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Founded in:
2001-12-14 -
Country:
China -
Address:
No. 518, Laodong East Road, Changzhou -
Tax NO.:
91320400137158490L -
Registered Funds:
108 million yuan -
Website:
-
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Ibuprofen |
This product can inhibit the synthesis of prostaglandins and has antipyretic, analgesic and anti-inflammatory effects.
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This product can inhibit the synthesis of prostaglandins and has antipyretic, analgesic and anti-inflammatory effects. |
15687-27-1 | 54 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Folic acid |
Folic acid is a water-soluble B vitamin composed of pteridine, p-aminobenzoic acid and glutamic acid residues. It is an essential substance for the growth and reproduction of body cells. It participates in many important reactions in the body and the synthesis of nucleic acids and amino acids, promotes cell DNA synthesis, and promotes cell division and maturation.
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Folic acid is a water-soluble B vitamin composed of pteridine, p-aminobenzoic acid and glutamic acid residues. It is an essential substance for the growth and reproduction of body cells. It participates in many important reactions in the body and the synthesis of nucleic acids and amino acids, promotes cell DNA synthesis, and promotes cell division and maturation. |
0.4mg | 59-30-3 | 17 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Clonidine hydrochloride |
Extract from the above information
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Extract from the above information |
4205-91-8 | 23 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| 1-[(2S)-2-methyl-3-mercapto-1-oxypropyl]-L-proline |
This product is a competitive angiotensin converting enzyme inhibitor, which prevents angiotensin I from converting into angiotensin II, thereby reducing peripheral vascular resistance and reducing water and sodium retention by inhibiting aldosterone secretion. This product can also dilate peripheral blood vessels by interfering with the degradation of bradykinin. For patients with heart failure, this product can also reduce pulmonary capillary wedge pressure and pulmonary vascular resistance, increase cardiac output and exercise tolerance time.
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This product is a competitive angiotensin converting enzyme inhibitor, which prevents angiotensin I from converting into angiotensin II, thereby reducing peripheral vascular resistance and reducing water and sodium retention by inhibiting aldosterone secretion. This product can also dilate peripheral blood vessels by interfering with the degradation of bradykinin. For patients with heart failure, this product can also reduce pulmonary capillary wedge pressure and pulmonary vascular resistance, increase cardiac output and exercise tolerance time. |
0 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Hydrochlorothiazide |
1. Effect on water and electrolyte excretion. ① Diuretic effect, increased excretion of urinary sodium, potassium, chloride, phosphorus and magnesium ions, and reduced excretion of urinary calcium. The mechanism of action of this type of drug is mainly to inhibit the reabsorption of sodium chloride in the distal tubule anterior segment and the proximal tubule (less severe), thereby increasing the Na-K exchange in the distal tubule and the collecting duct, and increasing K+ secretion. Its mechanism of action is not yet fully understood. This type of drug can inhibit carbonic anhydrase activity to varying degrees, so it can explain its effect on the proximal tubule. This type of drug can also inhibit phosphodiesterase activity, reduce the tubular uptake of fatty acids and mitochondrial oxygen consumption, thereby inhibiting the active reabsorption of Na and Cl- by the tubule. ② Antihypertensive effect. In addition to the diuretic and sodium excretion effects, there may be extrarenal mechanisms involved in antihypertensive treatment, which may be to increase the excretion of Na in the gastrointestinal tract. 2. Effect on renal hemodynamics and glomerular filtration function. Due to the reduced reabsorption of water and Na by the renal tubules, the increased pressure within the renal tubules, and the increased water and Na flowing through the distal convoluted tubules, the macula densa is stimulated to increase the secretion of renin and angiotensin in the kidney through the tubular-glomerular reflex, causing renal vasoconstriction, decreased renal blood flow, constriction of the glomerular afferent and efferent arterioles, and a decrease in the glomerular filtration rate.
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1. Effect on water and electrolyte excretion. ① Diuretic effect, increased excretion of urinary sodium, potassium, chloride, phosphorus and magnesium ions, and reduced excretion of urinary calcium. The mechanism of action of this type of drug is mainly to inhibit the reabsorption of sodium chloride in the distal tubule anterior segment and the proximal tubule (less severe), thereby increasing the Na-K exchange in the distal tubule and the collecting duct, and increasing K+ secretion. Its mechanism of action is not yet fully understood. This type of drug can inhibit carbonic anhydrase activity to varying degrees, so it can explain its effect on the proximal tubule. This type of drug can also inhibit phosphodiesterase activity, reduce the tubular uptake of fatty acids and mitochondrial oxygen consumption, thereby inhibiting the active reabsorption of Na and Cl- by the tubule. ② Antihypertensive effect. In addition to the diuretic and sodium excretion effects, there may be extrarenal mechanisms involved in antihypertensive treatment, which may be to increase the excretion of Na in the gastrointestinal tract. 2. Effect on renal hemodynamics and glomerular filtration function. Due to the reduced reabsorption of water and Na by the renal tubules, the increased pressure within the renal tubules, and the increased water and Na flowing through the distal convoluted tubules, the macula densa is stimulated to increase the secretion of renin and angiotensin in the kidney through the tubular-glomerular reflex, causing renal vasoconstriction, decreased renal blood flow, constriction of the glomerular afferent and efferent arterioles, and a decrease in the glomerular filtration rate. |
58-93-5 | 56 |