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(Synonyms: 库美香豆素; Dicumoxane; Ph 137) 目录号 : GC33781

Coumetarol (Dicumoxane) (Dicumoxane) 是一种维生素 K 拮抗剂。

Coumetarol (Dicumoxane) Chemical Structure

Cas No.:4366-18-1

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Sample solution is provided at 25 µL, 10mM.

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产品描述

Coumetarol (Dicumoxane) is a vitamin K antagonist.

Coumetarol (Dicumoxane), an oral anticoagulant, is active in both models. The vitamin K antagonist Coumetarol is effective in both models after oral treatment but inhibits the thrombus formation more strongly in the arterio-venous shunt model. Treatment with the vitamin K antagonist Coumetarol in a dose of 25 mg/kg p.o. twice daily for 2 days results in a significant reduction in thrombus weight by 50% in the venous stasis model and by 75% in the arterio-venous shunt model. In both experiments the coagulation time as measured by the Thrombotest is prolonged to the same extent[1].

[1]. Vogel GM, et al. Comparison of two experimental thrombosis models in rats effects of four glycosaminoglycans. Thromb Res. 1989 Jun 1;54(5):399-410.

Chemical Properties

Cas No. 4366-18-1 SDF
别名 库美香豆素; Dicumoxane; Ph 137
Canonical SMILES COCC(C1=C(O)C2=CC=CC=C2OC1=O)C3=C(O)C4=CC=CC=C4OC3=O
分子式 C21H16O7 分子量 380.35
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.6292 mL 13.1458 mL 26.2916 mL
5 mM 0.5258 mL 2.6292 mL 5.2583 mL
10 mM 0.2629 mL 1.3146 mL 2.6292 mL
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Research Update

Comparison of two experimental thrombosis models in rats effects of four glycosaminoglycans

Thromb Res 1989 Jun 1;54(5):399-410.PMID:2549654DOI:10.1016/0049-3848(89)90210-7

Two experimental thrombosis models in rats have been compared with regard to the composition of the formed thrombi and the effects of various treatments on thrombus formation. In the first model thrombosis is induced in the vena cava by a combination of venous stasis and hypercoagulability; these thrombi consist merely of red cells and fibrin with only a few platelets. In the second model thrombosis is induced in an arterio-venous shunt in which the formed thrombi consist of red cells, fibrin and a large amount of platelet aggregates adhering to the foreign material. Antiplatelet serum and acetylsalicylic acid, which reduce blood platelet activity, inhibited thrombus formation only in the arteriovenous shunt model. Dicumoxane, an oral anticoagulant, was active in both models. The glycosaminoglycans heparin, Org 10172, Fragmin and the pentasaccharide, representing the AT-III binding sequence of heparin, were active in both models. However, there were qualitative and quantitative differences between the effects of the glycosaminoglycans suggesting differences in their modes of action.