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Protein / target

Insulin-like growth factor-binding protein 2

Encoded byIGFBP2P18065Homo sapiensSwiss-Prot
UniProt: P18065Ensembl: ENSG00000115457HGNC: HGNC:5471NCBI Gene: 3485
Small-molecule tractable
Druggability
Druggable Family
1
Research papers

Protein at a glance

Biological role

Insulin-like growth factor II binding

Strongest disease association

Intelligence

Via encoding gene IGFBP2 · Genetic evidence · score 0.47

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

Multifunctional protein that plays a critical role in regulating the availability of IGFs such as IGF1 and IGF2 to their receptors and thereby regulates IGF-mediated cellular processes including proliferation, differentiation, and apoptosis in a cell-type specific manner.

View complete UniProt function annotation

Multifunctional protein that plays a critical role in regulating the availability of IGFs such as IGF1 and IGF2 to their receptors and thereby regulates IGF-mediated cellular processes including proliferation, differentiation, and apoptosis in a cell-type specific manner (PubMed:18563800, PubMed:38796567). Functions coordinately with receptor protein tyrosine phosphatase beta/PTPRB and the IGF1 receptor to regulate IGF1-mediated signaling by stimulating the phosphorylation of PTEN leading to its inactivation and AKT1 activation (PubMed:22869525). Plays a positive role in cell migration via interaction with integrin alpha5/ITGA5 through an RGD motif (PubMed:16569642). Additionally, interaction with ITGA5/ITGB1 enhances the adhesion of endothelial progenitor cells to endothelial cells (PubMed:26076738). Upon mitochondrial damage, facilitates apoptosis with ITGA5 of podocytes, and then activates the phosphorylation of focal adhesion kinase (FAK)-mediated mitochondrial injury (PubMed:38796567)

Subcellular location

Secreted
Domains and Gene Ontology detail (23)

Domains & features

IGFBP N-terminalThyroglobulin type-1

Gene Ontology

  • Capical plasma membrane
  • Cextracellular exosome
  • Cextracellular region
  • Cextracellular space
  • Finsulin-like growth factor I binding
  • Finsulin-like growth factor II binding
  • Freceptor ligand inhibitor activity
  • Fsignaling receptor binding
  • Pcellular response to hormone stimulus
  • Pfemale pregnancy
  • Pnegative regulation of canonical Wnt signaling pathway
  • Posteoblast differentiation

325 aa · 35 kDa

Biological roles

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

Growth-factor signallingGOCell migrationUniProt
View supporting evidence

Growth-factor signalling

  • ·insulin-like growth factor I binding
  • ·insulin-like growth factor II binding
  • ·regulation of insulin-like growth factor receptor signaling pathway

Cell migration

  • ·Multifunctional protein that plays a critical role in regulating the availability of IGF…

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 IGFBP2

Gene-level evidence surfaced through the gene IGFBP2that 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.

Intelligence
0.47Limited support

Genetic evidence dominant · Open Targets 0.29

Pregnancy Complications
0.47Limited support

Genetic evidence dominant · Open Targets 0.28

Glaucoma, Open-Angle
0.38Limited support

Genetic evidence dominant · Open Targets 0.23

Neurodegenerative Diseases
0.21Preliminary

Pathway evidence dominant · Open Targets 0.31 · no direct causal or clinical evidence

Glioblastoma
0.20Preliminary

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

View evidence synthesis (5)
IntelligenceLimited support
0.47
agreement 0.35–0.59
Genetic100%

Open Targets aggregate 0.29 · 1 independent evidence family

Pregnancy ComplicationsLimited support
0.47
agreement 0.34–0.58
Genetic100%

Open Targets aggregate 0.28 · 1 independent evidence family

Glaucoma, Open-AngleLimited support
0.38
agreement 0.26–0.50
Genetic100%

Open Targets aggregate 0.23 · 1 independent evidence family

Neurodegenerative DiseasesPreliminary
0.21
agreement 0.03–0.39
Pathway97%Literature4%

Open Targets aggregate 0.31 · 2 independent evidence families · no direct causal or clinical evidence

GlioblastomaPreliminary
0.20
agreement 0.01–0.39
Literature65%RNA expression35%

Open Targets aggregate 0.12 · 2 independent evidence families · 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
Neurodegenerative Diseases0.31
Intelligence0.29
Pregnancy Complications0.28
Glaucoma, Open-Angle0.23
Central Nervous System Neoplasms0.12
Glioblastoma0.12
Glioma0.11
Neoplasms0.11
Breast Neoplasms0.11

Tractability

Small molecules — Emerging

Feasibility evidence (druggable family) — 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 (database ubiquitination and small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (6)
SM · Druggable FamilyAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Small Molecule Binder

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

Disease-relevant upregulation of P2Y<sub>1</sub> receptor in astrocytes enhances neuronal excitability via IGFBP2.20 cites

Shigetomi E · Nature communications · 2024

Recent

Disease-relevant upregulation of P2Y<sub>1</sub> receptor in astrocytes enhances neuronal excitability via IGFBP2.

Shigetomi E · Nature communications · 2024

Europe PMC papers linked directly to this protein.