Each film coated tablet ROSWIN 10 contains: Rosuvastatin Calcium equivalent to Rosuvastatin 10 mg.
Each film coated tablet ROSWIN 20 contains: Rosuvastatin Calcium equivalent to Rosuvastatin 20 mg.
Each film coated tablet ROSWIN 40 contains: Rosuvastatin Calcium equivalent to Rosuvastatin 40 mg.
Pharmacology: Pharmacodynamics: Mechanism of action: Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl co-enzyme A to mevalonate, a precursor for cholesterol. The primary site of action of rosuvastatin is the liver, the target organ for cholesterol lowering.
Rosuvastatin increases the number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
Pharmacodynamic effects: Rosuvastatin reduces elevated LDL-cholesterol, total cholesterol and triglycerides and increases HDL-cholesterol. It also lowers ApoB, non HDL-C, VLDL-C, VLDL-TG and increases ApoA-I. Rosuvastatin also lowers the LDL-C/HDL-C, total C/HDL-C and non HDL-C/HDL-C and the ApoB/ApoA-I ratios.
A therapeutic response to rosuvastatin is evident within 1 week of commencing therapy and 90% of maximum response is usually achieved in 2 weeks. The maximum response is usually achieved by 4 weeks and is maintained after that.
Special populations: Age and sex: There was no clinically relevant effect of age or sex on the pharmacokinetics of rosuvastatin.
Renal insufficiency: The increase of plasma concentration only occurred in patients with sever renal impairment (CrCl <30 mL/min).
Hepatic impairment: There is no evidence of increased exposure to rosuvastatin in hepatic impairment patients with Child-Pugh scores lower than 8 and 9.
Rosuvastatin is indicated for patients with primary hypercholesterolemia (type IIa, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type IIb) as an adjunct to diet when response to diet and exercise is inadequate.
Rosuvastatin reduces elevated LDL-cholesterol, total cholesterol, triglycerides and ApoB, and increases HDL-cholesterol.
Rosuvastatin is also indicated in patients with homozygous familial hypercholesterolemia as an adjunct to diet and other lipid lowering treatments (e.g. LDL aphaeresis).
Before initiating treatment with rosuvastatin, the patient should be placed on a standard cholesterol-lowering diet that should continue during treatment. The dose of rosuvastatin should be individualized according to the goal of therapy and patient response, using current consensus guidelines.
The recommended start dose is 5 or 10 mg once daily in both statin naive patients or patients switched from another HMG-CoA reductase inhibitor. The choice of starting dose should take into account the individual patients cholesterol level and future cardiovascular risk as well as the potential risk for adverse reactions. A dose adjustment to the next dose level can be made after 4 weeks, if necessary. In light of the increased of adverse reactions with the 40 mg dose compare to lower dose, a final titration to the maximum dose of 40 mg should only be considered in patients with severe hypercholesterolemia at high cardiovascular risk (in particular those with familial hypercholesterolemia) who do not achieve their treatment goal on 20 mg, and in whom routine follow up will be performed. Specialist supervision is recommended when the 40 mg dose is initiated.
Rosuvastatin may be given at any time of day, with or without food.
Use in Children: Safety and efficacy have not been established in children. Pediatric experience is limited to a small number of children (aged 8 years or above) with homozygous familial hypercholesterolemia. Therefore, rosuvastatin is not recommended for pediatric use at this time.
Use in the Elderly: A start dose of 5 mg is recommended in patients > 70 years. No other dose adjustment is necessary in relation to age.
Dosage in Patients with Renal Insufficiency: No dose adjustment is necessary in patients with mild to moderate renal impairment.
For patients with severe renal impairment (CrCl < 30 mL/min/1.73m2) not on hemodialysis, dosing of rosuvastatin should be started at 5 mg once daily and not to exceeded 10 mg once daily.
Dosage in Patients with Hepatic Impairment: There was no increase in systemic exposure to rosuvastatin in patients with Child-Pugh scores of 7 or below. However, increased systemic exposure to rosuvastatin has been observed in patients with Child-Pugh scores of 8 and 9.
In these patients an assessment of renal function should be considered, therefore the dose of rosuvastatin should not exceed 20 mg once daily. There is no data in patients with Child-Pugh scores above 9.
Race: The increase of plasma concentration of rosuvastatin occured in Asian. Initiation of therapy with 5 mg once daily should be considered for Asian patients. The increased systemic exposure should be taken into consideration when treating Asian patients particularly in these whose hypercholesterolemia is not adequately controlled a doses up to 20 mg/daily.
Dosage in Patients with Pre-disposing Factors to Myopathy: The recommended start dose is 5 mg in patients with predisposing factors to myopathy.
Interactions requiring dose adjustment: Gemfibrozil: The concomitant use of rosuvastatin and gemfibrozil will increase systematic exposure of rosuvastatin (see PRECAUTIONS and INTERACTIONS).
