Molecular Formula | C13H12N2O2 |
Molar Mass | 228.25 |
Density | 1.17±0.1 g/cm3(Predicted) |
Melting Point | 223-224° |
Boling Point | 468.0±25.0 °C(Predicted) |
Flash Point | 236.8°C |
Solubility | Soluble in DMSO (10 mg/ml), DMF (5 mg/ml), 1:1 DMSO:PBS(pH 7.2) (~1 mg/ml), and ethano |
Vapor Presure | 1.47E-09mmHg at 25°C |
Appearance | Solid |
pKa | 4.43±0.10(Predicted) |
Storage Condition | Sealed in dry,Room Temperature |
Refractive Index | 1.593 |
Physical and Chemical Properties | Prismatic crystals from ethanol-diethyl ether, melting point 223-224 °c. Ozagrel Hydrochloride: C13H12N2O2? HCl. [78712-43-3]. Crystallized from ethanol-diethyl ether, melting point 214-217 °c. Ozagrel Sodium: C13 H11N2NaO2. White Crystal or crystalline powder, odorless, sour bitter. Soluble in water, soluble in methanol, a few insoluble in ethanol, acetone or ether. Acute toxicity LD50 male and female mice, male and female rats (mg/kg):1940,1580,1150,1300 intravenous injection; 5700, 2450 oral; 2100,2300,2250 subcutaneous injection. |
Use | A potent and selective thromboxane A2 inhibitor. |
In vivo study | In guinea pigs, Ozagrel prevents oleic acid (OA)-induced thromboxane A(2) production in bronchoalveolar lavage fluid and subsequent increases in total protein concentration, macrophages and neutrophil numbers, and increased expression of monocyte chemoattractant protein -1 and interleukin-8 mRNA throughout the lung. In rats, Ozagrel (3 mg/kg) reduced cortical infarct size and volume after middle cerebral artery ischemia-reperfusion. Ozagrel also had an inhibitory effect on neurological deficits in a rat model of microthrombosis. In a conscious cerebral ischemia-reperfusion mouse model, Ozagrel ameliorates reduced spontaneous motor activity and impairment of motor coordination. In the conscious cerebral ischemia-reperfusion SHR model, Ozagrel inhibited the decrease of brain tissue density induced by occlusion-reperfusion, and after middle cerebral artery occlusion-reperfusion in cats in vivo, restores the post-ischemic reduction of cortical PO(2). In a conscious mouse model of cerebral ischemia-reperfusion, Ozagrel also increases 6-keto-PGF(1Alpha), a prostaglandin I(2), in brain tissue after cerebral ischemia-reperfusion (PGI(2)) metabolite levels, and PGI(2) administration improves reduced spontaneous locomotor activity. In guinea pigs, intravenous administration of Ozagrel 30 minutes before oleic acid injection prevents the decrease of Pao(2) and pulmonary vascular hyperpermeability. In guinea pig bronchoalveolar lavage fluid, Ozagrel also prevents lactate dehydrogenase (a measure of lung cell injury) activity, TXB(2) and its effect on 6-keto prostaglandin F(1Alpha) increase in weight ratio. |
from ethanol ether prismatic crystals, melting point 223~224 deg C.
developed by Nishi Mino Pharmaceutical Industry Co., Ltd., was first launched in Japan in April 1988. Potent thromboxane synthase inhibitors. By inhibiting thromboxane synthase, lowering thromboxane A2(TXA2) in vivo, and promoting the production of prostacyclin (PGI2), to fight against the aggregation of platelets and spasm of cerebral vessels, however, it had little effect on other arachidonic acid metabolizing enzymes such as cyclooxygenase. For the improvement of vasospasm after subarachnoid hemorrhage surgery and its complicated cerebral ischemia symptoms.
male and female mice, male and female rats LD50 (mg/kg): 1940, 1580, 1150, 1300 intravenous injection; 3800, 3600, 5900, 5700 oral; 2450, 2250, 0.