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 |
|---|---|---|---|---|
| Stugeron |
This product is a piperazine calcium channel antagonist that can block calcium influx into vascular smooth muscle, causing vasodilation and improving cerebral and coronary circulation, especially having a certain selective effect on cerebral blood vessels. This product can inhibit phosphodiesterase, prevent cAMP from decomposing into inactive 5'-AMP, thereby increasing the intracellular cAMP concentration, inhibiting the release of various biologically active substances such as histamine, 5-hydroxytryptamine, bradykinin, and also inhibiting the activation of complement C4.
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This product is a piperazine calcium channel antagonist that can block calcium influx into vascular smooth muscle, causing vasodilation and improving cerebral and coronary circulation, especially having a certain selective effect on cerebral blood vessels. This product can inhibit phosphodiesterase, prevent cAMP from decomposing into inactive 5'-AMP, thereby increasing the intracellular cAMP concentration, inhibiting the release of various biologically active substances such as histamine, 5-hydroxytryptamine, bradykinin, and also inhibiting the activation of complement C4. |
298-57-7 | 15 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Tofacitinib citrate |
Tofacitinib is a Janus kinase (JAK) inhibitor. JAK is an intracellular enzyme that transmits signals generated by cytokine or growth factor-receptor interactions on the cell membrane, thereby affecting the cell hematopoietic process and cellular immune function. Tofacitinib regulates the signal transduction pathway at the JAK point to prevent STAT phosphorylation and activation.
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Tofacitinib is a Janus kinase (JAK) inhibitor. JAK is an intracellular enzyme that transmits signals generated by cytokine or growth factor-receptor interactions on the cell membrane, thereby affecting the cell hematopoietic process and cellular immune function. Tofacitinib regulates the signal transduction pathway at the JAK point to prevent STAT phosphorylation and activation. |
540737-29-9 | 70 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| DIGOXIN |
1. Positive inotropic effect: selectively inhibits the activity of Na-K-ATPase in myocardial cell membrane, increases intracellular Ca2 concentration, and enhances myocardial contractility. 2. Negative frequency effect: improves hemodynamic state, reduces sympathetic nerve tension and enhances vagal nerve tension to slow heart rate; large doses may directly inhibit the function of the sinoatrial node and atrioventricular node. 3. Cardiac electrophysiological effect: reduces the autonomy of the sinoatrial node, increases the autonomy of Purkinje fibers, slows down the conduction velocity of the atrioventricular node, prolongs the effective refractory period, and can be used to slow down the ventricular rate of atrial fibrillation or flutter, but may accelerate the atrial rate or cause atrial flutter to turn into fibrillation.
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1. Positive inotropic effect: selectively inhibits the activity of Na-K-ATPase in myocardial cell membrane, increases intracellular Ca2 concentration, and enhances myocardial contractility. 2. Negative frequency effect: improves hemodynamic state, reduces sympathetic nerve tension and enhances vagal nerve tension to slow heart rate; large doses may directly inhibit the function of the sinoatrial node and atrioventricular node. 3. Cardiac electrophysiological effect: reduces the autonomy of the sinoatrial node, increases the autonomy of Purkinje fibers, slows down the conduction velocity of the atrioventricular node, prolongs the effective refractory period, and can be used to slow down the ventricular rate of atrial fibrillation or flutter, but may accelerate the atrial rate or cause atrial flutter to turn into fibrillation. |
0 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Clotrimazole |
Unspecified
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Unspecified |
0 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Josamycin |
A macrolide antibiotic produced by Streptomyces, with an antibacterial spectrum similar to that of erythromycin. Its antibacterial effect on Staphylococcus and Streptococcus is slightly worse than that of erythromycin, but it still has antibacterial activity against induced resistant strains; meningococci and Bordetella pertussis are sensitive to this product; it has good antibacterial effect on anaerobic bacteria such as Peptococcus, Peptostreptococcus, Propionibacterium and Eubacterium; intracellular pathogens such as Mycoplasma, Chlamydia and Legionella are also sensitive to this product. This product does not induce Staphylococcus to macrolide resistance, and is a non-inducible antibiotic.
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A macrolide antibiotic produced by Streptomyces, with an antibacterial spectrum similar to that of erythromycin. Its antibacterial effect on Staphylococcus and Streptococcus is slightly worse than that of erythromycin, but it still has antibacterial activity against induced resistant strains; meningococci and Bordetella pertussis are sensitive to this product; it has good antibacterial effect on anaerobic bacteria such as Peptococcus, Peptostreptococcus, Propionibacterium and Eubacterium; intracellular pathogens such as Mycoplasma, Chlamydia and Legionella are also sensitive to this product. This product does not induce Staphylococcus to macrolide resistance, and is a non-inducible antibiotic. |
16846-24-5 | 3 |