Protein / target

Fibroblast growth factor 2

Encoded byFGF2P09038Homo sapiensSwiss-Prot

UniProt: P09038 Ensembl: ENSG00000138685 HGNC: HGNC:3676 NCBI Gene: 2247

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Fibroblast growth factor receptor binding

Strongest disease association

Dermatitis, Atopic

Via encoding gene FGF2 · Genetic evidence · score 0.56

Therapeutic position

Clinically advancing target

Research activity

Emerging research

3 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

Acts as a ligand for FGFR1, FGFR2, FGFR3 and FGFR4.

View complete UniProt function annotation

Acts as a ligand for FGFR1, FGFR2, FGFR3 and FGFR4 (PubMed:8663044). Also acts as an integrin ligand which is required for FGF2 signaling (PubMed:28302677). Binds to integrin ITGAV:ITGB3 (PubMed:28302677). Plays an important role in the regulation of cell survival, cell division, cell differentiation and cell migration (PubMed:28302677, PubMed:8663044). Functions as a potent mitogen in vitro (PubMed:1721615, PubMed:3732516, PubMed:3964259). Can induce angiogenesis (PubMed:23469107, PubMed:28302677). Mediates phosphorylation of ERK1/2 and thereby promotes retinal lens fiber differentiation (PubMed:29501879)

Subcellular location

SecretedNucleus

Domains and Gene Ontology detail (74)

Gene Ontology

Ccytoplasm
Cextracellular region
Cextracellular space
Cnuclear body
Cnucleoplasm
Cnucleus
Fchemoattractant activity
Fchemokine binding
Fcytokine activity
Ffibroblast growth factor receptor binding
Fgrowth factor activity
Fheparin binding

288 aa · 31 kDa · 4 isoforms

Biological roles

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

Cell migrationUniProt · GOCell proliferation & survivalUniProt · GOGrowth-factor signallingGOTranscriptional regulationGOKinase signallingGO

View supporting evidence

Cell migration

·Acts as a ligand for FGFR1, FGFR2, FGFR3 and FGFR4 (PubMed:8663044). Also acts as an int…
·cell migration involved in sprouting angiogenesis
·chemotaxis
·negative regulation of blood vessel endothelial cell migration

Cell proliferation & survival

·Acts as a ligand for FGFR1, FGFR2, FGFR3 and FGFR4 (PubMed:8663044). Also acts as an int…
·positive regulation of cell population proliferation

Growth-factor signalling

·fibroblast growth factor receptor binding
·fibroblast growth factor receptor signaling pathway
·negative regulation of fibroblast growth factor receptor signaling pathway
·positive regulation of endothelial cell chemotaxis to fibroblast growth factor

Transcriptional regulation

·negative regulation of gene expression
·positive regulation of miRNA transcription
·positive regulation of transcription by RNA polymerase II

Kinase signalling

·positive regulation of MAP kinase activity
·positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction

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 FGF2

Gene-level evidence surfaced through the gene FGF2that 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.

Dermatitis, Atopic

0.56Moderately supported

Genetic evidence dominant · Open Targets 0.34

Carcinoma, Hepatocellular

0.52Moderately supported

Clinical evidence dominant · Open Targets 0.38

Neoplasms

0.51Moderately supported

Pathway evidence dominant · Open Targets 0.63

Stroke

0.50Limited support

Genetic evidence dominant · Open Targets 0.28

Bone development disease

0.39Preliminary

Pathway evidence dominant · Open Targets 0.60 · no direct causal or clinical evidence

View evidence synthesis (5)

Dermatitis, AtopicModerately supported

0.56

agreement 0.44–0.68

Genetic100%

Open Targets aggregate 0.34 · 1 independent evidence family

Carcinoma, HepatocellularModerately supported

0.52

agreement 0.36–0.67

Clinical76%Literature24%

Open Targets aggregate 0.38 · 2 independent evidence families

NeoplasmsModerately supported

0.51

agreement 0.39–0.64

Pathway66%Literature23%Clinical11%

Open Targets aggregate 0.63 · 3 independent evidence families

StrokeLimited support

0.50

agreement 0.36–0.64

Genetic76%Literature24%

Open Targets aggregate 0.28 · 2 independent evidence families

Bone development diseasePreliminary

0.39

agreement 0.16–0.62

Pathway100%

Open Targets aggregate 0.60 · 1 independent evidence family · no direct causal or clinical evidence

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

Neoplasms0.63

Bone development disease0.60

Ovarian carcinoma0.49

Carcinoma, Hepatocellular0.38

Craniosynostoses0.37

Dermatitis, Atopic0.34

Stroke0.28

Liver Neoplasms0.27

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)

MUPARFOSTATPhase 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 ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

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

Protein degraders — Emerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (11)

SM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketSM · Druggable FamilyAB · UniProt loc high confAB · GO CC high confPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life DataPR · Small Molecule BinderOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Research activity

3 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

Adult spinal cord stem cells generate neurons after transplantation in the adult dentate gyrus.484 cites

Shihabuddin LS · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000

Resveratrol regulates neuro-inflammation and induces adaptive immunity in Alzheimer's disease.472 cites

Moussa C · Journal of neuroinflammation · 2017

Revisiting the Stress Concept: Implications for Affective Disorders.367 cites

McEwen BS · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020

Recent

Revisiting the Stress Concept: Implications for Affective Disorders.

McEwen BS · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020

Resveratrol regulates neuro-inflammation and induces adaptive immunity in Alzheimer's disease.

Moussa C · Journal of neuroinflammation · 2017

Adult spinal cord stem cells generate neurons after transplantation in the adult dentate gyrus.

Shihabuddin LS · The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000

Europe PMC papers linked directly to this protein.