Full Prescribing Info
Rosuvastatin calcium.
Rovastin 5mg Film Coated Tablet: Each tablet contains Rosuvastatin calcium equivalent to Rosuvastatin 5 mg.
Rovastin 10mg Film Coated Tablet: Each tablet contains Rosuvastatin calcium equivalent to Rosuvastatin 10 mg.
Pharmacology: Mechanism of Action: Rosuvastatin is a selective, potent and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. Triglycerides (TG) and cholesterol in the liver are incorporated with apolipoprotein B (ApoB), into very low density lipoprotein (VLDL) and released into the plasma for delivery to peripheral tissues. VLDL particles are TG-rich. Cholesterol-rich low density lipoprotein (LDL) is formed from VLDL and is cleared primarily through the high affinity LDL receptor in the liver.
Rosuvastatin produces its lipid-modifying effects in 2 ways; it 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 ofVLDL and LDL particles.
High density lipoprotein (HDL), which contains ApoA-I is involved, amongst other things, in transport of cholesterol from tissues back to the liver (reverse cholesterol transport).
The involvement of LDL-Cholesterol (LDL-C) in atherogenesis has been well documented. Epidemiological studies have established that high LDL-C, TG, low HDL-C and ApoA-I have been linked to a higher risk of cardiovascular (CV) disease. Intervention studies have shown the benefits on mortality and CV event rates of lowering LDL-C and TG or raising HDL-C. More recent data has linked the beneficial effects of HMG-CoA reductase inhibitors to lowering of non-HDL (ie, all circulating cholesterol not in HDL) and ApoB or reducing the ApoB/ApoA-I ratio.
Pharmacokinetics: Absorption: In clinical pharmacology studies in man, peak plasma concentrations of rosuvastatin were reached 3-5 hrs following oral dosing. Both peak concentration (Cmax) and area under the plasma concentration-time curve (AUC) increased in approximate proportion to rosuvastatin dose. The absolute bioavailability of rosuvastatin is approximately 20%.
Administration of rosuvastatin with food decreased the rate of drug absorption by 20% as assessed by Cmax, but there was no effect on the extent of absorption as assessed by AUC.
Plasma concentrations of rosuvastatin do not differ following evening or morning drug administration.
Significant LDL-C reductions are seen when rosuvastatin is given with or without food, and regardless of the time of day of drug administration.
Distribution: Mean volume of distribution at steady-state of rosuvastatin is approximately 134 L. Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations.
Metabolism: Rosuvastatin is not extensively metabolised; approximately 10% of a radio labeled dose is recovered as metabolite. The major metabolite is N-desmethyl rosuvastatin, which is formed principally by cytochrome P-450 2C9, and in vitro studies have demonstrated that N-desmethyl rosuvastatin has approximately ⅙ to ½ the HMG-CoA reductase inhibitory activity of rosuvastatin. Overall, >90% of active plasma HMG-CoA reductase inhibitory activity is accounted for by rosuvastatin.
Excretion: Following oral administration, rosuvastatin and its metabolite are primarily excreted in the faeces (90%). The elimination half-life (t½) of rosuvastatin is approximately 19 hrs.
After an IV dose, approximately 28% of total body clearance was via the renal route and 72% by the hepatic route.
Special Populations: Age and Sex: There was no clinically relevant effect of age or sex on the pharmacokinetics of rosuvastatin.
Race: Pharmacokinetic studies show an approximate 2-fold elevation in median AUC in Asian subjects compared with Caucasians. A population pharmacokinetic analysis revealed no clinically relevant differences in pharmacokinetics among Caucasian, Hispanic and Black or Afro-Caribbean groups.
Genetic polymorphisms: Disposition of HMG-CoA reductase inhibitors, including rosuvastatin, involves OATP1B1 and BCRP transporter proteins. In patients with SLCO1B1 (OATP1B1) and/or ABCG2 (BCRP) genetic polymorphisms there is a risk of increased rosuvastatin exposure. Individual polymorphisms of SLCO1B1 c.521CC and ABCG2 c.421AA are associated with a higher rosuvastatin exposure (AUC) compared to the SLCO1B1 c.521TT or ABCG2 c.421CC genotypes. This specific genotyping is not established in clinical practice, but for patients who are known to have these types of polymorphisms, a lower daily dose of Rovastin is recommended.
