Fenostad 160

Fenofibrate, a fibric acid derivative, is a hypolipidemic drug. By inhibiting the hepatic biosynthesis of cholesterol, fenofibrate reduces atherogenic fractions and raises the production of HDL and reduces blood triglycerides. Thus, the repartition of plasma cholesterol is markedly ameliorated.

Pack size Box of 30 tablets, 100 tablets
Shelf-life 48 months
Composition Fenofibrate
Dosage forms and strengths Film-coated tablet: 160 mg
Product code :



Fenostad 160 is indicated as an adjunct to diet and other non-pharmacological treatment (e.g. exercise, weight reduction) for the following:

  • Treatment of severe hypertriglyceridaemia with or without low HDL cholesterol.
  • Mixed hyperlipidaemia when a statin is contraindicated or not tolerated or in patients at high cardiovascular risk in addition to a statin when triglycerides and HDL cholesterol are not adequately controlled.


  • Adults, geriatric populations:
    The recommended dose is one tablet containing 160 mg fenofibrate taken once daily. Patients currently taking one fenofibrate 200 mg capsule can be changed to one fenofibrate 160 mg tablet without further dose adjustment.
  • Renal impairment:
    Dosage reduction is required.
  • Severe chronic kidney disease, hepatic impairment, children < 18 years:
    Fenofibrate is not recommended for use.


  • Fenostad 160 should be swallowed whole during a meal.
  • Dietary measures initiated before therapy should be continued.
  • Known hypersensitivity to any of the ingredients.
  • Severe renal dysfunction.
  • Hepatic insufficiency (including biliary cirrhosis and unexplained persistent liver function abnormality).
  • Chronic or acute pancreatitis with the exception of acute pancreatitis due to severe hypertriglyceridemia.
  • Known photoallergy or phototoxic reaction during treatment with fibrates or ketoprofen.
  • Known gallbladder disease.


  • Gastrointestinal disorders, epigastric fullness, nausea, meteorism, mild diarrhea;
  • Hives, urticaria, cutaneous non-specific rash;
  • Rise in serum transaminases;
  • Muscular pain.
  • Secondary causes of hyperlipidemia:
    Secondary cause of hypercholesterolemia, such as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver disease or alcoholism should be adequately treated before fenofibrate therapy is considered. Secondary cause of hypercholesterolemia related to pharmacological treatment can be seen with diuretics, β-blocking agents, estrogens, progestogens, combined oral contraceptives, immunosuppressive agents and protease inhibitors. In these cases, it should be ascertained whether the hyperlipidaemia is of primary or secondary nature (possible elevation of lipid values caused by these therapeutic agents).
  • Liver function:
    As with other lipid lowering agents, increases have been reported in transaminase levels in some patients. In the majority of cases, these elevations were transient, minor and asymptomatic. It is recommended that transaminase levels are monitored every 3 months during the first 12 months of treatment and thereafter periodically. Attention should be paid to patients who develop increase in transaminase levels and therapy should be discontinued if AST (SGOT) and ALT (SGPT) levels increase to more than 3 times the upper limit of the normal range. When symptoms indicative of hepatitis occur (e.g. jaundice, pruritus), and diagnosis is confirmed by laboratory testing, fenofibrate therapy should be discontinued.
  • Pancreas:
    Pancreatitis has been reported in patients taking fenofibrate. This occurrence may represent a failure of efficacy in patients with severe hypertriglyceridemia, a direct drug effect, or a secondary phenomenon mediated through biliary tract stone or sludge formation with obstruction of the common bile duct.
  • Muscle:
    Muscle toxicity, including rare cases of rhabdomyolysis, with or without renal failure, has been reported with administration of fibrates and other lipid-lowering agents. The incidence of this disorder increases in case of hypoalbuminaemia and previous renal insufficiency. Patients with pre-disposing factors for myopathy and/or rhabdomyolysis, including age above 70 years, personal or familial history of hereditary muscular disorders, renal impairment, hypothyroidism and high alcohol intake, may be at an increased risk of developing rhabdomyolysis. For these patients, the putative benefits and risks of fenofibrate therapy should be carefully weighed up.
    Muscle toxicity should be suspected in patients presenting diffuse myalgia, myositis, muscular cramps and weakness and/or marked increases in CPK (levels exceeding 5 times the upper normal range). In such cases treatment with fenofibrate should be stopped.
    The risk of muscle toxicity may be increased if the drug is administered with another fibrate or an HMG-CoA reductase inhibitor, especially in case of pre-existing muscular disease. Consequently, the co-prescription of fenofibrate with HMG-CoA reductase inhibitor or another fibrate should be reserved to patients with severe combined dyslipidaemia and high cardiovascular risk without any history of muscular disease and with a close monitoring of potential muscle toxicity.
  • Renal function:
    Fenofibrate 160 mg is contraindicated in severe renal impairment.
    Fenofibrate 160 mg should be used with caution in patients with mild to moderate renal insufficiency. Dose should be adjusted in patients whose estimated glomerular filtration rate is 30 to 59 mL/min/1.73 m2.
    Reversible elevations in serum creatinine have been reported in patients receiving fenofibrate monotherapy or co-administered with statins. Elevations in serum creatinine were generally stable over time with no evidence for continued increases in serum creatinine with long term therapy and tended to return to baseline following discontinuation of treatment.
    During clinical trials, 10% of patients had a creatinine increase from baseline greater than 30 μmol/L with co-administered fenofibrate and simvastatin versus 4.4% with statin monotherapy. 0.3% of patients receiving co-administration had clinically relevant increases in creatinine to values > 200 μmol/L.
    Treatment should be interrupted when creatinine level is 50% above the upper limit of normal. It is recommended that creatinine is measured during the first 3 months after initiation of treatment and periodically thereafter.
  • Fenostad 160 contains lactose. Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicine.
  • Fenostad 160 contains less than 1 mmol sodium (23 mg) per tablet, that is to say essentially “sodium-free”.
  • This drug should not be used during pregnancy and lactation.
  • None effect on ability to drive and use machines has been noted.