Back to discover

Protein / target

Tumor necrosis factor receptor superfamily member 8

Encoded byTNFRSF8P28908Homo sapiensSwiss-Prot
UniProt: P28908Ensembl: ENSG00000120949HGNC: HGNC:11923NCBI Gene: 943
Clinically validated
Therapeutic maturity
1
Approved medicines
Open Targets target-level
Antibody-tractable
Druggability
Advanced Clinical
1
Research papers

Protein at a glance

Biological role

Transmembrane signaling receptor

Strongest disease association

Asthma

Via encoding gene TNFRSF8 · Genetic evidence · score 0.92

Therapeutic position

Established drug 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

Receptor for TNFSF8/CD30L.

View complete UniProt function annotation

Receptor for TNFSF8/CD30L (PubMed:8391931). May play a role in the regulation of cellular growth and transformation of activated lymphoblasts. Regulates gene expression through activation of NF-kappa-B (PubMed:8999898)

Subcellular location

Cell membraneCytoplasm
Domains and Gene Ontology detail (11)

Gene Ontology

  • Ccytoplasm
  • Cextracellular exosome
  • Cplasma membrane
  • Fprotease binding
  • Ftransmembrane signaling receptor activity
  • Pcellular response to mechanical stimulus
  • Pnegative regulation of cell population proliferation
  • Ppositive regulation of apoptotic process
  • Ppositive regulation of TRAIL production
  • Ppositive regulation of tumor necrosis factor production
  • Psignal transduction

595 aa · 64 kDa · 3 isoforms

Biological roles

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

Cell proliferation & survivalGO
View supporting evidence

Cell proliferation & survival

  • ·negative regulation of cell population proliferation

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 TNFRSF8

Gene-level evidence surfaced through the gene TNFRSF8that 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.

Asthma
0.93Well supported

Genetic evidence dominant · Open Targets 0.57

Respiratory Tract Diseases
0.80Well supported

Genetic evidence dominant · Open Targets 0.48

Hodgkin's Disease
0.74Moderately supported

Clinical evidence dominant · Open Targets 0.60

Hypersensitivity
0.69Moderately supported

Genetic evidence dominant · Open Targets 0.42

Venous Thrombosis
0.69Moderately supported

Genetic evidence dominant · Open Targets 0.42

View evidence synthesis (5)
AsthmaWell supported
0.93
agreement 0.79–1.00
Genetic94%Literature6%

Open Targets aggregate 0.57 · 2 independent evidence families

Respiratory Tract DiseasesWell supported
0.80
agreement 0.68–0.92
Genetic100%

Open Targets aggregate 0.48 · 1 independent evidence family

Hodgkin's DiseaseModerately supported
0.74
agreement 0.59–0.90
Clinical85%Literature16%

Open Targets aggregate 0.60 · 2 independent evidence families

HypersensitivityModerately supported
0.69
agreement 0.55–0.83
Genetic97%Literature4%

Open Targets aggregate 0.42 · 2 independent evidence families

Venous ThrombosisModerately supported
0.69
agreement 0.57–0.81
Genetic100%

Open Targets aggregate 0.42 · 1 independent evidence family

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
Hodgkin's Disease0.60
Asthma0.57
Anaplastic large cell lymphoma0.53
Respiratory Tract Diseases0.48
Lymphoma, Non-Hodgkin's0.42
Hypersensitivity0.42
Venous Thrombosis0.42
Neoplasms0.40

Drug development

4 compounds recorded · 1 approved · 3 in clinical development

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

View all recorded compounds (4)
SGN-30Phase 2
IRATUMUMABPhase 2
BRENTUXIMAB VEDOTINApproval
HEFI-1Phase 1

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 UniProt loc high conf support this modality.

Protein degraders — Emerging

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

Other modalities — Strong

Approved Drug support this modality.

View underlying tractability evidence (8)
AB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · Database UbiquitinationPR · Half-life DataOC · Approved Drug

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

Brentuximab Vedotin-Driven Microtubule Disruption Results in Endoplasmic Reticulum Stress Leading to Immunogenic Cell Death and Antitumor Immunity.35 cites

Heiser RA · Molecular cancer therapeutics · 2024

Recent

Brentuximab Vedotin-Driven Microtubule Disruption Results in Endoplasmic Reticulum Stress Leading to Immunogenic Cell Death and Antitumor Immunity.

Heiser RA · Molecular cancer therapeutics · 2024

Europe PMC papers linked directly to this protein.