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Jits-40 (Esomeprazole pellets (enteric coated) 40mg)Luxafen Gel (Diclofenac Diethylammonium 1.16g)

Kolmark-10 Tablets(Atorvastatin (as calcium trihydrate)10mg)

Kolmark-10 Tablets(Atorvastatin (as calcium trihydrate)10mg)

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KOLMARK (c) is a synthetic lipid lowering agent. Atorvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-co-enzymes A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. Chemically, Atorvastatin calcium is [R-(R*, R*)]-2-(4-fluorophenyl)-ß, S- dihydroxy-5-(1-methylethyl)-3-phenyl-4[(phenylamino) carbonyl]-1 H-pyrrole-1 heptanoic acid, calcium salt (2:1) trihydrate.
The molecular formula is (C33H34FN2O5)2Ca*3H2O and the structural formula is:


KOLMARK (Atorvastatin) is available for oral administration as:

  • KOLMARK Tablet 10mg
    Each film-coated tablet contains:
    (as calcium trihydrate salt)
  • KOLMARK Tablet 20mg
    Each film-coated tablet contains:
    (as calcium trihydrate salt)


Mechanism of Action:
Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methyl-glutaryl-co-enzyme A (HMG-CoA) reductase, the rate-limiting enzyme responsible for the conversion of HMG-CoA to mevalonate, a precursor of sterols, including cholesterol. The primary site of action of HMG-CoA reductase inhibition 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, LDL-cholesterol and apo-Protein B in patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed dyslipidemias. Atorvastatin also reduces VLDL-cholesterol and triglyceroides and produces variable increases in HDL-cholesterol and Apo-Lipoprotein A 1.


Atorvastatin is rapidly absorbed after oral administration, maximum plasma concentrations occur within 1 to 2 hours. Extent of absorption increases in proportion to Atorvastatin dose. The absolute bioavailability of Atorvastatin is approximately 12% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%. The low systemic availability is attributed to presystemic clearance in gastrointestinal mucosa and/or hepatic first-pass metabolism. Although food decreases the rate and extent of drug absorption by approximately 25% and 9%, respectively, as assessed by Cmax and AUC, LDL-C reduction is similar whether Atorvastatin is given with or without food. Plasma Atorvastatin concentrations are lower (approximately 30% for Cmax and AUC) following evening drug administration compared with morning. However, LDL-C reduction is the same regardless of the time of day of drug administration.


Mean volume of distribution of Atorvastatin is approximately 381 Liters. Atorvastatin is 98% bound to plasma proteins. A blood/plasma ratio of approximately 0.25 indicates poor drug penetration into red blood cells.


Atorvastatin is metabolized by the cytochrome P450 isoenzyme CYP3A4 to ortho-and parahydroxylated derivatives and various beta-oxidation products. In vitro inhibition of HMG-CoA reductase by ortho-and parahydroxylated metabolites is equivalent to that of Atorvastatin. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites.


Atorvastatin and its metabolites are eliminated primarily in bile following hepatic and extra-hepatic metabolism. Mean plasma elimination half-life of atorvastatin in humans is approximately 14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20 to 30 hours due to the contribution of active metabolites.

Special Populations
Plasma concentrations of atorvastatin are higher (approximately 40% for Cmax and 30% for AUC) in healthy elderly subjects than in young adults.Studies suggest that there is a greater degree of LDL-Iowering at any dose of drug in the elderly patient population compared to younger.

Pharmacokinetic data in the pediatric population are not available.

Plasma concentrations of atorvastatin in women differ from those in men (approximately 20% higher for Cmax and 10% lower for AUC); however, there is no clinically significant difference in LDL -C reduction between men and women.

Renal Insufficiency
Renal disease has no influence on the plasma concentrations or LDL-C reduction of atorvastatin; thus, dose adjustment in patients with renal dysfunction is not necessary.

Hepatic Insufficiency
In patients with chronic alcoholic liver disease, plasma concentrations of atorvastatin are markedly increased. Cmax and AUC are each 4-fold greater in patients with Childs-Pugh A disease. Cmax and AUC are approximately 16-fold and 11-fold increased, respectively, in patients with Childs-Pugh B disease.


KOLMARK (Atorvastatin) is indicated:

  • As an adjunct to diet to reduce elevated Total-C, LDL-C, Apolipoprotein B, and Triglyceroides levels and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia.
  • As an adjunct to diet for the treatment of patients with elevated serum TG levels (Hypertrigiyceridaemia/Fredrickson Type IV).
  • For the treatment of patients with primary dysbetalipoproteinemia (Fredrickson Type III) who do not respond adequately to diet.
  • To reduce Total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to diet and other non-pharmacological or lipid lowering treatments (e.g. LDL apheresis) or if such treatments are unavailable or inadequate.
  • As an adjunct to diet to reduce Total-C, LDL-C, and Apolipoprotein B levels in children with heterozygous familial hypercholesterolemia, if after an adequate trial of diet therapy LDL-C remains 190mg/dl or LDL-C remains 160mg/dl with positive family history of premature cardiovascular disease and/or two or more other CVD risk factors are present in the pediatric patient.


