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Fukushima-shi, Japan

Toa Eiyo Ltd. and Nitto Denko Corporation | Date: 2012-07-13

A packaging structure (

TOA Eiyo Ltd. | Date: 2011-05-24

Provided is a novel compound which shows an antagonistic effect against T-type calcium channels, and is useful as a pharmaceutical product. A compound represented by general formula (I), and a pharmaceutical agent containing the same, are disclosed: wherein n represents the number of nitrogen atoms contained in the 6-membered fused aromatic ring, and is 0, 1 or 2; p represents the number of nitrogen atoms contained in the 6-membered aromatic ring, and is 0 or 1; X represents an oxygen atom, SO

Toa Eiyo Ltd. | Date: 2013-04-15

Provided is a pharmaceutical agent containing a compound represented by General Formula (1), a pharmaceutically acceptable salt thereof, or a solvate thereof: wherein A represents a C

Chiba T.,Toho University | Chiba T.,TOA EIYO LTD | Kondo N.,TOA EIYO LTD | Takahara A.,Toho University
Journal of Pharmacological Sciences | Year: 2016

Electrical remodeling plays a pivotal role in maintaining the reentry during atrial fibrillation. In this study, we assessed influence of electrical remodeling on pharmacological manipulation of the atrial refractoriness in rabbits. We used an atrial electrical remodeling model of the rabbit, subjected to rapid atrial pacing (RAP; 600 beats/min) for 2-4 weeks, leading to shortening of atrial effective refractory period (AERP). Intravenous administration of dl-sotalol (6 mg/kg), bepridil (1 mg/kg), amiodarone (10 mg/kg) or vernakalant (3 mg/kg) significantly prolonged the AERP both in the control and RAP rabbits. The extents in the RAP rabbits were similar to those in the control animals. On the other hand, prolonging effects of intravenously administered ranolazine (10 mg/kg) or tertiapin-Q (0.03 mg/kg) on the AERP in the RAP rabbits were more potent than those in the control animals. These results suggest that rapid pacing-induced electrical remodeling effectively modified the prolonging effects of ranolazine and tertiapin-Q on the AERP in contrast to those of clinically available antiarrhythmic drugs, dl-sotalol, bepridil amiodarone and vernakalant. © 2016 Japanese Pharmacological Society. Source

Murakami A.,TOA EIYO LTD | Takasugi H.,TOA EIYO LTD | Ohnuma S.,TOA EIYO LTD | Koide Y.,TOA EIYO LTD | And 12 more authors.
Molecular Pharmacology | Year: 2010

Sphingosine 1-phosphate (S1P) induces diverse biological responses in various tissues by activating specific G protein-coupled receptors (S1P 1-S1P5 receptors). The biological signaling regulated by S1P3 receptor has not been fully elucidated because of the lack of an S1P3 receptor-specific antagonist or agonist. We developed a novel S1P3 receptor antagonist, 1-(4-chlorophenylhydrazono)-1-(4- chlorophenylamino)-3,3-dimethyl-2-butanone (TY-52156), and show here that the S1P-induced decrease in coronary flow (CF) is mediated by the S1P3 receptor. In functional studies, TY-52156 showed submicromolar potency and a high degree of selectivity for S1P3 receptor. TY-52156, but not an S1P1 receptor antagonist [(R)-phosphoric acid mono-[2-amino-2-(3- octyl-phenylcarbamoyl)-ethyl] ester; VPC23019] or S1P2 receptor antagonist [1-[1,3-dimethyl-4-(2-methylethyl)-1H-pyrazolo[3,4-b]pyridin-6-yl]-4- (3,5-dichloro-4-pyridinyl)-semicarbazide; JTE013], inhibited the decrease in CF induced by S1P in isolated perfused rat hearts. We further investigated the effect of TY-52156 on both the S1P-induced increase in intracellular calcium ([Ca2+]i) and Rho activation that are responsible for the contraction of human coronary artery smooth muscle cells. TY-52156 inhibited both the S1P-induced increase in [Ca2+]i and Rho activation. In contrast, VPC23019 and JTE013 inhibited only the increase in [Ca2+]i and Rho activation, respectively. We further confirmed that TY-52156 inhibited FTY-720-induced S1P3 receptor-mediated bradycardia in vivo. These results clearly show that TY-52156 is both sensitive and useful as an S1P3 receptor-specific antagonist and reveal that S1P induces vasoconstriction by directly activating S1P 3 receptor and through a subsequent increase in [Ca 2+]i and Rho activation in vascular smooth muscle cells. Copyright © 2010 The American Society for Pharmacology and Experimental Therapeutics. Source

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