Statins – The Cornerstone Drugs Inhibiting Cholesterol Synthesis
Mechanism of action: Inhibit HMG-CoA reductase to block hepatic cholesterol synthesis.
Lipid-lowering features: Significantly reduce LDL-C (by 30%–50%), mildly reduce TG, and increase HDL-C.
Representative drugs: Atorvastatin, Rosuvastatin, Simvastatin, etc.
Clinical status: First-line medications for hypercholesterolemia, atherosclerosis, and cardiovascular disease prevention.
Fibrates – Key Triglyceride Regulators
Mechanism of action: Activate PPAR-α to promote TG breakdown and lipoprotein metabolism.
Lipid-lowering features: Significantly reduce TG (by 30%–50%), mildly reduce LDL-C, and increase HDL-C.
Representative drugs: Fenofibrate, Gemfibrozil.
Clinical application: Hypertriglyceridemia (especially when TG > 5.65 mmol/L) to prevent acute pancreatitis.
Cholesterol Absorption Inhibitors – Auxiliary Intestinal Lipid-lowering Drugs
Mechanism of action: Inhibit intestinal NPC1L1 protein to reduce dietary and biliary cholesterol absorption.
Lipid-lowering features: Monotherapy reduces LDL-C by ~15%, often combined with statins for enhanced efficacy.
Representative drugs: Ezetimibe, Hezetimibe.
Clinical application: For patients intolerant to statins or with insufficient response to monotherapy, as part of combination regimens.
PCSK9 Inhibitors – Potent Biological Agents
Mechanism of action: Inhibit PCSK9 via monoclonal antibodies, reducing LDL receptor degradation and accelerating LDL-C clearance.
Lipid-lowering features: Reduce LDL-C by 50%–70%, currently the most potent lipid-lowering drugs.
Representative drugs: Alirocumab, Evolocumab.
Clinical application: Familial hypercholesterolemia, refractory hyperlipidemia, or patients failing to achieve targets with statin + ezetimibe.
Niacin – Broad-spectrum Lipid-modifying Agents
Mechanism of action: Inhibit adipocyte lipolysis, reduce free fatty acid release, and suppress VLDL and LDL synthesis.
Lipid-lowering features: Reduce LDL-C and TG, increase HDL-C (the most comprehensive lipid regulation profile).
Representative drugs: Nicotinic acid, Acipimox (a derivative with fewer side effects).
Clinical status: Due to side effects like flushing and hyperglycemia, clinical use has decreased, reserved for specific mixed hyperlipidemia cases.
Bile Acid Sequestrants (Resins) – Intestinal Bile Acid Binding Agents
Mechanism of action: Bind to bile acids in the intestine, prompting the liver to convert cholesterol into bile acids, thus lowering blood cholesterol.
Lipid-lowering features: Reduce LDL-C with minimal effect on TG.
Representative drugs: Cholestyramine, Colestipol.
Clinical application: Suitable for hypercholesterolemia (e.g., pregnant women intolerant to statins), but less used as first-line due to poor palatability and interference with other drug absorption.
Supplementary Notes
Classification of novel drugs: Agents like omega-3 fatty acids, bempedoic acid (ACL inhibitor), and inclisiran (siRNA drug) are typically excluded from the "six classic categories" due to unique mechanisms or limited clinical prevalence, but they remain important adjuncts in lipid-lowering therapy.
Combination therapy principle: Clinically, these drugs are often combined (e.g., statin + ezetimibe, statin + PCSK9 inhibitor) to achieve optimal lipid-lowering effects and cardiovascular protection.
For further details on side effects or medication precautions for specific categories, please specify your needs.