YINGTAI TAIYUN Rosuvastatin Calcium Tablets For Hypercholesterolemia 10mg*7

[Drug Name]
Generic Name: Rosuvastatin Calcium Tablets
Trade Name: Taiyun Rosuvastatin Calcium Tablets 10mg x 7 tablets

[Main Ingredients]
The main active ingredient of this product is rosuvastatin calcium. Chemical Name: Calcium Bis[(7-(4-(4-fluorophenyl)-6-isopropyl)-2-(methyl(methylsulfonyl)complex)pyrimidin-5-[3R5-35-dihydroxy-hept-6-enoate)]
Molecular Formula: 22H27F306)2Ca
Molecular Weight: 101.14

[Properties]
This product is a film-coated tablet that appears white to pale yellow after removal of the coating.

[Indications/Main Functions]
This product is indicated for primary hypercholesterolemia (type Ia, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type Ib), whose dyslipidemia is not adequately controlled with diet and other non-drug therapies (e.g., exercise therapy, weight loss).

[Specifications]
10mg (7 tablets)

[Dosage and Administration]
Before treatment begins, patients should be prescribed a standard cholesterol-lowering diet and maintain this diet during treatment. The use of this product should be individualized, taking into account the patient's cholesterol level, expected cardiovascular risk, and potential for adverse reactions. Oral administration. The usual starting dose is 5 mg once daily. The starting dose of rosuvastatin calcium tablets should be selected based on the patient's individual cholesterol level, expected cardiovascular risk, and potential for adverse reactions. For patients requiring more potent LDL-C lowering, a starting dose of 10 mg once daily can be considered. This dose controls lipid levels in most patients. If necessary, the dose can be adjusted to the next higher dose level after 4 weeks of treatment. The maximum daily dose of this product is 20 mg. This product can be taken at any time of day, with or without food. Use in Patients with Renal Impairment: No dose adjustment is required for patients with mild and moderate renal impairment. All doses of this product are contraindicated in patients with severe renal impairment. Use in Patients with Hepatic Impairment: Systemic exposure to rosuvastatin was not increased in subjects with a Child-Pugh score of 7 or less. Increased systemic exposure was observed in subjects with Child-Pugh scores of 8 and 9. In these patients, an evaluation of renal function should be considered. There is no experience with the use of this product in patients with a Child-Pugh score of 9 or higher. This product is contraindicated in patients with active liver disease. Race: Increased systemic exposure has been observed in Asian subjects. In determining the efficacy of this product in patients of Asian descent, the use of this product in patients with active liver disease is contraindicated. This factor should be considered when considering dosing.

[Adverse Reactions]
Adverse reactions observed with this product are generally mild and transient. In controlled clinical trials, adverse events resulted in less than 4% of patients withdrawing from the trial. The frequency of adverse events is as follows: Common (incidence 1:10,000, highest, lowest, lowest, lowest, lowest, lowest, highest ... and rhabdomyolysis. Systemic disorders: Weakness is common. As with other HMG-COA reductase inhibitors, the incidence of adverse reactions tends to increase with increasing dose. Renal effects: Proteinuria (as determined by dipstick) has been observed in patients receiving rosuvastatin calcium tablets, with the majority of protein originating from the renal tubules. Approximately 1% of patients experienced an increase in proteinuria from none or trace to ++ or greater at some point during treatment with 10mg and 20mg, and approximately 3% of patients receiving 40mg experienced this increase. At the 20mg dose, Proteinuria has been observed, ranging from absent or minimal to mildly elevated. In most cases, proteinuria spontaneously decreased or resolved with continued treatment. Effects on skeletal muscle: Skeletal muscle effects, such as myalgia, myopathy, and rarely, rhabdomyolysis, have been reported in patients receiving all doses of this drug, particularly in patients receiving doses greater than 20 mg. Dose-related increases in creatine kinase (CK) levels have been observed in patients taking this drug; most cases have been mild, asymptomatic, and transient. If CK levels are elevated (>5× ULN), the patient should be monitored. ), treatment should be discontinued. Liver effects: As with other HMG-CoA reductase inhibitors, dose-related transaminase elevations have been observed in a small number of patients taking this product; most cases have been mild, asymptomatic, and transient. Postmarketing experience: In addition to the reactions described above, the following adverse events have been reported during postmarketing use of this product: Hepatobiliary disorders: Very rare jaundice, hepatitis; rare elevated liver transaminases. Musculoskeletal disorders: Rare arthralgia. Neurological disorders: Very rare polyneuropathy.

