Table 2.

Current therapies for primary hyperlipidemias

Drug	Mechanism of action	Indications	LDL-C	HDL-C	TG	Lp(a)	ApoB
Statins	Inhibits HMG-CoA reductase	Hypercholesterolemia	↓20–60%	↑5–15%	↓0–35%	↑8–24%	↓20–30%
Fibrates	PPAR alpha agonist	Hypertriglyceridemia	↓0–15%	↑5–15%	↓20–50%	↑12%	↓11%
Ezetimibe	Inhibits NPC1L1	Hypercholesterolemia	↓15–25%	↑1–3%	↓10–20%	-	↓11–17%
PCSK9 inhibitors	mAb targeting PCSK9	Hypercholesterolemia	↓50–60%	↑5–15%	↓5–20%	↓6.2–46.7%	↓40–62%
Bempedoic acid	ATP- citrate lyase	Hypercholesterolemia	↓15–25%	↓5–6%	No change	↑2.4%	↓8–13.2%
Volanesorsen	ASO inhibiting APOC3	MCS and mixed hyperlipidemia	↑136%	↓40%	↓58.9–88.5%	–	↑20%
Olezarsen	ASO inhibiting APOC3	MCS and mixed hyperlipidemia	↑7.7–9.9%	↑39.6%	↓49–53.1%	–	18.2–18.5%
Plozasiran	siRNA APOC3	Mixed hyperlipidemia	↓0.9–10%	↑37–50%	↓49–62%	↑19–33.9%	↓9.5–18.3%
Evinacumab	ASO inhibiting ANGPTL3	Mixed hyperlipidemia Hypercholesterolemia	↓29.9–47.2%	↓19–27.9%	↓38–53.4%	↓8.9–10.3%	↓19.9–38.8%
Zodasiran	siRNA-inhibiting ANGPTL3	Mixed hyperlipidemia	↓7.3–15.8%	↓7.8–24.5%	↓52–63%	↓3.3–20%	↓6.8–21.9%
Solbisiran	siRNA-inhibiting ANGPTL3	Mixed hyperlipidemia (Not published)	–	–	–	–	–
LYS3475766	mAb-targeting ANGPTL3/8 complex	Mixed hyperlipidemia (Not published)	↓17–37%	↓37%	↓59–70%	–	–

LDL-C low-density lipoprotein cholesterol, TG triglycerides, HDL-C high-density lipoprotein cholesterol, Lp(a) lipoprotein (a), apoB apolipoprotein B, HMG-CoA β-hydroxy β-methylglutaryl-CoA, PPAR β-hydroxy β-methylglutaryl-CoA, NPC1L1 Niemann–Pick C1-like 1, mAb monoclonal antibody, PCSK9 proprotein convertase subtilisin/kexin type 9, ATP adenosine triphosphate, ASO antisense oligonucleotide, APOC3 apolipoprotein C-III gene, siRNA silencing ribonucleic acid, ANGPTL3 angiopoietin-like protein 3