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Rosuvastatin Ethyl Ester 851443-04-4 Rosuvastatin Ethyl Ester 851443-04-4

Rosuvastatin Ethyl Ester 851443-04-4
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Basic Information of Rosuvastatin Ethyl Ester 851443-04-4

  • English name: Rosuvastatin ethyl ester
  • Molecular Formula: C24H32FN3O6S
  • Molecular Weight: 509.5908
  • CAS Registry Number: 851443-04-4
  • Quality: BP/EP/USP
  • Density: 1.294g/cm3
  • Boiling point: 699.1°C at 760 mmHg
  • Refractive index: 1.571
  • Flash point: 376.6°C
  • Vapour Pressure: 1.62E-20mmHg at 25°C

Usage of Rosuvastatin Ethyl Ester 851443-04-4

Rosuvastatin is a selective HMG-CoA reductase inhibitor. HMG-CoA reductase inhibitors are rate-limiting enzymes that convert 3-hydroxy-3-methylglutaryl coenzyme A into a precursor of mevalonate-cholesterol. Rosuvastatin's main site of action is liver-cholesterol-lowering target organ. Rosuvastatin increases the number of hepatic LDL cell surface receptors, promotes LDL uptake and catabolism, inhibits hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL microparticles.

1. Hypolipidemic effect
Rosuvastatin obvious lipid-lowering effect, the general statin lowering low-density lipoprotein cholesterol (LDL-C) levels of 17% to 54%. The phase II clinical trial of rosuvastatin showed that the LDL-C was reduced to 65% at a dose of 80 mg, which is currently the most effective statin. Rosuvastatin can increase the number of LDL receptors. In human hepatoma, rosuvastatin increases LDL receptor mRNA by about 10-fold more than pravastatin.

2. Selective effect on liver cells
Cholesterol, which is derived from hepatocytes, is a major cause of blood cholesterol, and cholesterol, which is derived from non-hepatocytes, is required for normal cells. The main site of action of lovastatin is the liver, from the perspective of inhibition of sterol synthesis, the drug on the rat liver selectivity than the peripheral tissue selectivity and higher than pravastatin or simvastatin on liver tissue selection Sex is high. Lovastatin is absorbed into liver cells through an active absorption process and it has a 1000-fold more potent inhibitory effect on cholesterol in rat hepatocytes than in fibroblasts.

3. Anti-atherosclerotic effect
Rosuvastatin can reduce blood lipids, reduce lipid infiltration and foam cell formation, the delay in atherosclerosis benefit; the drug also by blocking the methylol glutaric acid pathway, in particular, the inhibition of isoprenoid metabolites Formation and inhibition of smooth muscle cell proliferation and promote apoptosis and stabilize atherosclerotic plaque, slow the occurrence and development of atherosclerosis.

MORE_DETAIL Rosuvastatin Ethyl Ester 851443-04-4

Basic Information of Rosuvastatin Ethyl Ester 851443-04-4

  • English name: Rosuvastatin ethyl ester
  • Molecular Formula: C24H32FN3O6S
  • Molecular Weight: 509.5908
  • CAS Registry Number: 851443-04-4
  • Quality: BP/EP/USP
  • Density: 1.294g/cm3
  • Boiling point: 699.1°C at 760 mmHg
  • Refractive index: 1.571
  • Flash point: 376.6°C
  • Vapour Pressure: 1.62E-20mmHg at 25°C

Usage of Rosuvastatin Ethyl Ester 851443-04-4

Rosuvastatin is a selective HMG-CoA reductase inhibitor. HMG-CoA reductase inhibitors are rate-limiting enzymes that convert 3-hydroxy-3-methylglutaryl coenzyme A into a precursor of mevalonate-cholesterol. Rosuvastatin's main site of action is liver-cholesterol-lowering target organ. Rosuvastatin increases the number of hepatic LDL cell surface receptors, promotes LDL uptake and catabolism, inhibits hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL microparticles.

1. Hypolipidemic effect
Rosuvastatin obvious lipid-lowering effect, the general statin lowering low-density lipoprotein cholesterol (LDL-C) levels of 17% to 54%. The phase II clinical trial of rosuvastatin showed that the LDL-C was reduced to 65% at a dose of 80 mg, which is currently the most effective statin. Rosuvastatin can increase the number of LDL receptors. In human hepatoma, rosuvastatin increases LDL receptor mRNA by about 10-fold more than pravastatin.

2. Selective effect on liver cells
Cholesterol, which is derived from hepatocytes, is a major cause of blood cholesterol, and cholesterol, which is derived from non-hepatocytes, is required for normal cells. The main site of action of lovastatin is the liver, from the perspective of inhibition of sterol synthesis, the drug on the rat liver selectivity than the peripheral tissue selectivity and higher than pravastatin or simvastatin on liver tissue selection Sex is high. Lovastatin is absorbed into liver cells through an active absorption process and it has a 1000-fold more potent inhibitory effect on cholesterol in rat hepatocytes than in fibroblasts.

3. Anti-atherosclerotic effect
Rosuvastatin can reduce blood lipids, reduce lipid infiltration and foam cell formation, the delay in atherosclerosis benefit; the drug also by blocking the methylol glutaric acid pathway, in particular, the inhibition of isoprenoid metabolites Formation and inhibition of smooth muscle cell proliferation and promote apoptosis and stabilize atherosclerotic plaque, slow the occurrence and development of atherosclerosis.
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