Rovastin is indicated as an adjunct to diet, at least equivalent to the Adult Treatment Panel III (ATP III TLC diet), for the reduction of elevated total cholesterol, LDL-cholesterol, ApoB, the total cholesterol: HDL-cholesterol ration and triglycerides and for increasing HDL-C, in hyperlipidemic and dyslipidemic conditions, when response to diet and exercise alone has been inadequate including: Prevention of Cardiovascular Events: In adult patients with an increased risk of atherosclerotic cardiovascular disease based on the presence of cardiovascular disease based on the presence of cardiovascular disease risk markers such as an elevated hsCRP level, age, hypertension, low HDL-C, smoking or a family history of premature coronary heart disease. Rovastin is indicated to reduce total mortality and the risk of major cardiovascular events (cardiovascular death, stroke, MI, unstable angina, or arterial revascularization).
Rovastin is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia).
Primary hypercholesterolaemia (Type IIa including heterozygous familial hypercholesterolaemia and severe non-familial hypercholesterolaemia).
Combined (mixed) dyslipidemia (Type IIb).
Homozygous familial hypercholesterolaemia where Rovastin is used either alone or as an adjunct to diet and other lipid lowering treatment such as apheresis.
Rovastin is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels.
Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH): Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesteroleamia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or> 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors.
Dosage/Direction for Use
Patients should be placed on a standard cholesterol-lowering diet (at least equivalent to the ATP III TLC diet) before receiving Rovastin and should continue on this diet during treatment with Rovastin. If appropriate, a program of weight control and physical exercise should be implemented.
Prior to initiating therapy with Rovastin, secondary causes for elevations in plasma lipid levels should be excluded. A lipid profile should also be performed. After initiation or upon titration of Rovastin, lipid levels should be analyzed within 2-4 weeks and the dosage adjusted accordingly.
The usual recommended starting dose of Rovastin is 10 mg once daily. However, initiation of therapy with 5 mg once daily should be considered for special patient populations or patients requiring less aggressive LDL-C reductions. 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. Rovastin may be taken in the morning or evening, with or without food. The majority of patients are controlled at the 10-mg dose. However, if necessary, dose adjustments to the next dose level can be made after 4-week intervals. The maximum response is usually achieved within 2-4 weeks and is maintained during chronic therapy. Increasing the dose to 40 mg should be reserved for patients with severe hypercholesterolaemia at high cardiovascular risk (in particular those with familial hypercholesterolaemia), who do not achieve their treatment goal on 20 mg and should only be initiated under specialist supervision (see Precautions). The physician who elects to use Rovastin at a dose higher than 20 mg should periodically re-evaluate the long-term risk/benefit of Rovastin for the individual patient. Rovastin should be prescribed with caution in patients with pre-disposing factors for myopathy/rhabdomyolysis (see Precautions).
The dosage of Rovastin should be individualised according to baseline LDL-C, total-C/HDL-C ratio and/or TG levels, the recommended target lipid values and the patient response.
Lipid levels should be monitored periodically and, if necessary, the dose of Rovastin adjusted based on target lipid levels recommended by guidelines.
Patients with Renal Insufficiency: The usual dose range applies in patients with mild to moderate renal impairment. The use of Rovastin in patients with severe renal impairment is contraindicated.
Patients with Hepatic Insufficiency: Rovastin is contraindicated in patients with active liver disease.
Pediatric Patients (10-17 years of age): In pediatric patients (10-17 years) with heterozygous familial hypercholesterolemia (HeFH), the usual dose range of Rovastin is 5-20 mg/day; the maximum recommended dose is 20 mg/day (doses greater than 20 mg have not been studied in this patient population). Doses should be individualized according to the recommended goal of therapy. Adjustments should be made at intervals of 4 weeks or more.
Use in Children below 10 years: The safety and effectiveness in children have not been established. In children and adolescents with homozygous familial hypercholesterolemia, experience is limited to 8 patients (aged 8 years and above).
Dosage in Asian Patients: Initiation of Rovastin therapy with 5 mg once daily should be considered for Asian patients. The potential for increased systemic exposures relative to Caucasians is relevant when considering escalation of dose in cases where hypercholesterolaemia is not adequately controlled at doses of 5, 10 or 20 mg once daily.
Genetic polymorphisms: Specific types of genetic polymorphisms are known that can lead to increase rosuvastatin exposure (see Pharmacology: Pharmacokinetics under Actions). For patients who are known to have such specific types of polymorphisms, a lower daily dose of Rovastin is recommended.
