Protein / target

Interleukin-8

Encoded byCXCL8P10145Homo sapiensSwiss-Prot

UniProt: P10145 Ensembl: ENSG00000169429 HGNC: HGNC:6025 NCBI Gene: 3576

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

CXCR chemokine receptor binding

Strongest disease association

Coronary Artery Disease

Via encoding gene CXCL8 · Genetic evidence · score 0.54

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

8 papers · latest 2025

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

Chemotactic factor that mediates inflammatory response by attracting neutrophils, basophils, and T-cells to clear pathogens and protect the host from infection.

View complete UniProt function annotation

Chemotactic factor that mediates inflammatory response by attracting neutrophils, basophils, and T-cells to clear pathogens and protect the host from infection (PubMed:18692776, PubMed:7636208). Also plays an important role in neutrophil activation (PubMed:2145175, PubMed:9623510). Released in response to an inflammatory stimulus, exerts its effect by binding to the G protein-coupled receptors CXCR1 and CXCR2, primarily found in neutrophils, monocytes and endothelial cells (PubMed:1840701, PubMed:1891716). G protein heterotrimer (alpha, beta, gamma subunits) constitutively binds to CXCR1/CXCR2 receptor and activation by IL8 leads to beta and gamma subunits release from Galpha (GNAI2 in neutrophils) and activation of several downstream signaling pathways including PI3K and MAPK pathways (PubMed:11971003, PubMed:8662698)

Subcellular location

Secreted

Domains and Gene Ontology detail (40)

Gene Ontology

Cextracellular region
Cextracellular space
Cmembrane
Fchemokine activity
FCXCR chemokine receptor binding
Fheparin binding
Finterleukin-8 receptor binding
Pangiogenesis
Pantimicrobial humoral immune response mediated by antimicrobial peptide
Pcalcium-mediated signaling
Pcellular response to fibroblast growth factor stimulus
Pcellular response to interleukin-1

99 aa · 11 kDa

Biological roles

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

Cell migrationGOGrowth-factor signallingGOCell proliferation & survivalGOImmune signallingUniProt · GOG protein-coupled signallingUniProt · GOCell adhesionGO

View supporting evidence

Cell migration

·chemotaxis
·induction of positive chemotaxis
·neutrophil chemotaxis
·positive regulation of neutrophil chemotaxis

Growth-factor signalling

·cellular response to fibroblast growth factor stimulus

Cell proliferation & survival

·negative regulation of cell population proliferation

Immune signalling

·Chemotactic factor that mediates inflammatory response by attracting neutrophils, basoph…
·interleukin-8 receptor binding
·antimicrobial humoral immune response mediated by antimicrobial peptide
·cellular response to interleukin-1

G protein-coupled signalling

·Chemotactic factor that mediates inflammatory response by attracting neutrophils, basoph…
·G protein-coupled receptor signaling pathway
·negative regulation of G protein-coupled receptor signaling pathway

Cell adhesion

·negative regulation of cell adhesion molecule production
·regulation of cell adhesion

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 CXCL8

Gene-level evidence surfaced through the gene CXCL8that 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.

Coronary Artery Disease

0.60Moderately supported

Genetic evidence dominant · Open Targets 0.35

Myocardial Infarction

0.58Moderately supported

Genetic evidence dominant · Open Targets 0.35

Ischemic Stroke

0.57Moderately supported

Genetic evidence dominant · Open Targets 0.34

Endocrine System Diseases

0.31Limited support

Genetic evidence dominant · Open Targets 0.19

Carcinoma, Hepatocellular

0.25Limited support

Literature evidence dominant · Open Targets 0.14

View evidence synthesis (5)

Coronary Artery DiseaseModerately supported

0.60

agreement 0.46–0.74

Genetic81%Literature19%

Open Targets aggregate 0.35 · 2 independent evidence families

Myocardial InfarctionModerately supported

0.58

agreement 0.45–0.72

Genetic85%Literature15%

Open Targets aggregate 0.35 · 2 independent evidence families

Ischemic StrokeModerately supported

0.57

agreement 0.43–0.71

Genetic89%Literature11%

Open Targets aggregate 0.34 · 2 independent evidence families

Endocrine System DiseasesLimited support

0.31

agreement 0.19–0.43

Genetic100%

Open Targets aggregate 0.19 · 1 independent evidence family

Carcinoma, HepatocellularLimited support

0.25

agreement 0.12–0.39

Literature54%Clinical42%RNA expression5%

Open Targets aggregate 0.14 · 3 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

Coronary Artery Disease0.35

Myocardial Infarction0.35

Ischemic Stroke0.34

Endocrine System Diseases0.19

Carcinoma, Hepatocellular0.14

Melanoma0.14

Dermatitis, Contact0.14

Pulmonary Disease, Chronic Obstructive0.14

Carcinoma, Non-Small-Cell Lung0.13

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)

ABX-IL8Phase 2

ADAKITUGPhase 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

Small molecules — Emerging

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

Antibodies — Strong

Advanced Clinical and GO CC high conf support this modality.

Protein degraders — Emerging

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

View underlying tractability evidence (9)

SM · Structure with LigandSM · High-Quality LigandSM · Med-Quality PocketSM · Druggable FamilyAB · Advanced ClinicalAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of gene expressionToxCasthypertensionClinPGx

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.