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Protein / target

Angiopoietin-like protein 8

Encoded byANGPTL8Q6UXH0Homo sapiensSwiss-Prot
UniProt: Q6UXH0Ensembl: ENSG00000130173HGNC: HGNC:24933NCBI Gene: 55908
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Hormone

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene ANGPTL8 · Genetic evidence · score 0.31

Research activity

Emerging research

1 papers · latest 2024

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Hormone that acts as a blood lipid regulator by regulating serum triglyceride levels.

View complete UniProt function annotation

Hormone that acts as a blood lipid regulator by regulating serum triglyceride levels (PubMed:22569073, PubMed:22809513, PubMed:23150577). May be involved in the metabolic transition between fasting and refeeding: required to direct fatty acids to adipose tissue for storage in the fed state (By similarity)

Subcellular location

Secreted
Domains and Gene Ontology detail (7)

Gene Ontology

  • Cextracellular region
  • Fhormone activity
  • Plipid metabolic process
  • Ppositive regulation of protein processing
  • Pregulation of lipid metabolic process
  • Pregulation of lipoprotein metabolic process
  • Ptriglyceride homeostasis

198 aa · 22 kDa

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Lipid & lipoprotein metabolismUniProt · GO
View supporting evidence

Lipid & lipoprotein metabolism

  • ·Hormone that acts as a blood lipid regulator by regulating serum triglyceride levels (Pu…
  • ·lipid metabolic process
  • ·regulation of lipid metabolic process
  • ·regulation of lipoprotein metabolic process

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene ANGPTL8

Gene-level evidence surfaced through the gene ANGPTL8that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Diabetes Mellitus, Type 2
0.35Limited support

Genetic literature evidence dominant · Open Targets 0.21

Genetic Diseases, Inborn
0.31Limited support

Genetic evidence dominant · Open Targets 0.19

Hypertension
0.29Limited support

Genetic evidence dominant · Open Targets 0.15

Diabetes Mellitus, Type 1
0.29Limited support

Genetic literature evidence dominant · Open Targets 0.20

Obesity due to melanocortin 4 receptor deficiency
0.22Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

View evidence synthesis (5)
Diabetes Mellitus, Type 2Limited support
0.35
agreement 0.20–0.51
Genetic literature63%Literature38%

Open Targets aggregate 0.21 · 2 independent evidence families

Genetic Diseases, InbornLimited support
0.31
agreement 0.19–0.43
Genetic100%

Open Targets aggregate 0.19 · 1 independent evidence family

HypertensionLimited support
0.29
agreement 0.16–0.43
Genetic65%Literature36%

Open Targets aggregate 0.15 · 2 independent evidence families

Diabetes Mellitus, Type 1Limited support
0.29
agreement 0.14–0.45
Genetic literature78%Literature22%

Open Targets aggregate 0.20 · 2 independent evidence families

Obesity due to melanocortin 4 receptor deficiencyPreliminary
0.22
agreement 0.04–0.40
Literature56%Animal model44%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Diabetes Mellitus, Type 20.21
Diabetes Mellitus, Type 10.20
Genetic Diseases, Inborn0.19
Hypertension0.15
Obesity due to melanocortin 4 receptor deficiency0.12
Diabetes, Gestational0.12

Tractability

Antibodies — Emerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (3)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMM

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2024

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Inhibition of ANGPTL8 protects against diabetes-associated cognitive dysfunction by reducing synaptic loss via the PirB signaling pathway.10 cites

Meng X · Journal of neuroinflammation · 2024

Recent

Inhibition of ANGPTL8 protects against diabetes-associated cognitive dysfunction by reducing synaptic loss via the PirB signaling pathway.

Meng X · Journal of neuroinflammation · 2024

Europe PMC papers linked directly to this protein.