-5%
Atorvastatin selectively inhibits HMG-CoA reductase, the enzyme responsible for converting HMG-CoA into mevalonate, a precursor in cholesterol biosynthesis. By blocking this pathway, atorvastatin reduces cholesterol synthesis in the liver and increases hepatic LDL receptor expression, thereby enhancing LDL clearance from circulation.
- Absorption: Rapidly absorbed, with peak plasma levels in 1–2 hours. Oral bioavailability ≈ 14%, systemic inhibitory activity ≈ 30%.
- Distribution: Widely distributed (Vd ~381 L), ~98% protein bound, minimal entry into red blood cells. Likely excreted in breast milk.
- Metabolism: Extensively metabolized via CYP3A4 into active hydroxy metabolites, contributing ~70% of overall activity.
- Excretion: Primarily eliminated in bile; minimal urinary excretion (<2%). Half-life ≈ 14 hrs; inhibitory activity persists 20–30 hrs due to active metabolites.
Atova is prescribed alongside dietary measures to help lower elevated levels of total cholesterol, LDL cholesterol, apolipoprotein B (Apo-B), and triglycerides when lifestyle modification alone is insufficient. It is indicated for:
- Lowering total and LDL cholesterol in patients with heterozygous or homozygous familial hypercholesterolemia.
- Reducing elevated cholesterol and triglycerides in mixed dyslipidemia (Fredrickson Type IIa and IIb).
- Treating hypertriglyceridemia (Fredrickson Type IV).
- Managing dysbetalipoproteinemia (Fredrickson Type III).
- Reducing ischemic cardiac events in patients with asymptomatic or mild-to-moderate coronary artery disease who have elevated LDL-C.
- Lowering cholesterol in patients with hypercholesterolemia related to diabetes mellitus or renal transplantation.