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Protein / target

Tryptophan 2,3-dioxygenase

Encoded byTDO2P48775Homo sapiensSwiss-Prot
UniProt: P48775Ensembl: ENSG00000151790HGNC: HGNC:11708NCBI Gene: 6999
Small-molecule tractable
Druggability
Structure with Ligand
2
Research papers

Protein at a glance

Biological role

L-tryptophan 2,3-dioxygenase

Strongest disease association

Carcinoma, Hepatocellular

Via encoding gene TDO2 · Literature evidence · score 0.12

Research activity

Emerging research

2 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

Heme-dependent dioxygenase that catalyzes the oxidative cleavage of the L-tryptophan (L-Trp) pyrrole ring and converts L-tryptophan to N-formyl-L-kynurenine.

View complete UniProt function annotation

Heme-dependent dioxygenase that catalyzes the oxidative cleavage of the L-tryptophan (L-Trp) pyrrole ring and converts L-tryptophan to N-formyl-L-kynurenine. Catalyzes the oxidative cleavage of the indole moiety

Domains and Gene Ontology detail (13)

Gene Ontology

  • Ccytosol
  • Famino acid binding
  • Fheme binding
  • Fidentical protein binding
  • FL-tryptophan 2,3-dioxygenase activity
  • Fmetal ion binding
  • Foxygen binding
  • PL-tryptophan catabolic process to acetyl-CoA
  • PL-tryptophan catabolic process to L-kynurenine
  • Pprotein homotetramerization
  • Presponse to cortisol
  • Presponse to ethanol

406 aa · 48 kDa

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 TDO2

Gene-level evidence surfaced through the gene TDO2 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.

Carcinoma, Hepatocellular
0.20Preliminary

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

Neoplasms
0.13Preliminary

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

Alzheimer's Disease
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Glioma
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

Central Nervous System Neoplasms
0.11Preliminary

Literature evidence dominant · Open Targets 0.09 · no direct causal or clinical evidence

View evidence synthesis (5)
Carcinoma, HepatocellularPreliminary
0.20
agreement 0.01–0.39
Literature63%RNA expression37%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

NeoplasmsPreliminary
0.13
agreement 0.00–0.40
Literature100%

Open Targets aggregate 0.10 · 1 independent evidence family · no direct causal or clinical evidence

Alzheimer's DiseasePreliminary
0.11
agreement 0.00–0.30
Literature97%RNA expression3%

Open Targets aggregate 0.09 · 2 independent evidence families · no direct causal or clinical evidence

GliomaPreliminary
0.11
agreement 0.00–0.38
Literature100%

Open Targets aggregate 0.09 · 1 independent evidence family · no direct causal or clinical evidence

Central Nervous System NeoplasmsPreliminary
0.11
agreement 0.00–0.38
Literature100%

Open Targets aggregate 0.09 · 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
Carcinoma, Hepatocellular0.12
Neoplasms0.10
Alzheimer's Disease0.09
Glioma0.09
Central Nervous System Neoplasms0.09
Colonic Neoplasms0.09
Carcinoma, Renal Cell0.09

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 (human protein atlas loc) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (half-life data and small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (6)
SM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · Human Protein Atlas locPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 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

Blockade of the AHR restricts a Treg-macrophage suppressive axis induced by L-Kynurenine.366 cites

Campesato LF · Nature communications · 2020

The therapeutic potential of targeting tryptophan catabolism in cancer.227 cites

Opitz CA · British journal of cancer · 2020

Recent

The therapeutic potential of targeting tryptophan catabolism in cancer.

Opitz CA · British journal of cancer · 2020

Blockade of the AHR restricts a Treg-macrophage suppressive axis induced by L-Kynurenine.

Campesato LF · Nature communications · 2020

Europe PMC papers linked directly to this protein.