There is no specific treatment in the event of overdose. In the event of overdose, the patient should be treated symptomatically and supportive measures instituted as required. Liver function and Creatinine Kinase levels should be monitored. Hemodialysis is unlikely to be of benefit.
Rosuvastatin is contraindicated in patients: With hypersensitivity to any component of this product.
With active liver disease (including unexplained, persistent elevations of serum transaminases and any serum transaminase elevation exceeding 3x the upper limit of normal).
With myopathy.
Receiving concomitant cyclosporine.
During pregnancy and lactation and in women of childbearing potential not using appropriate contraceptive measures.
Liver: As with other HMG-CoA reductase inhibitors, rosuvastatin should be used with caution in patients who consume excessive quantities of alcohol and/or have a history of liver disease. It is recommended that liver function tests be carried out prior to, and 3 months following, the initiations of treatment with rosuvastatin. Rosuvastatin should be discontinued or the dose reduced if the level of serum transaminases is greater than 3 times the upper limit of normal. In patients with secondary hypercholesterolemia caused by the hypothyroidism or nephritic syndrome, the underlying disease should be treated prior to initiating therapy with rosuvastatin.
Skeletal Muscle: As with other HMG-CoA reductase inhibitors, effects on skeletal muscle e.g. uncomplicated myalgia, myopathy and, rarely, rhabdomyolysis, have been reported in rosuvastatin treated patients with all doses and in particular doses >20 mg. As with other HMG-CoA reductase inhibitors, the reporting rate of rhabdomyolysis is higher at the highest dose. Patients should be asked to report inexplicable muscle pain or weakness immediately, particularly if associated with malaise or fever. Creatinine Kinase (CK) levels should be discontinued if CK levels are markedly elevated (5 c ULN) or, if muscular symptoms are severe and cause daily discomfort (even if CK levels are <5 x ULN). If symptoms resolve and CK levels return to normal, then consideration should be given to-re-introducing resorvastatin or an alternative HMG-CoA reductase inhibitor at the lowest dose with close monitoring. Routine monitoring of CK levels in asymptomatic patients is not warranted.
Creatinine Kinase (CK) should not be measured following strenuous exercise or in the presence of a plausible alternative cause of CK increase which may confound interpretation of the result. If CK levels are significantly elevated at baseline >5x ULN, a confirmatory test should be carried out within 5-7 days. If the repeat test confirms a baseline CK >5x ULN, treatment should not be started.
There was no evidence of increased skeletal muscle effects in patients dosed with rosuvastatin and concomitant therapy. However, an increase in the incidence of myositis and myopathy has been seen in patients receiving other HMG-CoA reductase inhibitors together with fibric acid derivatives including gemfibrozil, cyclosporin, nicotinic acid, azole antifungals, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when given concomitantly with some HMG-CoA reductase inhibitors. The benefit of further alterations in lipid levels by the combined used of rosuvastatin with fibrates or niacin should be carefully weighed against the potential risk of such combination. The 40 mg dose is contraindicated with concomitant use of a fibrate.
Rosuvastatin should be prescribed with caution in patients with pre-disposing factors for myopathy/rhabdomyolysis. Such factors include renal impairment, hypothyroidism, personal or family history of hereditary muscular disorders, previous history of muscular toxicity with another HMG-CoA reductase inhibitor or fibrate, alcohol abuse, age >70 years, situations where an increase in plasma levels may occur, and concomitant use of fibrates. In such patients the risks of treatments should be considered in relation to possible benefit and clinical monitoring is recommended. If CK levels are significantly elevated at baseline >5x ULN, treatment should not be started.
Rosuvastatin should not be used in any patient with an acute, serious condition suggestive of myopathy or predisposing to the development or renal failure secondary to rhabdomyolysis (e.g. sepsis, hypotension, major surgery, trauma, severe metabolic endocrine and electrolyte disorders; or uncontrolled seizures).
Diabetes Mellitus: As with other HMG-CoA reductase inhibitors, increases in HbA1c and serum glucose levels have been observed in patients treated with rosuvastatin. An increased frequency or diabetes has been reported with rosuvastatin in patients with risk factors for diabetes (see SIDE EFFECTS).
Effects on ability to drive and use machines: There is no data that showed the effect of rosuvastatin on the ability to drive and use machines. However, rosuvastatin is unlikely to effect this ability. When driving vehicles or operating machines, it should be taken into account that dizziness may occur during treatment.
Rosuvastatin is contraindicated during pregnancy or lactation as the safety of rosuvastatin during pregnancy and whilst breast-feeding has not been established. Women of child bearing potential should use appropriate contraceptive measures.
Since cholesterol and other products of cholesterol biosynthesis are essential for the development of the foetus, the potential risk from inhibition of HMG-CoA reductase outweighs the advantage of treatment during pregnancy. If a patient becomes pregnant during the use of this product, treatment should be discontinued immediately.