[Contraindications]
This product is contraindicated for Hypersensitivity to rosuvastatin or any of the ingredients in this product. Patients with active liver disease, including unexplained persistent elevations in serum transaminases and any elevation of serum transaminases exceeding three times the upper limit of normal (ULN). Patients with severe renal impairment (creatinine clearance <30 m/min). Patients with myopathy. Patients taking cyclosporine concomitantly. Pregnant or lactating women, as well as women who may become pregnant and are not using adequate contraceptive measures.

[Drug Interactions]
1. Cyclosporine: When this product is co-administered with cyclosporine, the AUC of rosuvastatin is, on average, seven times higher than that observed in healthy volunteers (compared to the same dose of this product). Coadministration does not affect cyclosporine plasma concentrations. Vitamin K antagonists: As with other HMG-CoA reductase inhibitors, initiating or gradually increasing the dose of this product in patients taking vitamin K antagonists (e.g., warfarin) may result in an increase in the INR. Discontinuing or gradually decreasing the dose of this product may result in a decrease in the INR. In such cases, appropriate monitoring of the INR is necessary. 3. Gemfibrozil and other lipid-lowering products: Concomitant use of this product with gemfibrozil may increase the Cmax and AUC of rosuvastatin by 2-fold. Based on data from dedicated interaction studies, no interaction between this product and fenofibrate is expected. Pharmacokinetic interactions, but pharmacodynamic interactions are possible. Concomitant use of gemfibrozil, fenofibrate, other fibrates, and lipid-lowering doses of niacin (21 g/day) with HMG-CoA reductase inhibitors increases the risk of myopathy, possibly due to the myopathy-inducing effects of these drugs when administered alone. 4. Antacids: Concomitant administration of this drug with 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 administered 2 hours after taking this drug. The clinical significance of this drug interaction is unclear. This has not been studied. 5. Erythromycin: Coadministration of this product with erythromycin resulted in a 20% decrease in the AUC of rosuvastatin and a 30% decrease in Cmax. This interaction may be due to increased gastrointestinal motility caused by erythromycin. 6. Oral Contraceptives/HRT: Concomitant use of this product with oral contraceptives increased the AUC of ethinyl estradiol and norgestrel by 26% and 34%, respectively. These increased plasma concentrations should be considered when selecting oral contraceptive dosages. Pharmacokinetic data are not available in subjects who have used this product concurrently with HRT; therefore, it cannot be used for further information. The possibility of such an interaction has been ruled out. However, in clinical trials, this combination was widely used and well tolerated by patients. 7. Other Medications: Based on data from dedicated drug interaction studies, no clinically relevant interaction is expected between this product and digoxin. 8. Cytochrome P450 Inhibitors: In vitro and in vivo data indicate that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. Furthermore, rosuvastatin is a weak substrate for these enzymes. 9. No clinically relevant interactions have been observed between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3AA) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4). Coadministration with itraconazole (a CYP3A4 inhibitor) increased the AUC of rosuvastatin by 28%, an increase not considered clinically significant. Therefore, drug interactions due to cytochrome P4.0-mediated metabolism are not expected.

