HomeAboutRankingsData Sources
Β© 2026 GeneE
🧬
GeneE
25 sources retrieved Β· Most recent: April 2026 Β· Index updated 15 days ago
β“˜GeneE is for informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment.
APOC3
apolipoprotein C3
Chromosome 11 Β· 11q23.3
NCBI Gene: 345Ensembl: ENSG00000110245.13HGNC: HGNC:610UniProt: A3KPE2
469PubMed Papers
21Diseases
3Drugs
2Pathogenic Variants
FUNCTIONAL ROLE
Hub GeneTransporter
RESEARCH IMPACT
Highly StudiedTrending
CLINICAL
FDA Approved TargetOMIM Disease Gene
DATA QUALITY
βœ“ Experimental GO Evidenceβœ“ Swiss-Prot Reviewed
phospholipid bindingextracellular exosomechylomicronspherical high-density lipoprotein particleapolipoprotein c-III deficiencyHypertriglyceridemiacoronary artery diseasefamilial chylomicronemia syndrome
✦AI Summary

APOC3 encodes apolipoprotein C3, a key regulator of triglyceride homeostasis that plays a crucial role in lipid metabolism 1. The protein functions as a component of triglyceride-rich very low density lipoproteins (VLDL) and high density lipoproteins (HDL) in plasma, where it promotes hepatic VLDL assembly and secretion intracellularly while attenuating hydrolysis and clearance of triglyceride-rich lipoproteins extracellularly 1. APOC3 impairs lipolysis by inhibiting lipoprotein lipase and reduces hepatic uptake of triglyceride-rich lipoproteins by remnant receptors 1. Therapeutically, APOC3 has emerged as a genetically validated target for triglyceride lowering, with antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) targeting APOC3 showing significant efficacy in reducing triglyceride levels in clinical trials 234. These therapies demonstrate substantial triglyceride reductions of 49-62% compared to placebo in patients with hypertriglyceridemia 23. APOC3 inhibition represents a promising therapeutic approach for severe hypertriglyceridemia, which poses risks for atherosclerotic cardiovascular disease and acute pancreatitis 56. The protein's role in triglyceride metabolism makes it particularly relevant for treating familial chylomicronemia syndrome and mixed hyperlipidemia 6.

Sources cited
1
APOC3 is a regulator of triglyceride metabolism and component of VLDL and HDL that promotes VLDL assembly while attenuating triglyceride-rich lipoprotein clearance
PMID: 38583092
2
APOC3 is a genetically validated target for triglyceride lowering, with olezarsen ASO reducing triglyceride levels by 49-53% in clinical trials
PMID: 38587249
3
Plozasiran siRNA targeting APOC3 significantly reduced triglyceride levels by 49-62% compared to placebo in mixed hyperlipidemia patients
PMID: 38804517
4
Olezarsen treatment resulted in 58-61% placebo-adjusted reduction in triglyceride levels in patients with moderate hypertriglyceridemia
PMID: 40888739
5
Severe hypertriglyceridemia poses risks for acute pancreatitis, with APOC3-targeting therapies being developed as treatment options
PMID: 37642858
6
APOC3 inhibition is relevant for treating familial chylomicronemia syndrome and other triglyceride metabolism disorders
PMID: 40257687
Disease Associationsβ“˜21
apolipoprotein c-III deficiencyOpen Targets
0.61Moderate
HypertriglyceridemiaOpen Targets
0.52Moderate
coronary artery diseaseOpen Targets
0.51Moderate
familial chylomicronemia syndromeOpen Targets
0.50Moderate
familial lipoprotein lipase deficiencyOpen Targets
0.47Moderate
cardiovascular diseaseOpen Targets
0.41Moderate
cholesterol-ester transfer protein deficiencyOpen Targets
0.40Weak
HypercholesterolemiaOpen Targets
0.38Weak
diabetes mellitusOpen Targets
0.38Weak
hyperalphalipoproteinemiaOpen Targets
0.37Weak
small intestine neoplasmOpen Targets
0.37Weak
metabolic diseaseOpen Targets
0.36Weak
placental retentionOpen Targets
0.32Weak
familial hyperlipidemiaOpen Targets
0.31Weak
hyperlipoproteinemiaOpen Targets
0.26Weak
Disorder of lipid metabolismOpen Targets
0.22Weak
amyloidosisOpen Targets
0.20Weak
Abnormality of the cardiovascular systemOpen Targets
0.19Weak
familial partial lipodystrophyOpen Targets
0.19Weak
type 2 diabetes mellitusOpen Targets
0.12Weak
Hyperalphalipoproteinemia 2UniProt
Pathogenic Variants2
NM_000040.3(APOC3):c.232A>G (p.Lys78Glu)Pathogenic
Apolipoprotein c-III deficiency
β˜†β˜†β˜†β˜†1991β†’ Residue 78
NM_000040.3(APOC3):c.280A>G (p.Thr94Ala)Pathogenic
Apolipoprotein C-III, nonglycosylated
β˜†β˜†β˜†β˜†1987β†’ Residue 94
View on ClinVar β†—
Drug Targets3
OLEZARSENApproved
Apolipoprotein C-III mRNA antisense inhibitor
familial lipoprotein lipase deficiency
VOLANESORSENApproved
Apolipoprotein C-III mRNA 3'UTR antisense inhibitor
cardiovascular disease
VOLANESORSEN SODIUMPhase II
Apolipoprotein C-III mRNA 3'UTR antisense inhibitor
lipodystrophy
Related Genes
AHSGProtein interaction99%ALBProtein interaction99%AMBPProtein interaction99%LCATProtein interaction99%F2Protein interaction98%ABCA1Protein interaction98%
Tissue Expression6 tissues
Liver
100%
Ovary
0%
Brain
0%
Heart
0%
Lung
0%
Bone Marrow
0%
Gene Interaction Network
Click a node to explore
APOC3AHSGALBAMBPLCATF2ABCA1
PROTEIN STRUCTURE
Preparing viewer…
PDB2JQ3 Β· NMR
View on RCSB β†—
Constraintβ“˜
LOEUFβ“˜
1.68LoF Tolerant
pLIβ“˜
0.00Tolerant
Observed/Expected LoF0.97 [0.56–1.68]
RankingsWhere APOC3 stands among ~20K protein-coding genes
  • #573of 20,598
    Most Researched469 Β· top 5%
  • #513of 1,025
    FDA-Approved Drug Targets2
  • #4,197of 5,498
    Most Pathogenic Variants2
  • #16,018of 17,882
    Most Constrained (LOEUF)1.68
Genes detectedAPOC3
Sources retrieved25 papers
Response timeβ€”
πŸ“„ Sources
25β–Ό
1
Plozasiran (ARO-APOC3) for Severe Hypertriglyceridemia: The SHASTA-2 Randomized Clinical Trial.
PMID: 38583092
JAMA Cardiol Β· 2024
1.00
2
Updates in Drug Treatment of Severe Hypertriglyceridemia.
PMID: 37642858
Curr Atheroscler Rep Β· 2023
0.90
3
APOC3 siRNA and ASO therapy for dyslipidemia.
PMID: 38334488
Curr Opin Endocrinol Diabetes Obes Β· 2024
0.80
4
Advances in Treatment of Dyslipidemia.
PMID: 37686091
Int J Mol Sci Β· 2023
0.70
5
Characterising metabolomic signatures of lipid-modifying therapies through drug target mendelian randomisation.
PMID: 35213538
PLoS Biol Β· 2022
0.68