Rosuvastatin is excreted in the milk of rats. There are no data with respect to excretion in milk in human (see CONTRAINDICATIONS).
The adverse events seen with rosuvastatin are generally mild and transient.
Nervous system disorders: Common: headache, dizziness.
Very rare: polyneuropathy, memory loss.
Gastrointestinal disorders: Common: constipation, nausea, abdominal pain.
Rare: pancreatitis.
Musculoskeletal, connective tissue and bone disorders: Common: myalgia.
Rare: myopathy, including myositis and rhabdomyolysis.
As with other HMG-CoA reductase inhibitors, the reporting rate for rhabdomyolysis in post-marketing use is higher at the highest marketed dose.
Very rare: arthralgia.
General disorders: Common: asthenia.
Immune system disorders: Rare: hypersensitivity reactions including angioedema.
Skin disorders: Uncommon: pruritus, rash, urticaria.
As with other HMG-CoA reductase inhibitor, the incidence of adverse drug reactions tends to increase with increasing dose.
Skeletal Muscle Effects: Rare cases of rhabdomyolysis which were occasionally associated with impairment of renal function.
Laboratory Effects: As with other HMG-CoA reductase inhibitors, a dose-related increase in transaminases and CK have been observed in a small number of patients taking rosuvastatin; the majority of cases were mild, asymptomatic and transient. If CK levels are elevated (>5x ULN), treatment should be discontinued. Increases in HbA1c have also been observed in patients treated with rosuvastatin.
Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated with higher doses of rosuvastatin, in particular 40 mg. This is usually transients or intermittent, and not predictive of acute progressive renal disease. An assessment of renal function should be considered during routine follow up of patients treated with a dose of 40 mg.
Hepatobiliary disorders: Very rare: Jaundice, hepatitis.
Rare: increased hepatic transaminase.
Psychiatric disorders: Unknown: depression, sleep disorder (including insomnia and nightmares).
Vitamin K antagonists: As with other HMG-CoA reductase inhibitors, the initiation of treatment or dosage up-titration of rosuvastatin in patients treated concomitantly with Vitamin K antagonists (e.g. warfarin) may result in an increase in INR. Discontinuation or down-titration of rosuvastatin may result in a decrease in INR. In such situations, appropriate monitoring of INR is desirable.
Gemfibrozil: Concomitant use of rosuvastatin and gemfibrozil resulted in a 2-fold increase in rosuvastatin Cmax and AUC (see DOSAGE & ADMINISTRATION).
Gemfibrozil, fenofibrate, other fibrates and lipid lowering doses > or equal to 1 g/day of niacin (nicotinic acid) increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone. The 40 mg dose is contraindicated with concomitant use of fibrate. These patients should also start with the 5 mg dose.
Protease inhibitors: Consideration should be given both to the benefit of lipid lowering by the use of rosuvastatin in HIV patients receiving protease inhibitors and the potential for increased rosuvastatin plasma concentrations when initiating and up-titrating rosuvastatin doses in patients treated with protease inhibitors.
Cyclosporin: During concomitant treatment with rosuvastatin and cyclosporin, rosuvastatin plasma levels were on average 7 times higher than those observed in healthy volunteers (see CONTRAINDICATIONS).
Concomitant administration of rosuvastatin and cyclosporin did not affect plasma concentration of cyclosporin.
Antacid: The simultaneous dosing of rosuvastatin with an antacid suspension containing aluminum and magnesium hydroxide resulted in a decrease in rosuvastatin plasma concentration of approximately 50%. This effect was mitigated when the antacid was dosed 2 hours after rosuvastatin. The clinical relevance of this interactions has not been studied.
Cytochrome P450 enzymes: Rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a poor substrate for these isoenzymes.
No interactions have been observed between rosuvastatin and either fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4).
Concomitant administration of itraconazole (an inhibitor of CYP3A4) and rosuvastatin resulted in a 28% increase in AUC of rosuvastatin. This small increase is not considered clinically significant. Therefore, drug interactions resulting from cytochrome P450-mediated metabolism are not expected.
Erythromycin: Concomitant use of rosuvastatin and erythromycin resulted in a 20% decrease in AUC(0-t) and a 30% decrease in Cmax of rosuvastatin. This interaction may be caused by the increase in gut motility caused by erythromycin.
Oral contraceptive/hormone replacement therapy (HRT): Concomitant use of rosuvastatin and an oral contraceptive resulted in an increase in ethinyl estradiol and norgestrel AUC of 26% and 34% respectively. These increased plasma levels should be considered when selecting oral contraceptive doses.
Store at temperature below 30°C.
C10AA07 - rosuvastatin ; Belongs to the class of HMG CoA reductase inhibitors. Used in the treatment of hyperlipidemia.
Roswin FC tab 10 mg
3 × 10's
Roswin FC tab 20 mg
3 × 10's
Roswin FC tab 40 mg
3 × 10's
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