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Protein / target

Tumor necrosis factor receptor superfamily member 18

Encoded byTNFRSF18Q9Y5U5Homo sapiensSwiss-Prot
UniProt: Q9Y5U5Ensembl: ENSG00000186891HGNC: HGNC:11914NCBI Gene: 8784
Clinical-stage
Therapeutic maturity
2
Clinical candidates
Antibody-tractable
Druggability
Advanced Clinical
1
Research papers

Protein at a glance

Biological role

Tumor necrosis factor receptor

Strongest disease association

Conduct Disorder

Via encoding gene TNFRSF18 · Genetic evidence · score 0.26

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

1 papers · latest 2021

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

Receptor for TNFSF18.

View complete UniProt function annotation

Receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway

Subcellular location

Cell membraneSecreted
Domains and Gene Ontology detail (10)

Gene Ontology

  • Cexternal side of plasma membrane
  • Cextracellular region
  • Cplasma membrane
  • Ftumor necrosis factor receptor activity
  • Papoptotic process
  • Pnegative regulation of apoptotic process
  • Ppositive regulation of cell adhesion
  • Ppositive regulation of leukocyte migration
  • Ppositive regulation of tyrosine phosphorylation of STAT protein
  • Psignal transduction

241 aa · 26 kDa · 3 isoforms

Biological roles

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

Apoptosis & cell deathGO
View supporting evidence

Apoptosis & cell death

  • ·apoptotic process
  • ·negative regulation of apoptotic process

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 TNFRSF18

Gene-level evidence surfaced through the gene TNFRSF18 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.

Conduct Disorder
0.26Limited support

Genetic evidence dominant · Open Targets 0.16

Squamous Cell Carcinoma of Head and Neck
0.16Preliminary

Clinical evidence dominant · Open Targets 0.11

Neoplasms
0.15Preliminary

Literature evidence dominant · Open Targets 0.12

Glioblastoma
0.14Preliminary

Clinical evidence dominant · Open Targets 0.09

Miyoshi myopathy
0.12Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

View evidence synthesis (5)
Conduct DisorderLimited support
0.26
agreement 0.14–0.38
Genetic100%

Open Targets aggregate 0.16 · 1 independent evidence family

Squamous Cell Carcinoma of Head and NeckPreliminary
0.16
agreement 0.01–0.32
Clinical70%Literature30%

Open Targets aggregate 0.11 · 2 independent evidence families

NeoplasmsPreliminary
0.15
agreement 0.00–0.30
Literature97%Clinical3%

Open Targets aggregate 0.12 · 2 independent evidence families

GlioblastomaPreliminary
0.14
agreement 0.00–0.30
Clinical62%Literature38%

Open Targets aggregate 0.09 · 2 independent evidence families

Miyoshi myopathyPreliminary
0.12
agreement 0.00–0.39
Literature100%

Open Targets aggregate 0.10 · 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
Conduct Disorder0.16
Neoplasms0.12
Squamous Cell Carcinoma of Head and Neck0.11
Miyoshi myopathy0.10
Lupus Erythematosus, Systemic0.09
Infections0.09
Carcinoma, Hepatocellular0.09
Glioblastoma0.09

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)
TRX-518Phase 1 2
RAGIFILIMABPhase 2

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 — Strong

Advanced Clinical and GO CC high conf support this modality.

View underlying tractability evidence (4)
AB · Advanced ClinicalAB · 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 2021

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

Most cited

Galectin-9 interacts with PD-1 and TIM-3 to regulate T cell death and is a target for cancer immunotherapy.461 cites

Yang R · Nature communications · 2021

Recent

Galectin-9 interacts with PD-1 and TIM-3 to regulate T cell death and is a target for cancer immunotherapy.

Yang R · Nature communications · 2021

Europe PMC papers linked directly to this protein.