Dosage in patients with pre-disposing factors to myopathy: The recommended start dose is 5mg in patients with pre-disposing factors to myopathy.
Concomitant therapy: Rosuvastatin is a substrate of various transporter proteins (e.g. OATP1B1 and BCRP). The risk of myopathy (including rhabdomyolysis) is increased when rosuvastatin is administered concomitantly with certain medicinal products that may increase the plasma concentration of rosuvastatin due to interactions with these transporter proteins (e.g. certain protease inhibitors including combinations of ritonavir with atazanavir, lopinavir, and/or tipranavir). Whenever possible, alternative medications should be considered, and if necessary, consider temporarily discontinuing Rovastin therapy. In situations where co-administration of these medicinal products with rosuvastatin is unavoidable, the benefit and the risk of concurrent treatment and rosuvastatin dosing adjustments should be carefully considered.
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. Haemodialysis is unlikely to be of benefit.
Rovastin is contraindicated in patients with hypersensitivity to any component of this product.
Rovastin is contraindicated in patients with active liver disease including unexplained, persistent elevations of serum transaminases and any serum transaminase elevation exceeding 3x the upper limit of normal (ULN).
Rovastin is contraindicated during pregnancy, while breast-feeding and in women of child-bearing potential not using appropriate contraceptive measures.
Rovastin is contraindicated in patients with severe renal impairment (creatinine clearance <30ml/min).
Rovastin is contraindicated in patients with myopathy.
Rovastin is contraindicated in patients receiving concomitant cyclosporine.
Special Precautions
Renal Effects: Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated with higher doses of Rovastin, in particular 40 mg, where it was transient or intermittent in most cases. Proteinuria has not been shown to be predictive of acute or progressive renal disease. An assessment of renal function should be considered during routine follow-up of patients treated with a dose of 40 mg.
Skeletal Muscle Effects: Gemfibrozil increases the risk of myopathy when given concomitantly with some HMG-CoA reductase inhibitors. Therefore, the combination of rosuvastation and gemfibrozil is not recommended. The benefit of further alterations in lipid levels by the combined use of rosuvastation with fibrates or niacin should be carefully weighed against the potential risks of such combinations.
Effects on skeletal muscle e.g. myalgia, myopathy and, rarely, rhabdomyolysis have been reported in Rosuvastatin-treated patients with all doses and in particular with doses >20 mg. Very rare cases of rhabdomyolysis have been reported with the use of ezetimibe in combination with HMG-CoA reductase inhibitors. A pharmacodynamic interaction cannot be excluded (see Interactions) and caution should be exercised with their combined use.
As with other HMG-CoA reductase inhibitors, the reporting rate for rhabdomyolysis associated with Rosuvastatin in post-marketing use is higher at the 40 mg dose.
Creatine Kinase Measurement: Creatine 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 (>5xULN) a confirmatory test should be carried out within 5-7 days. If the repeat test confirms a baseline CK >5xULN, treatment should not be started.
Before Treatment: Rovastin, as with other HMG-CoA reductase inhibitors, 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 (see Pharmacology: Pharmacokinetics under Actions, Dosage & Administration and Interactions); Concomitant use of fibrates.
In such patients the risk of treatment should be considered in relation to possible benefit and clinical monitoring is recommended. If CK levels are significantly elevated at baseline (>5xULN) treatment should not be started.
Whilst on Treatment: Patients should be asked to report inexplicable muscle pain, weakness or cramps immediately, particularly if associated with malaise or fever. CK levels should be measured in these patients. Therapy should be discontinued if CK levels are markedly elevated (>5xULN) or if muscular symptoms are severe and cause daily discomfort ( even if CK levels are ≤5x ULN). If symptoms resolve and CK levels return to normal, then consideration should be given to re-introducing Rovastin 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. There have been very rare reports of an immune-mediated necrotising myopathy (IMNM) during or after treatment with statins, including rosuvastatin. IMNM is clinically characterised by proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment.
The combination of Rovastin and gemfibrozil is not recommended. The benefit of further alterations in lipid levels by the combined use of Rovastin with fibrates or niacin should be carefully weighed against the potential risks of such combinations (see Interactions).
Rovastin should not be used in any patient with an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (e.g. sepsis, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders; or uncontrolled seizures).
