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Founded in:
1993-10-26 -
Country:
China -
Address:
No. 2 Huangshan Road, New District, Wuxi -
Tax NO.:
91320214607915071G -
Registered Funds:
$191.2 million -
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| TERBUTALINE SULFATE |
It can selectively stimulate b2-receptors, relax bronchial smooth muscles, inhibit the release of endogenous spasm-inducing substances and edema caused by endogenous mediators, improve the clearance ability of bronchial mucosal ciliary epithelium, and relax uterine smooth muscles.
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It can selectively stimulate b2-receptors, relax bronchial smooth muscles, inhibit the release of endogenous spasm-inducing substances and edema caused by endogenous mediators, improve the clearance ability of bronchial mucosal ciliary epithelium, and relax uterine smooth muscles. |
23031-32-5 | 32 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| TICAGRELOR |
Ticagrelor is a cyclopentatriazole pyrimidine (CPTP) compound. Ticagrelor and its major metabolites can reversibly interact with platelet P2Y12ADP receptors, blocking signal transduction and platelet activation. Ticagrelor and its active metabolites have comparable activity.
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Ticagrelor is a cyclopentatriazole pyrimidine (CPTP) compound. Ticagrelor and its major metabolites can reversibly interact with platelet P2Y12ADP receptors, blocking signal transduction and platelet activation. Ticagrelor and its active metabolites have comparable activity. |
274693-27-5 | 92 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Felodipine |
Dihydropyridine calcium channel antagonists (calcium channel blockers) compete reversibly with nitrendipine and/or other calcium channel blockers for dihydropyridine binding sites, blocking voltage-dependent Ca2 currents in vascular smooth muscle and cultured rabbit atrial cells, and blocking K-induced rat portal vein contracture. In vitro studies have shown that this product has a stronger selective inhibitory effect on vascular smooth muscle than on myocardium; negative inotropic effects can be detected in vitro, but this effect has not been observed in whole animals.
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Dihydropyridine calcium channel antagonists (calcium channel blockers) compete reversibly with nitrendipine and/or other calcium channel blockers for dihydropyridine binding sites, blocking voltage-dependent Ca2 currents in vascular smooth muscle and cultured rabbit atrial cells, and blocking K-induced rat portal vein contracture. In vitro studies have shown that this product has a stronger selective inhibitory effect on vascular smooth muscle than on myocardium; negative inotropic effects can be detected in vitro, but this effect has not been observed in whole animals. |
86189-69-7 | 30 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Felodipine |
This product is a dihydropyridine calcium channel blocker that can block voltage-dependent Ca2 currents in vascular smooth muscle and cultured rabbit atrial cells, and block K-induced rat portal vein contracture. In vitro studies have shown that felodipine has a more selective inhibitory effect on vascular smooth muscle than on myocardium; no negative inotropic effect was observed in whole animals. Felodipine can reduce peripheral vascular resistance and lead to lower blood pressure. This pharmacological effect is dose-related and is accompanied by a reflex increase in heart rate. Long-term administration may cause an increase in heart rate of 5 to 10 beats per minute. Felodipine exerts anti-anginal and anti-ischemic effects by improving myocardial oxygen supply, reducing coronary vascular resistance, increasing coronary blood flow and myocardial oxygen supply, relieving coronary spasm, and reducing left ventricular afterload and myocardial oxygen demand. In addition, felodipine also has natriuretic and diuretic effects, reduces renal vascular resistance, does not affect glomerular filtration rate, improves early graft function, and is suitable for the treatment of stable exertional angina and vasospastic angina.
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This product is a dihydropyridine calcium channel blocker that can block voltage-dependent Ca2 currents in vascular smooth muscle and cultured rabbit atrial cells, and block K-induced rat portal vein contracture. In vitro studies have shown that felodipine has a more selective inhibitory effect on vascular smooth muscle than on myocardium; no negative inotropic effect was observed in whole animals. Felodipine can reduce peripheral vascular resistance and lead to lower blood pressure. This pharmacological effect is dose-related and is accompanied by a reflex increase in heart rate. Long-term administration may cause an increase in heart rate of 5 to 10 beats per minute. Felodipine exerts anti-anginal and anti-ischemic effects by improving myocardial oxygen supply, reducing coronary vascular resistance, increasing coronary blood flow and myocardial oxygen supply, relieving coronary spasm, and reducing left ventricular afterload and myocardial oxygen demand. In addition, felodipine also has natriuretic and diuretic effects, reduces renal vascular resistance, does not affect glomerular filtration rate, improves early graft function, and is suitable for the treatment of stable exertional angina and vasospastic angina. |
86189-69-7 | 30 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| 2,6-Dimethyl-4-(2,3-dichlorophenyl)-1,4-dihydro-3,5-pyridinedicarboxylic acid methyl ethyl ester |
This product is a dihydropyridine calcium channel antagonist (calcium channel blocker), which acts by reversibly competing for dihydropyridine binding sites, blocking the voltage-dependent Ca2 current of vascular smooth muscle and cultured rabbit atrial cells, and blocking K-induced rat portal vein contracture.
More
This product is a dihydropyridine calcium channel antagonist (calcium channel blocker), which acts by reversibly competing for dihydropyridine binding sites, blocking the voltage-dependent Ca2 current of vascular smooth muscle and cultured rabbit atrial cells, and blocking K-induced rat portal vein contracture. |
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