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Founded in:
2003-09-02 -
Country:
China -
Address:
No. 1, Kangle Street, Qi County, Jinzhong City, Shanxi Province -
Tax NO.:
911407277540502901 -
Registered Funds:
22.5 million yuan -
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Vitamin B12 |
It is converted into methylcobalt ammonium and coenzyme B12 in the body to become active. Methylcobalt ammonium participates in folic acid metabolism. When it is deficient, it hinders the recycling of tetrahydrofolate, thereby hindering the synthesis of thymidine deoxynucleotides, blocking DNA synthesis, and stagnating the maturation and division of blood cells, leading to megaloblastic anemia. Coenzyme B12 promotes the conversion of methylmalonyl coenzyme A, an intermediate product of fat metabolism, into succinyl coenzyme A to participate in the tricarboxylic acid cycle. When it is deficient in the human body, it causes increased excretion of methylmalonic acid and abnormal fatty acid metabolism, and at the same time affects the synthesis of nerve myelin lipids and the maintenance of the normal function of sheathed nerve fibers, resulting in clinical symptoms of nerve damage.
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It is converted into methylcobalt ammonium and coenzyme B12 in the body to become active. Methylcobalt ammonium participates in folic acid metabolism. When it is deficient, it hinders the recycling of tetrahydrofolate, thereby hindering the synthesis of thymidine deoxynucleotides, blocking DNA synthesis, and stagnating the maturation and division of blood cells, leading to megaloblastic anemia. Coenzyme B12 promotes the conversion of methylmalonyl coenzyme A, an intermediate product of fat metabolism, into succinyl coenzyme A to participate in the tricarboxylic acid cycle. When it is deficient in the human body, it causes increased excretion of methylmalonic acid and abnormal fatty acid metabolism, and at the same time affects the synthesis of nerve myelin lipids and the maintenance of the normal function of sheathed nerve fibers, resulting in clinical symptoms of nerve damage. |
68-19-9 | 16 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Gentamicin sulfate |
Aminoglycoside antibiotics have good antibacterial effects on Gram-negative and Gram-positive bacteria. Their mechanism of action is to bind to the 30S subunit of bacterial ribosomes and inhibit bacterial protein synthesis. In recent years, the number of Gram-negative bacteria resistant to gentamicin has increased significantly.
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Aminoglycoside antibiotics have good antibacterial effects on Gram-negative and Gram-positive bacteria. Their mechanism of action is to bind to the 30S subunit of bacterial ribosomes and inhibit bacterial protein synthesis. In recent years, the number of Gram-negative bacteria resistant to gentamicin has increased significantly. |
1405-41-0 | 29 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Sodium bicarbonate |
1. Treat metabolic acidosis. This product increases the concentration of carbonate in plasma and neutralizes hydrogen ions, thereby correcting acidosis. 2. Alkalinize urine. As the pH value increases after the concentration of bicarbonate in urine increases, uric acid, sulfonamide drugs and hemoglobin are not easy to form crystals or aggregate in urine. 3. Antacid. Oral administration can quickly neutralize or buffer gastric acid without directly affecting gastric acid secretion. Therefore, the pH in the stomach increases rapidly to relieve the symptoms caused by high gastric acid.
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1. Treat metabolic acidosis. This product increases the concentration of carbonate in plasma and neutralizes hydrogen ions, thereby correcting acidosis. 2. Alkalinize urine. As the pH value increases after the concentration of bicarbonate in urine increases, uric acid, sulfonamide drugs and hemoglobin are not easy to form crystals or aggregate in urine. 3. Antacid. Oral administration can quickly neutralize or buffer gastric acid without directly affecting gastric acid secretion. Therefore, the pH in the stomach increases rapidly to relieve the symptoms caused by high gastric acid. |
144-55-8 | 44 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| ATP disodium salt |
This product is a coenzyme that improves the body's metabolism and participates in the metabolism of fat, protein, sugar, nucleic acid and nucleotides in the body. It is also the main source of energy in the body. When energy is needed for absorption, secretion, muscle contraction and biochemical synthesis reactions in the body, adenosine triphosphate is decomposed into adenosine diphosphate and phosphate groups, and energy is released at the same time. Animal experiments have shown that this product can inhibit the slow calcium ion influx of slow-reacting fibers, block or delay the forward conduction in the atrioventricular node reentry pathway, and a large dose may also block or delay the forward and reverse conduction of the bypass; in addition, it also has a short-term and strong effect of enhancing the vagus nerve, thereby terminating arrhythmias caused by atrioventricular node reentry and bypass reentry mechanisms.
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This product is a coenzyme that improves the body's metabolism and participates in the metabolism of fat, protein, sugar, nucleic acid and nucleotides in the body. It is also the main source of energy in the body. When energy is needed for absorption, secretion, muscle contraction and biochemical synthesis reactions in the body, adenosine triphosphate is decomposed into adenosine diphosphate and phosphate groups, and energy is released at the same time. Animal experiments have shown that this product can inhibit the slow calcium ion influx of slow-reacting fibers, block or delay the forward conduction in the atrioventricular node reentry pathway, and a large dose may also block or delay the forward and reverse conduction of the bypass; in addition, it also has a short-term and strong effect of enhancing the vagus nerve, thereby terminating arrhythmias caused by atrioventricular node reentry and bypass reentry mechanisms. |
987-65-5 | 8 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Nitrofurantoin |
This product is an antibacterial drug. Escherichia coli is mostly sensitive to this product, and some strains of Enterobacteriaceae such as Enterobacter aerogenes, Enterobacter cloacae, Proteus, and Klebsiella are sensitive to this product. Aeruginosa is usually resistant to this product. This product has antibacterial effects on Gram-positive bacteria such as Enterococcus. The antibacterial activity of this product is not affected by pus and tissue decomposition products. It is more active in acidic urine. The antibacterial mechanism is to interfere with the oxidoreductase system in the bacteria, thereby blocking its metabolic process.
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This product is an antibacterial drug. Escherichia coli is mostly sensitive to this product, and some strains of Enterobacteriaceae such as Enterobacter aerogenes, Enterobacter cloacae, Proteus, and Klebsiella are sensitive to this product. Aeruginosa is usually resistant to this product. This product has antibacterial effects on Gram-positive bacteria such as Enterococcus. The antibacterial activity of this product is not affected by pus and tissue decomposition products. It is more active in acidic urine. The antibacterial mechanism is to interfere with the oxidoreductase system in the bacteria, thereby blocking its metabolic process. |
67-20-9 | 26 |