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Zimvastin contains Simvastatin, a cholesterol lowering agent, a synthetic derivative of a fermentation product from Aspergillus terreus.

Once orally absorbed, simvastatin, which is an inactive lactose, is transformed by hydrolysis into the corresponding B-hydroxy acid. The latter is a major metabolite and an inhibitor of 3-hydroxymethylglutaryl coenzyme A (HGM-CoA) reductase, an enzyme that catalyzes an early and speed limiting step in cholesterol biosynthesis. As a result, simvastatin reduces plasma concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, and very low-density lipoprotein (VLDL) cholesterol. In addition, simvastatin moderately increases high-density lipoprotein (HDL) cholesterol and lowers plasma triglycerides.

In animal studies, orally administered simvastatin had high selectivity for the liver, where it reached higher concentrations than in other tissues. Simvastatin undergoes considerable first-pass extraction from the liver, its primary point of action, with subsequent excretion of the drug into the bile. In man, the systemic exposure to the active form of simvastatin has been found to be less than 5% of the orally administered dose, and 95% of that portion binds to plasma proteins.


  • Decrease in elevated concentrations of total cholesterol and LDL cholesterol in patients with primary hypercholesterolemia, when the response to diet and other non-pharmacological measures alone has been insufficient. Simvastatin increases HDL cholesterol and therefore lowers LDL / HDL and total / HDL cholesterol.
  • Decrease in elevated concentrations of total cholesterol and LDL cholesterol in patients with primary hypercholesterolemia and combined hypertriglyceridemia, when hypercholesterolemia is the most important abnormality.
  • Treatment to slow the progression of coronary atherosclerosis, including the development of new lesions or total occlusions, in patients with coronary heart disease.

Coronary cardiopathy:

In patients with coronary heart disease simvastatin is indicated for:

  • Reduce the risk of coronary heart death and non-fatal myocardial infarction.
  • Decrease the likelihood of requiring myocardial revascularization operations (coronary bypass graft or percutaneous transluminal coronary angioplasty).
  • Delay the progression of coronary atherosclerosis including the development of new lesions and total occlusions.



Liver effects:

Liver function tests are recommended for all patients before starting treatment and periodically for the first year (every six months) or one year after the last dose adjustment. Attention should be paid to those with an increase in serum transaminases and the measurement of these should be repeated soon after and more frequently during treatment. If transaminases continue to increase, particularly if they reach three times the upper limit of their normal values ​​and the increase is persistent, the administration of the drug should be discontinued.

Simvastatin should be used with caution in patients whose unexplained increases in transaminases are contraindications to the use of simvastatin.

Muscle effects:

In rare cases, treatment with HMG-CoA reductase inhibitors has been associated with myopathy (minus 0.1%). This possibility should be considered in any patient who presents with diffuse myalgia, muscular hyperesthesia and / or a considerable increase in creatine phosphokinase (up to values ​​more than ten times greater than the upper limit of the normal limits).

Patients should be instructed to report unexplained pain, hyperesthesia, or muscle weakness promptly, and simvastatin should be discontinued if creatine phosphokinase is greatly increased or if myopathy is diagnosed or suspected.

The risk of myopathy is known to be increased when an HMG-CoA reductase inhibitor and immunosuppressants (including cyclosporins), fibrate or doses of niacin (nicotinic acid), lipid lowering, are used concurrently.

There have been rare reports of severe rhabdomyolysis with secondary acute renal failure. Therefore, the benefits and risks of concomitant use of simvastatin and immunosuppressive medications fibrates or doses of niacin (nicotinic acid), lipid lowering agents, should be carefully considered.

HMG-CoA reductase inhibitors and azole-derived antifungal agents inhibit cholesterol biosynthesis at different points. If they require systemic antifungal therapy with an azole derivative in patients receiving cyclosporine, the administration of simvastatin should be temporarily discontinued, and those taking cyclosporine should be carefully monitored.

Treatment with HMG-CoA reductase inhibitors should be temporarily discontinued or discontinued in all patients who have an acute severe disorder suggesting myopathy or who have a risk factor predisposing to the development of renal insufficiency in the event of rhabdomyolysis.

Pregnancy: Simvastatin is contraindicated during pregnancy. A few reports of congenital abnormalities have been received in newborns whose mothers were treated with HMG-CoA reductase inhibitors during pregnancy.

Nursing Mothers: It is not known whether simvastatin or its metabolites are excreted in human milk. As many medications are excreted by this route, and due to the risk of serious adverse reactions, mothers taking simvastatin should not breastfeed their children.

Use in children: Until now, the use of simvastatin in children is not recommended.

Homozygous familial hypercholesterolemia: in patients with the homozygous form of familial hypercholesterolemia, who are completely lacking in LDL receptors, treatment with simvastatin is unlikely to produce any clinical benefit.

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Drug interactions

Cumarin derivatives: in patients taking anticoagulants, the prothrombin time should be determined before starting treatment with simvastatin, and afterwards at the intervals usually recommended during the use of these anticoagulants.


Delicate medicine, use only under medical prescription.

Side effects

Simvastatin is generally well tolerated; Most of the observed side effects have been mild and transient.

In all controlled clinical studies, the side effects that occurred 1% higher were abdominal pain, constipation, and flatulence. Other side effects that occurred in 0.5% to 0.9% of the patients were asthenia and headache. In rare cases, myopathy has been observed.

The following additional side effects have been observed in uncontrolled clinical trials or since the product was placed on the market: nausea, diarrhea, skin rash, pruritus, dyspepsia, alopecia, dizziness, muscle cramps, myalgia, vomiting and anemia.


It is recommended before starting simvastatin treatment to put the patient on a standard diet to lower cholesterol and continue that diet throughout the treatment.

Hyperlipidemia: The usual initial dosage is 10mg daily, administered in a single dose at night. Dosage adjustments, if necessary, should be made at intervals of not less than four weeks.

If the plasma LDL cholesterol concentration decreases to less than 75 mg / dl (1.94mm / 1/1) or the total cholesterol concentration decreases to less than 140 mg / dl (3.5 mm / 1/1), it is it is advisable to decrease the dosage of simvastatin.

Coronary atherosclerosis: The initial dosage is simvastatin 20 mg daily in a single dose at night, and the dosage is reduced if the total plasma cholesterol concentration decreases to less than 110mg / dl (285mm / 1/1).

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Zimvastin 20

Each coated tablet contains:

Simvastatin 20mg

C.S.P. excipients

Zimvastin 40

Each coated tablet contains:

Simvastatin 40mg

C.S.P. excipients

Administration route



Zimvastin 20: Box with 20 coated tablets.

Zimvastin 40: Box with 20 coated tablets.

Storage recommendation

Store below 30 ° C. Protect it from moisture.


    • Hypersensitivity to any component of this product.
    • Active liver disease or unexplained persistent increase in serum transminases.
    • Pregnancy and lactation.


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