 hydrochloride, reduced COX-2 mRNA levels as well as PGE2 production induced by IL-1beta or the combination of IL-1beta and EGF whereas COX-1 mRNA levels were not affected. Furthermore, the COX-2 specific inhibitor, NS-398, abolished the PGE2 production induced by IL-1beta, EGF, or the combination.
2.Electrophysiological characterization of BRL-32872 in canine Purkinje fiber and ventricular muscle. Effect on early after-depolarizations and repolarization dispersion.
Faivre JF1, Forest MC, Gout B, Bril A. Eur J Pharmacol. 1999 Oct 27;383(2):215-22.
Amongst the different pharmacological approaches to the treatment of cardiac arrhythmias, compounds with multiple electrophysiological activities appear to exhibit a reduced adverse effect profile. BRL-32872 (N-(3,4-dimethoxyphenyl)-N-[3[[2-(3,4-dimethoxyphenyl) ethyl] propyl]-4-nitrobenzamide hydrochloride) is a typical example of an antiarrhythmic agent with combined K(+) and Ca(2+) blocking actions. In this study, we investigated the effects of BRL-32872 on early after-depolarizations and on dispersion of repolarization. Action potentials were recorded either in canine cardiac Purkinje fibers alone or in preparations containing both ventricular muscle and the attached Purkinje fibers. In Purkinje fibers, BRL-32872 (0. 3-10 microM) induced a bell-shaped concentration-dependent increase in action potential duration. At 90% of repolarization, the action potential was prolonged at concentrations up to 1 microM and was shortened when the concentration of BRL-32872 was further increased.
3.Antiarrhythmic and electrophysiological effects of GYKI-16638, a novel N-(phenoxyalkyl)-N-phenylalkylamine, in rabbits.
Baczkó I1, El-Reyani NE, Farkas A, Virág L, Iost N, Leprán I, Mátyus P, Varró A, Papp JG. Eur J Pharmacol. 2000 Sep 15;404(1-2):181-90.
The effect of N-[4-[2-N-methyl-N-[1-methyl-2-(2, 6-dimethylphenoxy)ethylamino]-ethyl]-phenyl]-methanesulfonamide. hydrochloride (GYKI-16638; 0.03 and 0.1 mg/kg, i.v.), a novel antiarrhythmic compound, was assessed and compared to that of D-sotalol (1 and 3 mg/kg, i.v.) on arrhythmias induced by 10 min of coronary artery occlusion and 10 min of reperfusion in anaesthetized rabbits. Also, its cellular electrophysiological effects were studied in rabbit right ventricular papillary muscle preparations and in rabbit single isolated ventricular myocytes. In anaesthetized rabbits, intravenous administration of 0.03 and 0.1 mg/kg GYKI-16638 and 1 and 3 mg/kg D-sotalol significantly increased survival during reperfusion (GYKI-16638: 82% and 77%, D-sotalol: 75% and 83% vs. 18% in controls, P<0.05, respectively). GYKI-16638 (0.1 mg/kg) significantly increased the number of animals that did not develop arrhythmias during reperfusion (46% vs. 0% in controls, P<0.
4.In vivo antiarrhythmic and cardiac electrophysiologic effects of a novel diphenylphosphine oxide IKur blocker (2-isopropyl-5-methylcyclohexyl) diphenylphosphine oxide.
Stump GL1, Wallace AA, Regan CP, Lynch JJ Jr. J Pharmacol Exp Ther. 2005 Dec;315(3):1362-7. Epub 2005 Sep 12.
The antiarrhythmic efficacy of the novel ultrarapid delayed rectifier potassium current (IKur) blocker (2-isopropyl-5-methylcyclohexyl) diphenylphosphine oxide (DPO-1) was compared with efficacies of the standard class III rapidly activating component of delayed rectifier potassium current (IKr) blockers [+-N-[1'-(6-cyano-1,2,3,4-tetrahydro-2-napthalenyl)-3,4-dihydro-4-hydroxyspiro[2H-1-benzopyran-2,4'-piperidin]-6-yl] methanesulfonamide hydrochloride (MK499) and ibutilide and the class IC agent propafenone in a canine model of Y-shaped intracaval and right atrial free wall surgical lesions producing the substrate for reentrant atrial flutter. Electrocardiographic and cardiac electrophysiologic effects also were assessed at the effective antiarrhythmic doses of test agents. DPO-1 terminated atrial arrhythmia (six/six preparations; 5.5 +/- 2.0 mg/kg i.v.) while significantly increasing atrial relative and effective refractory periods (+15.
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