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- UMETSU Teruhiko
- Pharmacological Laboratory, Kaken Pharmaceutical Co., Ltd.
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- MURATA Takahiko
- Pharmacological Laboratory, Kaken Pharmaceutical Co., Ltd.
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- TANAKA Yoshie
- Pharmacological Laboratory, Kaken Pharmaceutical Co., Ltd.
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- OSADA Eizaburo
- Pharmacological Laboratory, Kaken Pharmaceutical Co., Ltd.
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- NISHIO Shintaro
- Basic Research Laboratories, Toray Industries, Inc.
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抄録
TR K 100, a stable PGI2 analogue structurally different from carbacyclines, was compared with other antiplatelet drugs for its effect on platelet functions using animal models. TRK-100 (10-300 nM) inhibited rat platelet aggregation induced by ADP (3 μM), collagen (12.5 μg/ml) and A23187 (10 μM), and its potency was about 1 /3-1 /7 that of PGI2. TRK-100 (0.3-3 mg/kg, p.o.) dose-dependently inhibited rabbit platelet adhesion (ED50: 2.2 mg/kg), and its effect lasted over at least 5 hr. In contrast, aspirin and ticlopidine (both at 300 mg/kg, p.o.) showed only a slight inhibition (4-7%). In the thrombocytopenia induced by collagen injection in rats, TRK-100 (3-300 μg/kg, i.v.; 0.1-3 mg/kg, p.o.) dose-dependently inhibited a decrease in platelet number, and its ED50 was 0.48-0.62 mg/kg orally and 13.7-16.4 μg/kg intravenously, while the inhibition by aspirin and ticlopidine (both at 1000 mg/kg, p.o.) was 40 and 37%, respectively. In the experimental thread thrombosis in rats, TRK-100 (0.03-3 mg/kg, p.o.) dose-dependently inhibited thrombus formation, and its ED50 was 0.46 mg/kg, being 21 and 87 times as potent as aspirin and ticlopidine, respectively. These results reveal that TRK-100 has a potent antiplatelet activity and is orally and intravenously effective for a variety of thrombosis models, suggesting that it may have a therapeutic value as an antithrombotic drug.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 43 (1), 81-90, 1987
公益社団法人 日本薬理学会
