Rosuvastatin calcium

The main ingredient of this product is rosuvastatin calcium.

1. Cyclosporine: When this product is used in combination with cyclosporine, the AUC of rosuvastatin is 7 times higher than the average observed in healthy volunteers (compared with taking the same dose of this product). Co-administration does not affect the plasma concentration of cyclosporine. 2. Vitamin K antagonists: Like other HMG-CoA reductase inhibitors, for patients who are also taking vitamin K antagonists (such as warfarin), starting this product or gradually increasing the dose of this product may lead to an increase in INR. Discontinuation of this product or gradually reducing the dose of this product may lead to a decrease in INR. In this case, appropriate monitoring of INR is necessary. 3. Gemfibrozil and other lipid-lowering products: When this product is used simultaneously with gemfibrozil, the Cmax and AUC of rosuvastatin can be increased by 2 times. Based on the data from special interaction studies, it is expected that this product has no pharmacokinetic interaction with fenofibrate, but pharmacodynamic interactions may occur. The risk of myopathy increases when gemfibrozil, fenofibrate, other fibrates, and lipid-lowering doses of niacin (1 g/day) are used in combination with HMG-CoA reductase inhibitors, which may be due to their ability to cause myopathy when administered alone. 4. Protease inhibitors: Although the mechanism of drug interaction is not clear, the simultaneous use of protease inhibitors may greatly increase the exposure of rosuvastatin. In a pharmacokinetic study, healthy volunteers took 20 mg of this product and a combination product of two protease inhibitors (400 mg lopinavir/100 mg ritonavir) at the same time. The results showed that the steady-state AUC (0-24) and Cmax of rosuvastatin increased by approximately 2 times and 5 times, respectively. Therefore, the simultaneous use of this product is not recommended in HIV patients receiving protease inhibitor treatment (see [Precautions]). 5. Antacids: The simultaneous administration of this product and an antacid suspension containing aluminum magnesium hydroxide can reduce the plasma concentration of rosuvastatin by approximately 50%. This effect can be mitigated if the antacid is given 2 hours after taking this product. The clinical significance of this drug interaction has not been studied. 6. Erythromycin: The co-administration of this product with erythromycin resulted in a 20% decrease in the AUC (0-t) of rosuvastatin and a 30% decrease in Cmax. This interaction may be due to the increased gastrointestinal motility caused by erythromycin. 7. Oral contraceptives, hormone replacement therapy (HRT): The simultaneous use of this product and oral contraceptives increased the AUC of estradiol and norgestrel by 26% and 34%, respectively. These increases in blood concentrations should be considered when selecting the dose of oral contraceptives. There are no pharmacokinetic data on subjects who use this product and HRT at the same time, so similar interactions cannot be ruled out. However, in clinical trials, this combination was widely used and well tolerated by patients. 8. Other drugs: Based on data from dedicated drug interaction studies, it is estimated that this product does not have a clinically relevant interaction with digoxin. 9. Cytochrome P450 enzymes: Data from both in vitro and in vivo studies have shown that rosuvastatin is neither an inhibitor nor an enzyme inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a weak substrate for these enzymes. There are no clinically relevant interactions between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4). Co-administration with itraconazole (an inhibitor of CYP3A4) increased the AUC of rosuvastatin by 28%, an increase that is not considered clinically significant. Therefore, drug interactions due to cytochrome P450-mediated metabolism are not expected.

The main ingredient of this product is rosuvastatin calcium.

