Each film-coated tablet contains

Atorvastatin calcium equivalent to Atorvastatin....... 10 mg

Fenofibrate BP (micronised)............. 160 mg



Atorvastatin is a selective competitive inhibitor of 3-hydroxy-3-methyl-glutarylcoenzymeA (HMG-CoA) reductase enzyme. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate limiting step in the synthesis of cholesterol.
The primary site of action of HMG-CoA reductase inhibitors is the liver. Inhibition of cholesterol synthesis in the liver leads to upregulation of LDL-receptors and an increase in LDL- catabolism. There is also some reduction of LDL-production as a result of inhibition of hepatic synthesis of very low density lipoprotein (VLDL), the precursor of LDL-cholesterol. Atorvastatin reduces total cholesterol, LDLcholesterol and apo B in patients with homozygous and heterozygous familial hypercholesterolemia, non familial forms of hypercholesterolemia and mixed dyslipidemias. Atorvastatin also reduces VLDL-cholesterol and triglycerides and produces variable increases in HDL-cholesterol and apolipoprotein A1.Atorvastatin reduces total cholesterol, LDL-cholesterol, VLDL-cholesterol, apoB,triglycerides, and non-HDL- cholesterol, and increases HDL-cholesterol in patients with isolated hypertriglyceridemia. Atorvastatin also reduces intermediate density lipoprotein (IDL) cholesterol in patients with dysbetalipoproteinemia.
Atorvastatin as well as some of its metabolites are pharmacologically active in humans. Drug dosage rather than systemic drug concentration correlates better with LDL-cholesterol reduction. Individualization of drug dosage should be based on therapeutic response.
Fenofibrate (micronized) is a lipid regulating agent. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total-C, LDL-C, apo B, total triglycerides and VLDL in treated patients. In addition, treatment with fenofibrate results in increases in HDL-C and apoproteins apoAI and apoAII. The effects of fenofibric acid seen in clinical practice have been explained by the activation of peroxisome proliferator activated receptor (alpha) [PPAR (alpha)]. Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity). The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. Activation of PPAR (alpha) also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol. 
Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Combined hyperlipidemia
ATORNET-F is indicated as an adjunct to diet to reduce elevated total-C,LDL-C, apo B, and TG levels and to increase HDL-C in these patients. Lipid altering agents should be used in addition to diet restricted in saturated fat and cholesterol only when the response to diet and other nonpharmacological measures has been inadequate [ see National Cholesterol Education Program (NCEP) Guidelines, summarized in the table below]
Risk category LDL goal (mg/dl) LDL level at which to consider drug therapy (mg/dl)
CHD or CHD risk equivalents* 
(10-yr risk>20%)
<100 >=130 
(100 - 129: drug optional)
2+ risk factors ** (10-yr risk < 20%) <130 10 - yr risk 10%-20%: >=130 
10-yr risk <10%: >=160
0-1 risk factor ** <160 (160-189; LDL-lowering drug optional)

*Coronary heart disease or peripheral vascular disease (including symptomatic carotid artery disease).** Other risk factors for coronary heart disease (CHD) include: age (males>=45 years, females>=55 years or premature menopause without estrogen replacement therapy); family history of premature CHD; current cigarette smoking; hypertension, confirmed HDL-C =<40 mg/dL ( =< 0.91 mmol/L); and diabetes mellitus. Subtract 1 risk factor if HDL-C is>=60 mg/dL ( >=1.6 mmol/L). After the LDL - C goal has been achieved, if the triglyceride level is still >=200 mg/dl, non HDL-C (total cholesterol minus HDL-C) becomes a secondary target of therapy. Non HDL - C goals are set 30 mg/dl higher than LDL-C goals for each risk category.

Patients should be placed on an appropriate lipid-lowering diet before receiving ATORNET-F, and should continue this diet during treatment. ATORNET-F should be given with meals, thereby optimizing the bioavailability of the medication. The recommended dosage is one tablet once daily Dosage in patients taking Cyclosporine, Clarithromycin or A combination of Ritonavir plus Saquinavir or Lopinavir plus Ritonavir. In patients taking cyclosporine, therapy should be limited to atorvastatin 10 mg once daily. In patients taking clarithromycin or in patients with HIV taking a combination of ritonavir plus saquinavir or lopinavir plus ritonavir, for doses of atorvastatin exceeding 20 mg appropriate clinical assessment is recommended to ensure that the lowest dose necessary of atorvastatin is employed.

        Hypersensitivity to either component
        Hepatic or severe renal dysfunction, including primary biliary cirrhosis, and patients with                       unexplained persistent liver function abnormality
        Unexplained persistent elevations of serum transaminases exceeding three times the upper                  limit of normal
        Preexisting gallbladder disease
        Pregnancy and Lactation