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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 TNFRSF18that 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
Stomach Neoplasms0.09
Colorectal Neoplasms0.09
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.