Liver Effects: As with other HMG-CoA reductase inhibitors, Rovastin 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 initiation of treatment. Rovastin should be discontinued or the dose reduced if the level of serum transaminases is greater than 3 times the upper limit of normal. The reporting rate for serious hepatic events (consisting mainly of increased hepatic transaminases) in post-marketing use is higher at the 40 mg dose. In patients with secondary hypercholesterolaemia caused by hypothyroidism or nephrotic syndrome, the underlying disease should be treated prior to initiating therapy with Rovastin.
Race: Pharmacokinetic studies show an increase in exposure in Asian subjects compared with Caucasians (see Pharmacology: Pharmacokinetics under Actions and Dosage & Administration).
Protease Inhibitors: Increased systemic exposure to rosuvastatin has been observed in subjects receiving rosuvastatin concomitantly with various protease inhibitors in combination with ritonavir. Consideration should be given both to the benefit of lipid lowering by use of Rovastin in HIV patients receiving protease inhibitors and the potential for increased rosuvastatin plasma concentrations when initiating and up titrating Rovastin doses in patients treated with protease inhibitors. The concomitant use with certain protease inhibitors is not recommended unless the dose of Rovastin is adjusted (see Dosage & Administration and Interactions).
Lactose Intolerance: Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
Interstitial Lung Disease: Exceptional cases of interstitial lung disease have been reported with some statins, especially with long term therapy (see Side Effects). Presenting features can include dyspnoea, non-productive cough and deterioration in general health (fatigue, weight loss and fever). If it is suspected a patient has developed interstitial lung disease, statin therapy should be discontinued.
Diabetes Mellitus: Some evidence suggests that statins as a class raise blood glucose and in some patients, at high risk of future diabetes, may produce a level of hyperglycaemia where formal diabetes care is appropriate. This risk, however, is outweighed by the reduction in vascular risk with statins and therefore should not be a reason for stopping statin treatment. Patients at risk (fasting glucose 5.6 to 6.9 mmol/L, BMI >30 kg/m2, raised triglycerides, hypertension) should be monitored both clinically and biochemically according to national guidelines.
Effects on the Ability to Drive or Operate Machinery: From the safety profile, Rovastin is not expected to adversely affect the ability to drive or use machines.
Use In Pregnancy & Lactation
The safety of Rovastin during pregnancy and whilst breastfeeding has not been established. Women of childbearing potential should use appropriate contraceptive measures.
Side Effects
There have been rare post-marketing reports of cognitive impairment (e.g. memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These issues have been reported for all statins. The reports are generally non-serious and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median 3 weeks).
Increases in HbAlc and fasting blood glucose have been reported with statins. The risk of hyperglycemia, however, is outweighed by the reduction in vascular risk with statins.
The adverse reactions seen with Rosuvastatin are generally mild and transient.
Tabulated list of adverse reactions: The frequencies of adverse reactions are ranked according to the following convention: Common (≥1/100 to <1/10); Uncommon (≥1/1,000 to <1/100); Rare (≥1/10,000 to <1/1000); Very rare (<1/10,000); Not known (cannot be estimated from the available data). (See table.)

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As with other HMG-CoA reductase inhibitors, the incidence of adverse drug reactions tends to be dose dependent.
Skeletal muscle effects: A dose-related increase in CK levels has been observed in patients taking rosuvastatin; the majority of cases were mild, asymptomatic and transient. If CK levels are elevated (>5xULN), treatment should be discontinued.
Liver effects: As with other HMG-CoA reductase inhibitors, a dose-related increase in transaminases has been observed in a small number of patients taking rosuvastatin; the majority of cases were mild, asymptomatic and transient.
The following adverse events have been reported with some statins: Sexual dysfunction.
Exceptional cases of interstitial lung disease, especially with long term therapy.
Tendon disorders, sometimes complicated by rupture.
The reporting rates for rhabdomyolysis, serious renal events and serious hepatic events (consisting mainly of increased hepatic transaminases) is higher at the 40 mg dose.
Drug Interactions
Effect of co-administered medicinal products on rosuvastatin: Transporter protein inhibitors: Rosuvastatin is a substrate for certain transporter proteins including the hepatic uptake transporter OATP1B1 and efflux transporter BCRP. Concomitant administration of Rovastin with medicinal products that are inhibitors of these transporter proteins may result in increased rosuvastatin plasma concentrations and an increased risk of myopathy.
Ciclosporin: Rovastin is contraindicated in patients receiving concomitant ciclosporin.
Protease inhibitors: Although the exact mechanism of interaction is unknown, concomitant protease inhibitor use may strongly increase rosuvastatin exposure. For instance, in a pharmacokinetic study, co-administration of 10 mg rosuvastatin and a combination product of two protease inhibitors (300 mg atazanavir/100 mg ritonavir) in healthy volunteers was associated with an approximately three-fold and seven-fold increase in rosuvastatin AUC and Cmax respectively. The concomitant use of Rovastin and some protease inhibitor combinations may be considered after careful consideration of Rovastin dose adjustments based on the expected increase in rosuvastatin exposure.
Gemfibrozil and other lipid-lowering products: Concomitant use of Rovastin and gemfibrozil resulted in a 2-fold increase in rosuvastatin Cmax and AUC (see Precautions).
Based on data from specific interaction studies no pharmacokinetic relevant interaction with fenofibrate is expected, however a pharmacodynamic interaction may occur. 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. These patients should also start with the 5 mg dose.
Ezetimibe: Concomitant use of 10 mg Rovastin and 10 mg ezetimibe resulted in a 1.2 fold increase in AUC of rosuvastatin in hypercholesterolaemic subjects. A pharmacodynamic interaction, in terms of adverse effects, between Rovastin and ezetimibe cannot be ruled out (see Precautions).
Antacid: The simultaneous dosing of Rovastin with an antacid suspension containing aluminium 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 Rovastin. The clinical relevance of this interaction has not been studied.
Fusidic Acid: Interaction studies with rosuvastatin and fusidic acid have not been conducted. As with other statins, muscle related events, including rhabdomyolysis, have been reported in post-marketing experience with rosuvastatin and fusidic acid given concurrently. Patients should be closely monitored and temporary suspension of rosuvastatin treatment may be appropriate.
Erythromycin: Concomitant use of Rovastin 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.
Cytochrome P450 enzymes: Results from in vitro and in vivo studies show that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a poor substrate for these isoenzymes. Therefore, drug interactions resulting from cytochrome P450-mediated metabolism are not expected. No clinically relevant interactions have been observed between rosuvastatin and either fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4).
Interactions requiring rosuvastatin dose adjustments: When it is necessary to co-administer Rovastin with other medicinal products known to increase exposure to rosuvastatin, doses of Rovastin should be adjusted. Start with a 5 mg once daily dose of Rovastin if the expected increase in exposure (AUC) is approximately 2-fold or higher. The maximum daily dose of Rovastin should be adjusted so that the expected rosuvastatin exposure would not likely exceed that of the recommended maximum daily dose of Rovastin taken without interacting medicinal products. For example, where the recommended dose of Rovastin is 20mg; the dose of Rovastin taken with a ritonavir/atazanavir combination (3.1-fold increase) should not exceed 5mg, and the dose of Rovastin taken with gemfibrozil (1.9 fold increase) should not exceed 10mg.
Other medications: Concurrent use of fibrates may cause severe myositis and myoglobinuria.
Effect of rosuvastatin on co-administered medicinal products: Vitamin K antagonists: As with other HMG-CoA reductase inhibitors, the initiation of treatment or dosage up-titration of Rovastin in patients treated concomitantly with vitamin K antagonists (e.g. warfarin or another coumarin anticoagulant) may result in an increase in International Normalised Ratio (INR). Discontinuation or down-titration of Rovastin may result in a decrease in INR. In such situations, appropriate monitoring of INR is desirable.
Oral contraceptive/hormone replacement therapy (HRT): Concomitant use of Rovastin and an oral contraceptive may increase ethinyl estradiol and norgestrel. These increased plasma levels should be considered when selecting oral contraceptive doses. There are no pharmacokinetic data available in subjects taking concomitant Rovastin and HRT and therefore a similar effect cannot be excluded. However, the combination has been extensively used in women in clinical trials and was well tolerated.
Other medicinal products: Digoxin: No clinically relevant interaction with digoxin is expected.
Paediatric population: The extent of interactions in the paediatric population is not known.
Store below 30°C. Store in the original package in order to protect from moisture.
ATC Classification
C10AA07 - rosuvastatin ; Belongs to the class of HMG CoA reductase inhibitors. Used in the treatment of hyperlipidemia.
FC tab 5 mg (round, yellow, engraved with
Click on icon to see table/diagram/image
on one side and plain on the reverse) x 2 x 14's. 10 mg (round, pink, engraved with
Click on icon to see table/diagram/image
on one side and plain on the reverse) x 2 x 14's.
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