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Protein / target

Hepatocyte growth factor

Encoded byHGFP14210Homo sapiensSwiss-Prot
UniProt: P14210Ensembl: ENSG00000019991HGNC: HGNC:4893NCBI Gene: 3082
Clinical-stage
Therapeutic maturity
2
Clinical candidates
Small-molecule tractable
Druggability
Structure with Ligand
1
Research papers

Protein at a glance

Biological role

Signaling receptor binding

Strongest disease association

Hearing loss, autosomal recessive

Via encoding gene HGF · Genetic evidence · score 0.74

Therapeutic position

Clinically advancing target

Antibodies

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

Potent mitogen for mature parenchymal hepatocyte cells, seems to be a hepatotrophic factor, and acts as a growth factor for a broad spectrum of tissues and cell types.

View complete UniProt function annotation

Potent mitogen for mature parenchymal hepatocyte cells, seems to be a hepatotrophic factor, and acts as a growth factor for a broad spectrum of tissues and cell types (PubMed:20624990). Activating ligand for the receptor tyrosine kinase MET by binding to it and promoting its dimerization (PubMed:15167892, PubMed:20977675). Activates MAPK signaling following TMPRSS13 cleavage and activation (PubMed:20977675)

Domains and Gene Ontology detail (30)

Domains & features

PANKringle 1Kringle 2Kringle 3Kringle 4Peptidase S1

Gene Ontology

  • Cextracellular region
  • Cextracellular space
  • Cmembrane
  • Cplatelet alpha granule lumen
  • Fchemoattractant activity
  • Fgrowth factor activity
  • Fidentical protein binding
  • Fsignaling receptor binding
  • Pcell chemotaxis
  • Pcellular response to hepatocyte growth factor stimulus
  • Pepithelial to mesenchymal transition
  • Phepatocyte growth factor receptor signaling pathway

728 aa · 83 kDa · 6 isoforms

Biological roles

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

Cell migrationGOReceptor tyrosine kinase signallingUniProtGrowth-factor signallingGOCell-cycle regulationGOApoptosis & cell deathGO
View supporting evidence

Cell migration

  • ·cell chemotaxis
  • ·positive regulation of cell migration

Receptor tyrosine kinase signalling

  • ·Potent mitogen for mature parenchymal hepatocyte cells, seems to be a hepatotrophic fact…

Growth-factor signalling

  • ·hepatocyte growth factor receptor signaling pathway

Cell-cycle regulation

  • ·mitotic cell cycle

Apoptosis & cell death

  • ·negative regulation of apoptotic process
  • ·negative regulation of hydrogen peroxide-mediated programmed cell death

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 HGF

Gene-level evidence surfaced through the gene HGFthat 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.

Hearing loss, autosomal recessive
0.82Well supported

Genetic evidence dominant · Open Targets 0.61

Prostate carcinoma
0.70Moderately supported

Genetic evidence dominant · Open Targets 0.40

Gastric adenocarcinoma
0.59Moderately supported

Clinical evidence dominant · Open Targets 0.41

Gastroesophageal junction adenocarcinoma
0.59Moderately supported

Clinical evidence dominant · Open Targets 0.40

Deafness
0.58Moderately supported

Genetic literature evidence dominant · Open Targets 0.39

View evidence synthesis (5)
Hearing loss, autosomal recessiveWell supported
0.82
agreement 0.69–0.94
Genetic72%Animal model28%Genetic literaturedup

Open Targets aggregate 0.61 · 2 independent evidence families · 1 not counted as duplicate

Prostate carcinomaModerately supported
0.70
agreement 0.59–0.81
Genetic58%Somatic mutation33%Literature9%

Open Targets aggregate 0.40 · 3 independent evidence families

Gastric adenocarcinomaModerately supported
0.59
agreement 0.47–0.71
Clinical57%Somatic mutation41%Literature3%

Open Targets aggregate 0.41 · 3 independent evidence families

Gastroesophageal junction adenocarcinomaModerately supported
0.59
agreement 0.47–0.71
Clinical58%Somatic mutation42%Literature1%

Open Targets aggregate 0.40 · 3 independent evidence families

DeafnessModerately supported
0.58
agreement 0.46–0.71
Genetic literature55%Animal model41%Literature5%

Open Targets aggregate 0.39 · 3 independent evidence families

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
Hearing loss, autosomal recessive0.61
Gastric adenocarcinoma0.41
Gastroesophageal junction adenocarcinoma0.40
Prostate carcinoma0.40
Melanoma0.40
Lung carcinoma0.40
Neoplasms0.40
Deafness0.39
Adenocarcinoma of Lung0.39

Drug development

2 compounds recorded · 2 in clinical development

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

View all recorded compounds (2)
FICLATUZUMABPhase 3
RILOTUMUMABPhase 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

Small molecules — Emerging

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

Antibodies — Strong

Advanced Clinical and GO CC high conf support this modality.

Protein degraders — Emerging

Feasibility evidence (small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (7)
SM · Structure with LigandSM · High-Quality PocketSM · Druggable FamilyAB · Advanced ClinicalAB · GO CC high confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of transcription factor activityToxCast

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

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

Inhibiting Hippo pathway kinases releases WWC1 to promote AMPAR-dependent synaptic plasticity and long-term memory in mice.17 cites

Stepan J · Science signaling · 2024

Recent

Inhibiting Hippo pathway kinases releases WWC1 to promote AMPAR-dependent synaptic plasticity and long-term memory in mice.

Stepan J · Science signaling · 2024

Europe PMC papers linked directly to this protein.