Statins: Rosuvastatin, Sinvastatin, Pravastatin, Lovastatin, Fluvastatin, Atorvastatin, Pitavastatin.

These drugs act by inhibiting the enzyme HMG-CoA reductase, thus reducing the synthesis of cholesterol in the liver.

Through this effect, through a negative feedback mechanism, it increases the synthesis of LDL-cholesterol receptors, which increase the uptake of blood cholesterol by the liver, thereby decreasing its plasma concentration, favoring cardiovascular health.

Fibrates: Fenofibrate, Gemfibrozil, Bezafibrate

act as agonists of the PPAR-α receptor, thus decreasing the synthesis and export of TAG by the liver, in addition to increasing the production of HDL molecules.

Ezetimibe

It acts by inhibiting the NCP 1L1 enzyme, which is found at the level of intestinal vellosities (this enzyme allows the lipids to be incorporated into the micelles for later digestion and absorption). This leads to a decrease in the absorption of cholesterol from the diet.

Through a negative feedback mechanism, at the liver level, it increases the synthesis of LDL-cholesterol receptors to increase the plasma uptake of the same.

PSK-9 Inhibitors: Alirocumab, Evolocumab

They are monoclonal antibodies that act by inhibiting PCSK-9, which is a mediator that acts by binding to LDL-receptors to lead them to cytoplasmic internalization and subsequent destruction. Thus, LDL-cholesterol receptors remain active in the plasma membrane.

Bile acid binders: Cholestyramine, Colestipol, Colesevelam

These drugs bind to bile acids at the level of intestinal lysis, in a non-resorbable manner, inhibiting the entero-hepatic circuit, thus increasing fecal excretion of cholesterol.

Other: Omega-3, Nicotinic acid, Phytosterols

They decrease the synthesis of LDL, LDL and TAG.