Protein / target

Interleukin-1 receptor antagonist protein

Encoded byIL1RNP18510Homo sapiensSwiss-Prot

UniProt: P18510 Ensembl: ENSG00000136689 HGNC: HGNC:6000 NCBI Gene: 3557

Small-molecule tractable

Druggability

High-Quality Ligand

Research papers

Protein at a glance

Biological role

Interleukin-1 type II receptor antagonist

Strongest disease association

Gout

Via encoding gene IL1RN · Genetic evidence · score 0.89

Research activity

Emerging research

7 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

Anti-inflammatory antagonist of interleukin-1 family of proinflammatory cytokines such as interleukin-1beta/IL1B and interleukin-1alpha/IL1A.

View complete UniProt function annotation

Anti-inflammatory antagonist of interleukin-1 family of proinflammatory cytokines such as interleukin-1beta/IL1B and interleukin-1alpha/IL1A. Protects from immune dysregulation and uncontrolled systemic inflammation triggered by IL1 for a range of innate stimulatory agents such as pathogens

Subcellular location

SecretedCytoplasm

Domains and Gene Ontology detail (18)

Gene Ontology

Ccytosol
Cextracellular exosome
Cextracellular space
Cplasma membrane
Fcytokine activity
Finterleukin-1 receptor antagonist activity
Finterleukin-1 receptor binding
Finterleukin-1 type I receptor antagonist activity
Finterleukin-1 type II receptor antagonist activity
Finterleukin-1, type I receptor binding
Finterleukin-1, type II receptor binding
Pacute-phase response

177 aa · 20 kDa · 4 isoforms

Biological roles

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

Immune signallingUniProt · GO

View supporting evidence

Immune signalling

·Anti-inflammatory antagonist of interleukin-1 family of proinflammatory cytokines such a…
·cytokine activity
·interleukin-1 receptor antagonist activity
·interleukin-1 receptor binding

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 IL1RN

Gene-level evidence surfaced through the gene IL1RNthat 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.

Gout

0.91Well supported

Genetic evidence dominant · Open Targets 0.56

Ischemic Stroke

0.61Moderately supported

Genetic evidence dominant · Open Targets 0.37

Coronary Artery Disease

0.61Moderately supported

Genetic evidence dominant · Open Targets 0.37

Venous Thromboembolism

0.59Moderately supported

Genetic evidence dominant · Open Targets 0.36

Diabetic Retinopathy

0.49Limited support

Genetic literature evidence dominant · Open Targets 0.37

View evidence synthesis (5)

GoutWell supported

0.91

agreement 0.77–1.00

Genetic90%Literature10%

Open Targets aggregate 0.56 · 2 independent evidence families

Ischemic StrokeModerately supported

0.61

agreement 0.47–0.75

Genetic90%Literature10%

Open Targets aggregate 0.37 · 2 independent evidence families

Coronary Artery DiseaseModerately supported

0.61

agreement 0.47–0.75

Genetic91%Literature9%

Open Targets aggregate 0.37 · 2 independent evidence families

Venous ThromboembolismModerately supported

0.59

agreement 0.47–0.71

Genetic100%

Open Targets aggregate 0.36 · 1 independent evidence family

Diabetic RetinopathyLimited support

0.49

agreement 0.34–0.64

Genetic literature98%Literature2%

Open Targets aggregate 0.37 · 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

Gout0.56

Diabetic Retinopathy0.37

Ischemic Stroke0.37

Coronary Artery Disease0.37

Venous Thromboembolism0.36

Hypothyroidism0.30

Cardiomyopathy, Hypertrophic0.27

Tractability

Small molecules — Emerging

Feasibility evidence (high-quality ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging