* Composition: Each tablet cotains: Rosuvastatin 10 mg (as Rosuvastatin calcium 10.4 mg)* INDICATIONS AND USAGE:  1- As an adjunct to diet o reduce elevated Total-C, LDL-C, ApoB, non-HDL-C, and TG levels and to increase HDL-C in patients with primary  hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson Type IIa and IIb).  2- As an adjunct to diet for the treatment of patients with elevated serum TG levels (Fredrickson Type IV).  3- To reduce LDL-C, total-C, and ApoB in patients with homozygous familial hypercholesterolemia as an adjunct  to other lipid-lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable.  ADVOCHOL has not been studied in Fredrickson Type I, III, and V dyslipidemias.* DOSAGE & ADMINISTRATION:  - The patient should be placed on a standard cholesterol-lowering diet before receiving ADVOCHOL and should  continue on this diet treatment during treatment.  - ADVOCHOL can be administered as a single dose at any time of day, with or without food.  - The recommended starting dose of ADVOCHOL is 10 mg once daily.  # Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia (Fredrickson Type IIa and IIb):  The dose range for ADVOCHOL is 5 to 40 mg once daily. Therapy with ADVOCHOL should be individualized  according to goal of therapy and response. The recommended starting dose of ADVOCHOL is 10 mg once  daily. However, initiation of therapy with 5 mg once daily should be considered for patients requiring less  aggressive LDL-C reductions, who have predisposing factors for myopathy, and as noted below for special  populations such as patients taking cyclosporin, Asian patients, and patients with severe renal insufficiency.  For patients with marked hypercholesterolemia (LDL-C >190 mg/dL) and aggressive lipid targets, a 20-mg  starting dose may be considered. After initiation and/or upon titration of ADVOCHOL, lipid levels should be  analyzed within 2 to 4 weeks and dosage adjusted accordingly.  # Homozygous Familial Hypercholesterolemia:  The recommended starting dose of ADVOCHOL is 20 mg once daily in patients with homozygous FH.  The maximum recommended daily dose is 40 mg. ADVOCHOL should be used in these patients as an adjunct  to other lipid-lowering treatments (e.g., LDL aphaeresis) or if such treatments are unavailable. Response to  therapy should be estimated from pre-aphaeresis LDL-C levels.  # Dosage in patients taking Cyclosporine:  In patients taking cyclosporine, therapy should be limited to ADVOCHOL 5 mg once daily. Concomitant lipid-  lowering therapy. The effect of ADVOCHOL on LDL-C and total-C may be enhanced when used in  combination with a bile acid binding resin. If ADVOCHOL is used in combination with Gemfibrozil, the dose of  ADVOCHOL should be limted to 10 mg once daily.  # Dosage in patients with renal insufficiency: No modification of dosage is necessary for patients with mild  to moderate renal insufficiency. For patients with severe renal impairment (CL cr <30 mL/min/1.73 m2) not on  Hemodialysis, dosing of ADVOCHOL should be started at 5 mg once daily and not to exceed 10 mg once daily.* CONTRAINDICATIONS:  - ADVOCHOL is contraindicated in patients with a known hypersensitivity to any component of this product.  - ADVOCHOL is contraindicated in patients with active liver disease or with unexplained persistent elevations of  serum transaminases.  - Pregnancy and Lactation: ADVOCHOL should be administered to women of childbearing age only when such  patients are highly unlikely to conceive and have been informed of the potential hazards. If the patient becomes  pregnant while taking this drug, therapy should be discontinued immediately and the patient apprised of the  potential hazard to the fetus.* WARNINGS:  - Liver enzymes: HMG-CoA reductase inhibitors, like some other lipid-lowering therapies, have been associated  with biochemical abnormalities of liver function. The incidence of persistent elevations (<3 times the upper limit  of normal [ULN] occuring on 2 or more consecutive occasions) in serum transaminases in fixed dose studies  was 0.4, 0, 0, and 0.1% in patients who received rosuvastatin 5, 10, 20, 40 mg, respectively. In most cases, the  elevations were transient and resolved or improved on continued therapy or after a brief interruption in therapy.  There were no cases of liver failure or irreversible liver disease in these trials. It is recommended that liver function  tests be performed before and at 12 weeks following both the initiation of therapy and any elevation of dose, and  periodically (e.g., semiannually) thereafter. Liver enzyme changes generally occur in the first 3 months of  treatment with rosuvastatin. Patients who develop increased transaminase levels should be monitored until the  abnormalities have resolved. Should an increase in ALT or AST of >3 times ULN persist, reduction of dose or  withdrawal of rosuvastatin is recommended. Rosuvastatin should be used with caution in patients who consume  substantial quantities of alcohol and/or have a history of liver disease. (Active liver disease or unexplained  persistent transaminase elevations are contraindications of the use of rosuvastatin).* PRECAUTIONS:  # General:  Before instituting therapy with rosuvastatin, any attempt should be made to control hypercholesterolemia with  appropriate diet and exercise, weight reduction in obese patients, and treatment of underlying medical problems.  Administration of rosuvastatin 20 mg to patients with severe renal impairment (CL cr <30 mL/min/1.73 m2)  resulted in a 3-fold increase in plasma concentrations of rosuvastatin compared with healthy volunteers.  # Endocrine Function:  Although clinical studies have shown that rosuvastatin alone does not reduce basal plasma cortisol concentration  or impair adrenal reserve, caution should be exercised if any HMG-CoA reductase inhibitor or other agent used to  lower cholesterol levels is administered concomitantly with drugs that may decrease the levels or activity of  endogenous steroid hormones such as ketoconazole, spironolactone, and cimetidine.  # Carcinogenesis, Mutagenesis, Impairment of Fertility:  Rosuvastatin was not mutagenic or clastogenic with or without metabolic activation in the Ames test with  Salmonella typhimurium and Escherichia coli, the mouse lymphoma assay, and the chromosomal aberration assay  in Chinese hamster lung cells. Rosuvastatin was negative in the in-vivo mouse micronucleus tests.* PREGNANCY CATEGORY X:  Rosuvastatin may cause fetal harm when administered to a pregnant woman. Rosuvastatin is contraindicated in  women who are or may become pregnant. Safety in pregnant women has not been established. There are no  adequate and well-controlled studies of rosuvastatin in pregnant women. If this drug is administered to a woman  with reproductive potential, the patient should be apprised of the potential hazard to a fetus. Rosuvastatin was not  teratogenic in rats   exposure at 40 mg/day based on AUC or body surface comparison, respectively.* NURSING MOTHERS:  It is not known whether rosuvastatin is excreted in human milk. A decision should be made whether to discontinue  nursing or administration of rosuvastatin taking into account the importance of the drug to the lactating woman.* Pediatric Use: The safety and effectiveness in pediatric patients have not been established.* Geriatric Use: The efficacy of rosuvastatin in the geriatric population (>/=65 years of age) was comparable  to the efficacy observed in the non-elderly.* Store at room temperature. Keep in a temperature below 30 degrees C, in a dry place. Protect from moisture.* Produced by: El-obour, for: Delta Pharma S.A.E. - A.R.E. Sole Agent: Advocure Pharmaceutical Co.