AT1 receptor; NPC1L1; HMG-CoA reductase

Class

Triple fixed-dose combination — fimasartan (angiotensin II receptor blocker) + ezetimibe (cholesterol absorption inhibitor) + atorvastatin (HMG-CoA reductase inhibitor/statin)

Pathway

Combined blood-pressure lowering (renin-angiotensin system blockade) and lipid-lowering (intestinal cholesterol absorption inhibition + hepatic cholesterol synthesis inhibition)

This combination targets three distinct molecular points that together govern two major cardiovascular risk factors: elevated blood pressure and abnormal blood lipids. The angiotensin II type 1 (AT1) receptor is the primary site through which angiotensin II raises blood pressure by constricting blood vessels and promoting sodium retention; blocking it lowers blood pressure and reduces the workload on the heart. Separately, cholesterol levels are governed by two supply routes: absorption from the intestine, mediated by the transporter NPC1L1, and synthesis in the liver, catalyzed by the enzyme HMG-CoA reductase. Inhibiting NPC1L1 reduces cholesterol uptake from the diet and bile, while inhibiting HMG-CoA reductase reduces the liver's own cholesterol production; used together, these two lipid-lowering actions are complementary because blocking one pathway partially unmasks compensatory upregulation of the other, and combining them allows lower doses of each. Fixed-dose combination of an AT1 blocker with a cholesterol-absorption inhibitor and a statin addresses hypertension and dyslipidemia simultaneously, which is clinically relevant because these risk factors frequently coexist and jointly drive atherosclerotic disease and cardiovascular events. This approach broadly matters wherever multiple risk factors must be controlled concurrently with a single regimen.