CSPC OUYI Pharmaceutical Co., Ltd.
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Founded in:
2001-03-29 -
Country:
China -
Address:
No. 88, Yangzi Road, Shijiazhuang Economic and Technological Development Zone -
Tax NO.:
91130100601289268L -
Registered Funds:
298 million yuan -
Website:
-
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Isosorbide 5-mononitrate |
It relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), and increases cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby dilating peripheral arteries and veins, reducing the amount of blood returning to the heart, lowering left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload), reducing peripheral vascular resistance, systolic arterial pressure and mean arterial pressure (afterload), and increasing coronary artery perfusion, ultimately reducing myocardial oxygen consumption and increasing oxygen supply.
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It relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), and increases cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby dilating peripheral arteries and veins, reducing the amount of blood returning to the heart, lowering left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload), reducing peripheral vascular resistance, systolic arterial pressure and mean arterial pressure (afterload), and increasing coronary artery perfusion, ultimately reducing myocardial oxygen consumption and increasing oxygen supply. |
16051-77-7 | 23 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| 1,4:3,6-dianhydro-D-sorbitol-5-mononitrate |
It relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), increases cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby dilating peripheral arteries and veins, reducing the amount of blood returning to the heart, lowering left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload), lowering peripheral vascular resistance, systolic arterial pressure and mean arterial pressure (afterload), dilating coronary arteries to increase coronary perfusion, and ultimately reducing myocardial oxygen consumption and increasing oxygen supply.
More
It relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), increases cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby dilating peripheral arteries and veins, reducing the amount of blood returning to the heart, lowering left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload), lowering peripheral vascular resistance, systolic arterial pressure and mean arterial pressure (afterload), dilating coronary arteries to increase coronary perfusion, and ultimately reducing myocardial oxygen consumption and increasing oxygen supply. |
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| Isosorbide 5-mononitrate |
Relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), increases cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby relaxing vascular smooth muscle, dilating peripheral arteries and veins, reducing myocardial oxygen consumption and increasing oxygen supply.
More
Relaxes vascular smooth muscle, activates guanylate cyclase by releasing nitric oxide (NO), increases cyclic guanosine monophosphate (cGMP) in smooth muscle cells, thereby relaxing vascular smooth muscle, dilating peripheral arteries and veins, reducing myocardial oxygen consumption and increasing oxygen supply. |
16051-77-7 | 23 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Dexamethasone sodium phosphate |
Adrenal cortex hormone drugs. It has anti-inflammatory, anti-allergic, anti-rheumatic and immunosuppressive effects. Its mechanism of action is as follows: 1. Anti-inflammatory effect: This product reduces and prevents tissue response to inflammation, thereby reducing the manifestations of inflammation. It can inhibit the accumulation of inflammatory cells, including macrophages and leukocytes, at the site of inflammation, and inhibit phagocytosis, the release of lysosomal enzymes, and the synthesis and release of inflammatory chemical mediators. 2. Immunosuppressive effect: including preventing or inhibiting cell-mediated immune responses, delayed allergic reactions, reducing the number of T lymphocytes, monocytes, and eosinophils, reducing the ability of immunoglobulins to bind to cell surface receptors, and inhibiting the synthesis and release of interleukins, thereby reducing the transformation of T lymphocytes into lymphoblasts.
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Adrenal cortex hormone drugs. It has anti-inflammatory, anti-allergic, anti-rheumatic and immunosuppressive effects. Its mechanism of action is as follows: 1. Anti-inflammatory effect: This product reduces and prevents tissue response to inflammation, thereby reducing the manifestations of inflammation. It can inhibit the accumulation of inflammatory cells, including macrophages and leukocytes, at the site of inflammation, and inhibit phagocytosis, the release of lysosomal enzymes, and the synthesis and release of inflammatory chemical mediators. 2. Immunosuppressive effect: including preventing or inhibiting cell-mediated immune responses, delayed allergic reactions, reducing the number of T lymphocytes, monocytes, and eosinophils, reducing the ability of immunoglobulins to bind to cell surface receptors, and inhibiting the synthesis and release of interleukins, thereby reducing the transformation of T lymphocytes into lymphoblasts. |
55203-24-2 | 25 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| (S)-Amlodipine |
Amlodipine is a calcium ion blocker that blocks calcium ions from entering myocardial and vascular smooth muscle cells across the membrane. Its antihypertensive mechanism is to directly relax vascular smooth muscle. The exact mechanism of relieving angina pectoris has not been fully confirmed, but it can dilate peripheral arterioles and coronary arteries, reduce total peripheral vascular resistance, and relieve coronary artery spasm. It reduces the afterload of the heart, reduces the heart's energy consumption and oxygen demand, and thus relieves angina pectoris.
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Amlodipine is a calcium ion blocker that blocks calcium ions from entering myocardial and vascular smooth muscle cells across the membrane. Its antihypertensive mechanism is to directly relax vascular smooth muscle. The exact mechanism of relieving angina pectoris has not been fully confirmed, but it can dilate peripheral arterioles and coronary arteries, reduce total peripheral vascular resistance, and relieve coronary artery spasm. It reduces the afterload of the heart, reduces the heart's energy consumption and oxygen demand, and thus relieves angina pectoris. |
103129-82-4 | 0 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Furosemide |
1. Effect on water and electrolyte excretion: It can increase the excretion of water, sodium, chloride, potassium, calcium, magnesium, phosphorus, etc., inhibit the active reabsorption of NaCl by the thick-walled segment of the renal tubular loop, reduce the osmotic pressure gradient difference of the medullary interstitial fluid, and reduce the reabsorption of Ca2+ and Mg2+. Short-term use can increase uric acid excretion, and long-term use can cause hyperuricemia. 2. Effect on hemodynamics: It inhibits the activity of prostaglandin degrading enzymes, dilates renal blood vessels and pulmonary capacitance veins, reduces the permeability of pulmonary capillaries, and helps in the treatment of acute left heart failure and adult respiratory distress syndrome.
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1. Effect on water and electrolyte excretion: It can increase the excretion of water, sodium, chloride, potassium, calcium, magnesium, phosphorus, etc., inhibit the active reabsorption of NaCl by the thick-walled segment of the renal tubular loop, reduce the osmotic pressure gradient difference of the medullary interstitial fluid, and reduce the reabsorption of Ca2+ and Mg2+. Short-term use can increase uric acid excretion, and long-term use can cause hyperuricemia. 2. Effect on hemodynamics: It inhibits the activity of prostaglandin degrading enzymes, dilates renal blood vessels and pulmonary capacitance veins, reduces the permeability of pulmonary capillaries, and helps in the treatment of acute left heart failure and adult respiratory distress syndrome. |
54-31-9 | 49 |