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Protein / target

Interleukin-10 receptor subunit alpha

Encoded byIL10RAQ13651Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
1
Clinical candidates
7
Clinical trials
Antibody-tractable
Druggability
UniProt loc high conf

Protein at a glance

Biological role

Interleukin-10 receptor

Strongest disease association

Inflammatory Bowel Diseases

Via encoding gene IL10RA · Genetic literature evidence · score 0.61

Therapeutic position

Clinically advancing target

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

Cell surface receptor for the cytokine IL10 that participates in IL10-mediated anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation.

View complete UniProt function annotation

Cell surface receptor for the cytokine IL10 that participates in IL10-mediated anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation. Upon binding to IL10, induces a conformational change in IL10RB, allowing IL10RB to bind IL10 as well (PubMed:16982608). In turn, the heterotetrameric assembly complex, composed of two subunits of IL10RA and IL10RB, activates the kinases JAK1 and TYK2 that are constitutively associated with IL10RA and IL10RB respectively (PubMed:12133952). These kinases then phosphorylate specific tyrosine residues in the intracellular domain in IL10RA leading to the recruitment and subsequent phosphorylation of STAT3. Once phosphorylated, STAT3 homodimerizes, translocates to the nucleus and activates the expression of anti-inflammatory genes. In addition, IL10RA-mediated activation of STAT3 inhibits starvation-induced autophagy (PubMed:26962683)

Subcellular location

Cell membraneCytoplasm
Domains and Gene Ontology detail (18)

Gene Ontology

  • Capical plasma membrane
  • Ccytosol
  • Cplasma membrane
  • Finterleukin-10 binding
  • Finterleukin-10 receptor activity
  • Fsignaling receptor activity
  • Pcell surface receptor signaling pathway via JAK-STAT
  • Pcytokine-mediated signaling pathway
  • Pinterleukin-10-mediated signaling pathway
  • Pintestinal epithelial structure maintenance
  • Pnegative regulation of autophagy
  • Pnegative regulation of inflammatory response

578 aa · 63 kDa

Biological roles

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

Synaptic signallingGOCell proliferation & survivalGOImmune signallingUniProt · GO
View supporting evidence

Synaptic signalling

  • ·regulation of synapse organization

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Immune signalling

  • ·Cell surface receptor for the cytokine IL10 that participates in IL10-mediated anti-infl…
  • ·interleukin-10 binding
  • ·interleukin-10 receptor activity
  • ·cytokine-mediated signaling pathway

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Drugs targeting this protein

1

How approved and investigational drugs engage this protein — mechanism and action type, direct vs complex targeting, and how broadly each acts across other targets. A drug-first view (the section above groups the approved ones disease-first); direct binders with few recorded targets are listed first.

Pegilodecakin
Phase 3Agonist

IL-10 receptor agonist

Acts on a complex — shared with IL10RB · 1 of 2 recorded protein targets — narrow recorded profile

ChEMBL mechanism, action type, target identity and approved indications. Open Targets clinical status.

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 IL10RA

Gene-level evidence surfaced through the gene IL10RAthat 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.

Inflammatory Bowel Diseases
0.54Moderately supported

Genetic literature evidence dominant · Open Targets 0.39

Colitis, Ulcerative
0.50Moderately supported

Genetic literature evidence dominant · Open Targets 0.37

Carcinoma, Pancreatic Ductal
0.33Limited support

Clinical evidence dominant · Open Targets 0.26

Pancreatic adenocarcinoma
0.32Limited support

Clinical evidence dominant · Open Targets 0.26

Genetic Diseases, Inborn
0.32Limited support

Genetic evidence dominant · Open Targets 0.19

View evidence synthesis (5)
Inflammatory Bowel DiseasesModerately supported
0.54
agreement 0.390.69
Genetic literature82%Literature18%

Open Targets aggregate 0.39 · 2 independent evidence families

Colitis, UlcerativeModerately supported
0.50
agreement 0.370.64
Genetic literature94%Literature4%RNA expression2%

Open Targets aggregate 0.37 · 3 independent evidence families

Carcinoma, Pancreatic DuctalLimited support
0.33
agreement 0.190.46
Clinical97%RNA expression2%Literature1%

Open Targets aggregate 0.26 · 3 independent evidence families

Pancreatic adenocarcinomaLimited support
0.32
agreement 0.170.47
Clinical99%Literature1%

Open Targets aggregate 0.26 · 2 independent evidence families

Genetic Diseases, InbornLimited support
0.32
agreement 0.180.46
Genetic99%Literature1%

Open Targets aggregate 0.19 · 2 independent evidence families

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
Inflammatory Bowel Diseases0.39
Colitis, Ulcerative0.37
Carcinoma, Pancreatic Ductal0.26
Pancreatic adenocarcinoma0.26
Genetic Diseases, Inborn0.19

Drug development

1 compounds recorded · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines. Distinct from the 1 drug that targets this protein in Forefront's canonical graph: these count different sets and are not a subset relation.

View all recorded compounds (1)
PEGILODECAKINPhase 3

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

AntibodiesEmerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

Feasibility evidence (uniprot ubiquitination) — no clinical-stage drug of this modality recorded.

Other modalitiesStrong

Advanced Clinical support this modality.

View underlying tractability evidence (6)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · UniProt UbiquitinationOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Clinical trials

7

Trials of drugs that target this protein — reached indirectly through those drugs, so a trial listed here studies the drug, not the protein. Ranked by active status, then clinical phase and recency, and spread across the targeting drugs.

ClinicalTrials.gov via the drug-target graph.