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Protein / target

Vasopressin-neurophysin 2-copeptin

Encoded byAVPP01185Homo sapiensSwiss-Prot
UniProt: P01185Ensembl: ENSG00000101200HGNC: HGNC:894NCBI Gene: 551
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Neurohypophyseal hormone

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene AVP · 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

Precursor of Arg-vasopressin, an antidiuretic hormone, and neurophysin 2, its carrier protein

Subcellular location

Cytoplasmic vesicle, secretory vesicleSecreted
Domains and Gene Ontology detail (49)

Gene Ontology

  • Cclathrin-coated endocytic vesicle membrane
  • Ccytosol
  • Cdendrite
  • Cextracellular region
  • Cextracellular space
  • Cneuronal dense core vesicle
  • Csecretory granule
  • Fhormone activity
  • Fneurohypophyseal hormone activity
  • Fneuropeptide hormone activity
  • Fprotein kinase activity
  • Fsignaling receptor binding

164 aa · 17 kDa

Biological roles

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

Cell proliferation & survivalGO
View supporting evidence

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

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 AVP

Gene-level evidence surfaced through the gene AVP that 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.

Genetic Diseases, Inborn
0.32Limited support

Genetic evidence dominant · Open Targets 0.19

Autistic Disorder
0.30Preliminary

Animal model evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Stroke
0.14Preliminary

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

Hydrops fetalis
0.14Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Diabetes Mellitus
0.14Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

View evidence synthesis (5)
Genetic Diseases, InbornLimited support
0.32
agreement 0.18–0.46
Genetic98%Literature2%

Open Targets aggregate 0.19 · 2 independent evidence families

Autistic DisorderPreliminary
0.30
agreement 0.12–0.48
Animal model65%Literature35%

Open Targets aggregate 0.11 · 2 independent evidence families · no direct causal or clinical evidence

StrokePreliminary
0.14
agreement 0.00–0.41
Literature100%

Open Targets aggregate 0.12 · 1 independent evidence family · no direct causal or clinical evidence

Hydrops fetalisPreliminary
0.14
agreement 0.00–0.41
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Diabetes MellitusPreliminary
0.14
agreement 0.00–0.41
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · 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
Genetic Diseases, Inborn0.19
Stroke0.12
Hydrops fetalis0.11
Diabetes Mellitus0.11
Polycystic Kidney, Autosomal Dominant0.11
Autistic Disorder0.11

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

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

View underlying tractability evidence (4)
SM · Structure with LigandAB · GO CC high confAB · UniProt loc med 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

GLP-1 receptor agonists may enhance the effects of desmopressin in individuals with AVP deficiency: a case series and proposed mechanism.7 cites

Nakhleh A · Pituitary · 2024

Recent

GLP-1 receptor agonists may enhance the effects of desmopressin in individuals with AVP deficiency: a case series and proposed mechanism.

Nakhleh A · Pituitary · 2024

Europe PMC papers linked directly to this protein.