How lipid-lowering medicines work

Click a numbered badge, a table row or a pathway tour. Filled badge = approved in the US · open badge = investigational in the US · colour = type of drug. Status as of 25 Oct 2026.

Lowers
Status
Type
SMALL INTESTINE BLOOD LIVER CELL (HEPATOCYTE) Gut lumendietary + biliarycholesterol bile acids enterocyte NPC1L1 cholesterol → cholesteryl ester + apoB-48 + triglyceride MTP chylomicron(TG-rich) via lymph to blood Less cholesterol absorbed, or more bile acid lost → the liver pulls more LDL out of the blood. PCSK9 in circulation binds LDL receptors → destroyed PCSK9 LDL Lp(a)LDL particle + apo(a) tail LDLapoB-100 cleared by LDL receptors HDL CETP moves cholesteryl ester HDL → apoB particles VLDL /chylomicron apoC-III remnants → LDL capillary wall LPL TG lipolysis ANG3 ANGPTL3 and apoC-III brake LPL LDL receptor endosome recycles lysosome with PCSK9 → destroyed nucleus protein secretedto blood ← mRNAgene (DNA) PCSK9 PCSK9 ANGPTL3 ANGPTL3 LPA apo(a) APOC3 apoC-III PPARα ↑ LPL, ↓ apoC-III SREBP-2: low cholesterol→ more LDLR (and PCSK9) siRNA: RISC cuts the mRNAASO: RNase H1 degrades it GalNAc tag → liver uptake gene editing: one-time DNA change Cholesterol synthesis Citrate Acetyl-CoA HMG-CoA Mevalonate ACL HMGCR Cholesterol apoB-100 + TG MTP VLDL assembly and secretion
US-approvedInvestigational (US)Dashed moving arrows = particle flow · bar-ended lines = inhibition
#AgentTarget · siteType · dosingMain effectUS status

Main effect = placebo-adjusted change where reported, from the pivotal or largest published trial of each agent (linked to PubMed). These are not head-to-head comparisons. Investigational agents are available only in clinical trials. Educational material prepared by Preval Health; not medical advice or prescribing guidance. Background artwork is AI-generated illustration and is decorative only; all labels and data are in the diagram layer.