The patient should be placed on a standard cholesterol-lowering diet before receiving KOLMARK and should continue on this diet during treatment with KOLMARK.
Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia (Fredrickson Types IIa and lib) The recommended starting dose of KOLMARK is 10mg or 20mg once daily. Patients who require a large reduction in LDL-C (more than 45%) may be started at 40mg once daily. The dosage range of KOLMARK is 10mg to 80mg once daily. KOLMARK can be administered as a single dose at any time of the day, with or without food. The starting dose and maintenance doses of KOLMARK should be individualized according to patient characteristics such as goal of therapy and response. After initiationt he recommended starting dose of KOLMARK is 10mg or 20mg once daily. Patients who require a large reduction in LDL-C (more than 45%) may be started at 40mg once daily. The dosage range of KOLMARK is 10mg to 80mg once daily. KOLMARK can be administered as a single dose at any time of the day, with or without food. The starting dose and maintenance doses of KOLMARK should be individualized according to patient characteristics such as goal of therapy and response. After initiation and/or upon titration of KOLMARK. lipid levels should be analyzed within 2 to 4 weeks and dosage adjusted accordingly. Heterozygous Familial Hypercholesterolemia in Children (10-17 years of age). The recommended starting dose of KOLMARK is 10mg once daily; or 20mg once daily. Adjustments should be made at intervals of 4 weeks or more. Homozygous Familial Hypercholesterolemiat the dosage of KOLMARK in patients with homozygous FH is 10mg to 80mg daily. Kolmark should be used as an adjunct to other lipid-lowering treatments (e.g. LDL apheresis) in these patients or if such treatments are unavailable.

The following Guidelines may be used to establish treatment goals:

  • 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 35mg/dL ( 0.91 mmol/l); and diabetes mellitus. Subtract 1 risk factor if HDL-C is > 60mg/dl ( 1.6mmol/l).


Atorvastatin is generally well tolerated. Adverse effects reported commonly include constipation, flatulence, dyspepsia, abdominal pain, headache, dizziness, nausea, myalgia, diarrhoea, asthenia and insomnia, skin rashes, infection.
The following additional adverse effects have been reported very rarely: pancretitis, hepatitis, hypersensitivity syndrome including angioedema, muscle pain or weakness associated with elevated serum CPK levels.


  • Atorvastatin is contraindicated in patients with hypersensitivity to any component of this medication.
  • Atorvastatin is also contraindicated in patients with active liver disease or unexplained persistent elevations of serum transaminases.
  • Safety of atorvastatin in pregnancy has not been established, and is contraindicated for use during pregnancy.
  • Use of atorvastatin during breast feeding is not recommended, because of the potential for serious adverse effects in nursing infants.


Before initiation of therapy with atorvastatin, an attempt should be made to control hypercholesterolemia with appropriate diet, exercise, and weight reduction in obese patients, and to treat other underlying medical problems.

Liver function abnormalities:
HMG-CoA reductase inhibitors, like some other lipid lowering therapies, have been associated with biochemical abnormalities of liver function. Liver function tests should be performed before treatment starts, at 6 weeks and 12 weeks after initiation of therapy and any elevation in dose, and periodically thereafter. Liver enzyme changes generally occur in the first three months of treatment with atorvastatin. Patients who develop increased transaminase levels should be monitored until the abnormalities resolved. Should a dose-related and reversible increase in serum ALT or AST of >3 times the upper limit of normal persists; reduction of dose or withdrawal of atorvastatin is recommended. The drug should be used with caution in patients who consume substantial quantities of alcohol and/or have past history of liver disease.

Skeletal Muscle:
Atorvastatin therapy should be temporarily withheld or discontinued in any patient with an acute, serious condition suggestive of a myopathy of having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (e.g. severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures). Patients should be advised to report promptly any unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever.

Atorvastatin should be administered to women of childbearing age only when such patients are unlikely to conceive and have been informed of the potential hazards. Women of childbearing potential should use adequate contraceptive measures while taking atorvastatin.

Pediatric use:
Treatment experience in a pediatric population is limited to doses of atorvastatin upto 80mg daily for 1 year. No clinical and biochemical abnormalities reported in these patients.

Drug Interactions:
Cyclosporine, fibric acid derivatives, erythromycin, azole antifungals or niacin:
The risk ot myopathy during treatment with drugs belonging to the class of HMG-CoA reductase inhibitors is increased with concurrent administration of these agents.
Antacid: Decreased plasma concentration of atorvastatin may occur when administered along with an oral antacid suspension containing magnesium and aluminium hydroxides, however LDL-cholesterol reduction is not altered.
Digoxin: When multiple doses of atorvastatin and digoxin were coadministered, steady state plasma digoxin concentrations increased by approximately 20%. Patients taking digoxin should be monitored appropriately.
Erythromycin: Plasma concentrations of atorvastatin increased approximately 40% with coadministration of atorvastatin and erythromycin, a known inhibitor of cytochrome P450.
Oral Contraceptives: Coadministration of atorvastatin and an oral contraceptive increased AUC values for nor ethindrone and ethinyl estradiol by approximately 30% and 20%. These increases should be considered when selecting an oral contraceptive for a woman taking atorvastatin.

Store below 30°C.
Protect from sunlight and moisture.
The expiration date refers to the product correctly stored at the required conditions.

KOLMARK (Atorvastatin) Tablets 10mg are available in blister pack of 10's.

KOLMARK (Atorvastatin) Tablets 20mg are available in blister pack of 10's.

Keep out of reach of children.

Please read the contents carefully before use.
This package insert is continually updated from time to time.