1. Cyclosporine: When this product is used in combination with cyclosporine, the AUC of rosuvastatin is 7 times higher than the average observed in healthy volunteers (compared with taking the same dose of this product). Co-administration does not affect the plasma concentration of cyclosporine. 2. Vitamin K antagonists: Like other HMG-CoA reductase inhibitors, for patients who are also taking vitamin K antagonists (such as warfarin), starting this product or gradually increasing the dose of this product may lead to an increase in INR. Discontinuation of this product or gradually reducing the dose of this product may lead to a decrease in INR. In this case, appropriate monitoring of INR is necessary. 3. Gemfibrozil and other lipid-lowering products: When this product is used simultaneously with gemfibrozil, the Cmax and AUC of rosuvastatin can be increased by 2 times. Based on the data from special interaction studies, it is expected that this product has no pharmacokinetic interaction with fenofibrate, but pharmacodynamic interactions may occur. The risk of myopathy increases when gemfibrozil, fenofibrate, other fibrates, and lipid-lowering doses of niacin (1 g/day) are used in combination with HMG-CoA reductase inhibitors, which may be due to their ability to cause myopathy when administered alone. 4. Protease inhibitors: Although the mechanism of drug interaction is not clear, the simultaneous use of protease inhibitors may greatly increase the exposure of rosuvastatin. In a pharmacokinetic study, healthy volunteers took 20 mg of this product and a combination product of two protease inhibitors (400 mg lopinavir/100 mg ritonavir) at the same time. The results showed that the steady-state AUC (0-24) and Cmax of rosuvastatin increased by approximately 2 times and 5 times, respectively. Therefore, the simultaneous use of this product is not recommended in HIV patients receiving protease inhibitor treatment (see [Precautions]). 5. Antacids: The simultaneous administration of this product and an antacid suspension containing aluminum magnesium hydroxide can reduce the plasma concentration of rosuvastatin by approximately 50%. This effect can be mitigated if the antacid is given 2 hours after taking this product. The clinical significance of this drug interaction has not been studied. 6. Erythromycin: The co-administration of this product with erythromycin resulted in a 20% decrease in the AUC (0-t) of rosuvastatin and a 30% decrease in Cmax. This interaction may be due to the increased gastrointestinal motility caused by erythromycin. 7. Oral contraceptives, hormone replacement therapy (HRT): The simultaneous use of this product and oral contraceptives increased the AUC of estradiol and norgestrel by 26% and 34%, respectively. These increases in blood concentrations should be considered when selecting the dose of oral contraceptives. There are no pharmacokinetic data on subjects who use this product and HRT at the same time, so similar interactions cannot be ruled out. However, in clinical trials, this combination was widely used and well tolerated by patients. 8. Other drugs: Based on data from dedicated drug interaction studies, it is estimated that this product does not have a clinically relevant interaction with digoxin. 9. Cytochrome P450 enzymes: Data from both in vitro and in vivo studies have shown that rosuvastatin is neither an inhibitor nor an enzyme inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a weak substrate for these enzymes. There are no clinically relevant interactions between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4). Co-administration with itraconazole (an inhibitor of CYP3A4) increased the AUC of rosuvastatin by 28%, an increase that is not considered clinically significant. Therefore, drug interactions due to cytochrome P450-mediated metabolism are not expected.

The main ingredient of this product is rosuvastatin calcium.

1. Cyclosporine: When this product is used in combination with cyclosporine, the AUC of rosuvastatin is 7 times higher than the average observed in healthy volunteers (compared with taking the same dose of this product). Co-administration does not affect the plasma concentration of cyclosporine. 2. Vitamin K antagonists: Like other HMG-CoA reductase inhibitors, for patients who are also taking vitamin K antagonists (such as warfarin), starting this product or gradually increasing the dose of this product may lead to an increase in INR. Discontinuation of this product or gradually reducing the dose of this product may lead to a decrease in INR. In this case, appropriate monitoring of INR is necessary. 3. Gemfibrozil and other lipid-lowering products: When this product is used simultaneously with gemfibrozil, the Cmax and AUC of rosuvastatin can be increased by 2 times. Based on the data from special interaction studies, it is expected that this product has no pharmacokinetic interaction with fenofibrate, but pharmacodynamic interactions may occur. The risk of myopathy increases when gemfibrozil, fenofibrate, other fibrates, and lipid-lowering doses of niacin (1 g/day) are used in combination with HMG-CoA reductase inhibitors, which may be due to their ability to cause myopathy when administered alone. 4. Protease inhibitors: Although the mechanism of drug interaction is not clear, the simultaneous use of protease inhibitors may greatly increase the exposure of rosuvastatin. In a pharmacokinetic study, healthy volunteers took 20 mg of this product and a combination product of two protease inhibitors (400 mg lopinavir/100 mg ritonavir) at the same time. The results showed that the steady-state AUC (0-24) and Cmax of rosuvastatin increased by approximately 2 times and 5 times, respectively. Therefore, the simultaneous use of this product is not recommended in HIV patients receiving protease inhibitor treatment (see [Precautions]). 5. Antacids: The simultaneous administration of this product and an antacid suspension containing aluminum magnesium hydroxide can reduce the plasma concentration of rosuvastatin by approximately 50%. This effect can be mitigated if the antacid is given 2 hours after taking this product. The clinical significance of this drug interaction has not been studied. 6. Erythromycin: The co-administration of this product with erythromycin resulted in a 20% decrease in the AUC (0-t) of rosuvastatin and a 30% decrease in Cmax. This interaction may be due to the increased gastrointestinal motility caused by erythromycin. 7. Oral contraceptives, hormone replacement therapy (HRT): The simultaneous use of this product and oral contraceptives increased the AUC of estradiol and norgestrel by 26% and 34%, respectively. These increases in blood concentrations should be considered when selecting the dose of oral contraceptives. There are no pharmacokinetic data on subjects who use this product and HRT at the same time, so similar interactions cannot be ruled out. However, in clinical trials, this combination was widely used and well tolerated by patients. 8. Other drugs: Based on data from dedicated drug interaction studies, it is estimated that this product does not have a clinically relevant interaction with digoxin. 9. Cytochrome P450 enzymes: Data from both in vitro and in vivo studies have shown that rosuvastatin is neither an inhibitor nor an enzyme inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a weak substrate for these enzymes. There are no clinically relevant interactions between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4). Co-administration with itraconazole (an inhibitor of CYP3A4) increased the AUC of rosuvastatin by 28%, an increase that is not considered clinically significant. Therefore, drug interactions due to cytochrome P450-mediated metabolism are not expected.