Atorlip Tablets (Atorvastatin Calcium)

Composition

ATORLIP-5

Each film-coated tablet contains:

Atorvastatin Calcium

equivalent to Atorvastatin: 5 mg

ATORLIP-10

Each film-coated tablet contains:

Atorvastatin Calcium

equivalent to Atorvastatin: 10 mg

ATORLIP-20

Each film-coated tablet contains:

Atorvastatin Calcium

equivalent to Atorvastatin: 20 mg

ATORLIP-40

Each film-coated tablet contains:

Atorvastatin Calcium

equivalent to Atorvastatin: 40 mg

ATORLIP-80

Each film-coated tablet contains:

Atorvastatin Calcium

equivalent to Atorvastatin: 80 mg

Dosage Form

Film-coated tablet
Pharmacology
Pharmacodynamics

Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme that converts HMG-CoA to mevalonate, a precursor of sterols, including cholesterol. Atorvastatin reduces low density lipoprotein (LDL) production and the number of LDL particles. Triglycerides (TG) and cholesterol in the liver are incorporated into very low density lipoprotein (VLDL) and released into the plasma for delivery to peripheral tissues. LDL is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor.

In animal models, atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL; atorvastatin also reduces LDL production and the number of LDL particles. Atorvastatin reduces LDL-C in some patients with homozygous familial hypercholesterolemia (HoFH), a population that rarely responds to other lipid-lowering medication(s).

Atorvastatin has been shown to reduce concentrations of total-C (30%-46%), LDL-C (41%-61%), ApoB (34%-50%), and TG (14%-33%) while producing variable increases in HDL-C and ApoA1 in a dose response study. These results are consistent in patients with heterozygous familial hypercholesterolemia (HeFH), nonfamilial forms of hypercholesterolemia, and mixed hyperlipidemia, including patients with noninsulin-dependent diabetes mellitus. Reductions in total-C, LDL-C, and ApoB have been proven to reduce risk for cardiovascular events and cardiovascular mortality.

Atorvastatin, as well as some of its metabolites, are pharmacologically active in humans. The liver is the primary site of action and the principal site of cholesterol synthesis and LDL clearance. Drug dosage, rather than systemic drug concentration, correlates better with LDL-C reduction. Individualization of drug dosage should be based on therapeutic response.