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Founded in:
1995-09-13 -
Country:
China -
Address:
The First Pharmaceutical Park, Datong Economic and Technological Development Zone, Shanxi Province -
Tax NO.:
91140200602167297K -
Registered Funds:
138.8 million yuan -
Website:
-
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Sodium ferulic |
This product is a non-peptide endothelin receptor antagonist, which can antagonize endothelin-induced vasoconstriction, blood pressure increase and vascular smooth muscle cell proliferation, reduce vascular endothelial damage; increase NO synthesis, relax vascular smooth muscle; inhibit platelet aggregation, anti-coagulation, and improve blood rheology characteristics. This product can also inhibit cholesterol synthesis, lower blood lipids, scavenge free radicals, prevent lipid peroxidation damage; affect complement, enhance immune function, and have certain analgesic and antispasmodic effects.
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This product is a non-peptide endothelin receptor antagonist, which can antagonize endothelin-induced vasoconstriction, blood pressure increase and vascular smooth muscle cell proliferation, reduce vascular endothelial damage; increase NO synthesis, relax vascular smooth muscle; inhibit platelet aggregation, anti-coagulation, and improve blood rheology characteristics. This product can also inhibit cholesterol synthesis, lower blood lipids, scavenge free radicals, prevent lipid peroxidation damage; affect complement, enhance immune function, and have certain analgesic and antispasmodic effects. |
24276-84-4 | 8 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Propyl gallate |
1. It can obviously inhibit the synthesis of thromboxane A2 (TXA2), counteract the platelet aggregation caused by arachidonic acid (AA), and has a stronger and faster antiplatelet aggregation effect than aspirin (ASP). 2. It can enhance the fibrinolytic activity and promote the dissolution of thrombus. 3. It can reduce the specific viscosity of whole blood and plasma, and accelerate the electrophoresis of red blood cells. 4. It can relax the vascular smooth muscle, dilate the artery, and increase the blood flow of the coronary artery and cerebral artery. 5. It can improve the ability to resist hypoxia. 6. It can strongly scavenge free radicals. 7. It can inhibit the inflammatory exudation of capillaries.
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1. It can obviously inhibit the synthesis of thromboxane A2 (TXA2), counteract the platelet aggregation caused by arachidonic acid (AA), and has a stronger and faster antiplatelet aggregation effect than aspirin (ASP). 2. It can enhance the fibrinolytic activity and promote the dissolution of thrombus. 3. It can reduce the specific viscosity of whole blood and plasma, and accelerate the electrophoresis of red blood cells. 4. It can relax the vascular smooth muscle, dilate the artery, and increase the blood flow of the coronary artery and cerebral artery. 5. It can improve the ability to resist hypoxia. 6. It can strongly scavenge free radicals. 7. It can inhibit the inflammatory exudation of capillaries. |
121-79-9 | 10 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Isosorbide dinitrate |
Directly relaxes smooth muscle, especially vascular smooth muscle; the dilation effect on post-capillary veins is more persistent than that on arteries. It has no obvious direct effect on the myocardium. Due to the dilation of capacitance vessels, the venous return to the heart is reduced, reducing the preload of the heart. At the same time, the peripheral resistance vessels expand, blood pressure drops, the left ventricular ejection resistance is reduced, and the afterload of the heart is reduced. The reduction of the preload and afterload of the heart reduces the oxygen consumption of the myocardium.
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Directly relaxes smooth muscle, especially vascular smooth muscle; the dilation effect on post-capillary veins is more persistent than that on arteries. It has no obvious direct effect on the myocardium. Due to the dilation of capacitance vessels, the venous return to the heart is reduced, reducing the preload of the heart. At the same time, the peripheral resistance vessels expand, blood pressure drops, the left ventricular ejection resistance is reduced, and the afterload of the heart is reduced. The reduction of the preload and afterload of the heart reduces the oxygen consumption of the myocardium. |
87-33-2 | 23 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Isosorbide dinitrate |
Directly relaxes smooth muscle, especially vascular smooth muscle; the dilation effect on post-capillary veins is more persistent than that on arterioles. No significant direct effect on the myocardium. Reduces myocardial oxygen consumption by reducing the preload and postload of the heart.
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Directly relaxes smooth muscle, especially vascular smooth muscle; the dilation effect on post-capillary veins is more persistent than that on arterioles. No significant direct effect on the myocardium. Reduces myocardial oxygen consumption by reducing the preload and postload of the heart. |
87-33-2 | 23 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Naloxone hydrochloride |
This product is an opioid receptor antagonist, which has almost no pharmacological activity itself, but can competitively antagonize various opioid receptors and has a strong affinity for m receptors. It can completely or partially correct the central inhibitory effects of opioid substances, such as respiratory depression, sedation and hypotension; it has a wake-up effect on animals with acute ethanol poisoning; it is a pure opioid receptor antagonist and does not cause respiratory depression, psychotomimetic reactions or miotic reactions; there is no drug resistance, nor physiological or mental dependence.
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This product is an opioid receptor antagonist, which has almost no pharmacological activity itself, but can competitively antagonize various opioid receptors and has a strong affinity for m receptors. It can completely or partially correct the central inhibitory effects of opioid substances, such as respiratory depression, sedation and hypotension; it has a wake-up effect on animals with acute ethanol poisoning; it is a pure opioid receptor antagonist and does not cause respiratory depression, psychotomimetic reactions or miotic reactions; there is no drug resistance, nor physiological or mental dependence. |
357-08-4 | 32 |