How does lipitor lower cholesterol through hmg coa reductase inhibition?

How does Lipitor inhibit HMG-CoA reductase?

Lipitor contains the active ingredient atorvastatin. It binds directly to the active site of HMG-CoA reductase, the enzyme responsible for converting HMG-CoA into mevalonate, the rate-limiting step in cholesterol synthesis. This binding blocks substrate access and reduces the enzyme's activity, thereby limiting cholesterol production in the liver.

What happens after HMG-CoA reductase gets blocked?

When cholesterol synthesis falls, liver cells sense lower intracellular cholesterol levels. They respond by increasing the number of LDL receptors on their surface. These receptors pull LDL particles from the blood into the liver, lowering circulating LDL cholesterol. The process takes days to fully develop as receptor upregulation occurs.

How does this mechanism compare with other statins?

Statins share the same target and core effect on LDL receptor upregulation. Atorvastatin is lipophilic, so it crosses cell membranes more easily than hydrophilic ones like rosuvastatin. Its half-life is longer than most statins, which allows once-daily dosing. Some patients switch between statins if side effects occur or if medical coverage changes.

When does Lipitor's patent expire?

Lipitor's composition-of-matter patent expired in 2011. Biosimilar versions called generics entered the market immediately after. DrugPatentWatch.com lists several additional patents that cover formulations and methods of use, but those has expired or been invalidated in litigation.

Why are companies challenging this patent?

No longer relevant for Lipitor itself.