[Precautions]
Renal Effects: Proteinuria (as determined by dipstick) has been observed in patients treated with high doses, particularly 40 mg. The majority of the protein originates from the renal tubules and, in most cases, is transient or intermittent.
Skeletal Muscle Effects: Skeletal muscle effects, such as myalgia, myopathy, and, rarely, rhabdomyolysis, have been reported in patients treated with all doses of this drug, particularly in doses greater than 20 mg.
Creatine Kinase Assay: Creatine kinase (CK) should not be measured after strenuous exercise or in the presence of plausible factors causing CK elevation, as this can confound interpretation of the results.
If baseline CK values ​​are significantly elevated (>5×ULN), retest within 5-7 days. If repeat testing confirms a baseline CK value >5×ULN, treatment should not be initiated.
Pre-treatment: As with other HMG-CoA reductase inhibitors, rosuvastatin calcium tablets should be used with caution in patients with predisposing factors for myopathy/rhabdomyolysis. These factors include: renal impairment, hypothyroidism, personal or family history of hereditary muscle disorders, a history of muscle toxicity with other HMG-CoA reductase inhibitors or fibrates, alcohol abuse, age >70 years, conditions that may increase blood concentrations, and concomitant use of fibrates. For these patients, the potential benefits of treatment should be balanced against the potential risks, and clinical monitoring is recommended. Treatment should not be initiated if the patient's baseline CK value is significantly elevated (>5×ULN). During treatment, patients should be asked to immediately report unexplained muscle pain, weakness, or cramping, especially if accompanied by malaise and fever. CK levels should be measured in these patients. If CK values ​​are significantly elevated (>5×ULN) or muscle symptoms are severe and cause daylong discomfort (even if CK is ≤5×ULN), treatment should be discontinued. If symptoms resolve and CK levels return to normal, consider restarting this product or switching to the lowest dose of another HMG-CoA reductase inhibitor and closely monitoring the patient. Routine CK level monitoring is not necessary for asymptomatic patients. In clinical studies, there was no evidence of increased effects on skeletal muscle in the small number of patients receiving this medication concomitantly with other therapies. However, an increased incidence of myositis and myopathy has been observed in patients receiving other HMG-CoA reductase inhibitors concomitantly with fibrates (including gemfibrozil), cyclosporine, niacin, azole antifungals, protease inhibitors, or macrolide antibiotics. Concomitant use of gemfibrozil with some HMG-CoA reductase inhibitors may increase the risk of myopathy. Therefore, concomitant use of this medication with gemfibrozil is not recommended. The benefits of combining this medication with fibrates or niacin to further improve lipid profiles should be carefully weighed against the potential risks of such a combination. This medication should not be used in any patient with an acute, severe illness suggestive of myopathy or with a predisposing condition to renal failure secondary to rhabdomyolysis (e.g., sepsis, hypotension, major surgery, trauma, severe metabolic, endocrine, or electrolyte abnormalities, or uncontrolled epilepsy). Effects on the Liver: As with other HMG-CoA reductase inhibitors, this drug should be used with caution in patients who consume alcohol excessively and/or have a history of liver disease. Liver function tests are recommended before starting treatment and in the third month after initiation. If serum transaminases are elevated more than three times the upper limit of normal, this drug should be discontinued or the dose reduced. For hypercholesterolemia secondary to hypothyroidism or nephrotic syndrome, the underlying disease should be treated before initiating this drug. Ethnicity: Pharmacokinetic studies have shown that drug exposure is higher in Asian subjects than in Caucasians. Effects on Driving and Operating Machinery: Studies have not been conducted to determine the effects of this drug on driving and operating machinery. However, based on its pharmacodynamic properties, this drug is unlikely to affect these abilities. The potential for dizziness during treatment should be considered. [Use in Pregnant and Lactating Women] This drug is contraindicated in pregnant and lactating women. Women of childbearing potential should use appropriate contraceptive measures. Because cholesterol and other cholesterol biosynthesis products are important for fetal development, the risks of HMG-COA reductase inhibition outweigh the benefits of treatment for pregnant women. Animal studies provide limited evidence of reproductive toxicity. If a patient becomes pregnant while taking this drug, treatment should be discontinued immediately. Rosuvastatin is excreted in rat milk. There are no data on the excretion of rosuvastatin in human milk.

[Overdose]
There is no specific treatment for suftan overdose. In the event of an overdose, symptomatic treatment should be initiated, with supportive measures as needed. Liver function and CK levels should be monitored. Hemodialysis may not be significantly effective.

[Pharmacology and Toxicology]
1) Rosuvastatin is a selective, competitive HMG-COA reductase inhibitor. HMG-COA reductase is the rate-limiting enzyme in the conversion of 3-hydroxy-3-methylglutaryl-CoA to mevalonate, a precursor of cholesterol. Results from animal and cell culture studies have shown that rosuvastatin is highly and selectively taken up by the liver, which is the target organ for cholesterol reduction. In vivo and in vitro studies have shown that rosuvastatin can increase the number of hepatic LDL receptors on the cell surface, thereby enhancing the uptake and catabolism of LDL, and inhibiting the synthesis of VLDL in the liver, thereby reducing the total number of VLDL and LDL particles. (2) For patients with homozygous and heterozygous familial hypercholesterolemia, patients with non-familial hypercholesterolemia, and patients with mixed dyslipidemia, rosuvastatin can reduce total cholesterol, LDL-C, ApoB, and non-HDL-C levels. Rosuvastatin can also reduce TG and increase HDL-C levels. For patients with simple hypertriglyceridemia, rosuvastatin can reduce total cholesterol, LDL-C, VLDL-C, ApoB, non-HDL-C, TG levels, and increase HDL-C levels. The effects of rosuvastatin on cardiovascular morbidity and mortality have not yet been determined.