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Protein / target

Vascular endothelial growth factor C

Encoded byVEGFCP49767Homo sapiensSwiss-Prot
UniProt: P49767Ensembl: ENSG00000150630HGNC: HGNC:12682NCBI Gene: 7424
Clinical-stage
Therapeutic maturity
1
Clinical candidates
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Vascular endothelial growth factor receptor 3 binding

Strongest disease association

Hypothyroidism

Via encoding gene VEGFC · Genetic evidence · score 0.87

Therapeutic position

Clinically advancing target

Research activity

Emerging research

1 papers · latest 2020

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

Growth factor active in angiogenesis, and endothelial cell growth, stimulating their proliferation and migration and also has effects on the permeability of blood vessels.

View complete UniProt function annotation

Growth factor active in angiogenesis, and endothelial cell growth, stimulating their proliferation and migration and also has effects on the permeability of blood vessels. May function in angiogenesis of the venous and lymphatic vascular systems during embryogenesis, and also in the maintenance of differentiated lymphatic endothelium in adults. Binds and activates KDR/VEGFR2 and FLT4/VEGFR3 receptors

Subcellular location

Secreted
Domains and Gene Ontology detail (27)

Gene Ontology

  • Cextracellular region
  • Cextracellular space
  • Cmembrane
  • Cplatelet alpha granule lumen
  • Fchemoattractant activity
  • Fgrowth factor activity
  • Fvascular endothelial growth factor receptor 3 binding
  • Pcell differentiation
  • Pinduction of positive chemotaxis
  • Pnegative regulation of blood pressure
  • Pnegative regulation of osteoblast differentiation
  • Ppositive regulation of angiogenesis

419 aa · 47 kDa

Biological roles

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

Cell migrationGOGrowth-factor signallingGOCell proliferation & survivalGOImmune signallingGO
View supporting evidence

Cell migration

  • ·induction of positive chemotaxis
  • ·positive regulation of blood vessel endothelial cell migration
  • ·positive regulation of mast cell chemotaxis
  • ·substrate-dependent cell migration

Growth-factor signalling

  • ·regulation of vascular endothelial growth factor receptor signaling pathway
  • ·vascular endothelial growth factor receptor signaling pathway

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Immune signalling

  • ·positive regulation of mast cell chemotaxis
  • ·substrate-dependent cell migration

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 VEGFC

Gene-level evidence surfaced through the gene VEGFCthat 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.

Hypothyroidism
0.87Well supported

Genetic evidence dominant · Open Targets 0.53

Milroy disease
0.79Well supported

Genetic evidence dominant · Open Targets 0.62

Thyroid Diseases
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.41

Alzheimer's Disease
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

Diabetic macular edema
0.42Limited support

Clinical evidence dominant · Open Targets 0.34

View evidence synthesis (5)
HypothyroidismWell supported
0.87
agreement 0.73–1.00
Genetic100%Literature0%

Open Targets aggregate 0.53 · 2 independent evidence families

Milroy diseaseWell supported
0.79
agreement 0.67–0.91
Genetic75%Animal model23%Literature2%Genetic literaturedup

Open Targets aggregate 0.62 · 3 independent evidence families · 1 not counted as duplicate

Thyroid DiseasesModerately supported
0.68
agreement 0.54–0.82
Genetic98%Literature2%

Open Targets aggregate 0.41 · 2 independent evidence families

Alzheimer's DiseaseModerately supported
0.55
agreement 0.41–0.69
Genetic88%Literature12%

Open Targets aggregate 0.33 · 2 independent evidence families

Diabetic macular edemaLimited support
0.42
agreement 0.26–0.57
Clinical98%Literature2%

Open Targets aggregate 0.34 · 2 independent evidence families

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. 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
Milroy disease0.62
Hypothyroidism0.53
Thyroid Diseases0.41
Neurodegenerative Diseases0.37
Diabetic macular edema0.34
Alzheimer's Disease0.33
Macular retinal edema0.33
Choroidal neovascularization0.28

Drug development

1 compounds recorded · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (1)
CONBERCEPTPhase 3

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Antibodies — Emerging

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

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (4)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2020

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

Most cited

Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis.292 cites

Bolte AC · Nature communications · 2020

Recent

Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis.

Bolte AC · Nature communications · 2020

Europe PMC papers linked directly to this protein.