Protein / target

C-X-C chemokine receptor type 2

Encoded byCXCR2P25025Homo sapiensSwiss-Prot

UniProt: P25025 Ensembl: ENSG00000180871 HGNC: HGNC:6027 NCBI Gene: 3579

Clinical-stage

Therapeutic maturity

Clinical candidates

Clinical trials

Small-molecule tractable

Druggability

Advanced Clinical

Protein at a glance

Biological role

G protein-coupled receptor

Strongest disease association

Colitis, Ulcerative

Via encoding gene CXCR2 · Genetic evidence · score 0.80

Therapeutic position

Clinically advancing target

Small molecules

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 interleukin-8 which is a powerful neutrophil chemotactic factor.

View complete UniProt function annotation

Receptor for interleukin-8 which is a powerful neutrophil chemotactic factor (PubMed:1891716). Binding of IL-8 to the receptor causes activation of neutrophils. This response is mediated via a G-protein that activates a phosphatidylinositol-calcium second messenger system (PubMed:8662698). Binds to IL-8 with high affinity. Also binds with high affinity to CXCL3, GRO/MGSA and NAP-2 (PubMed:1891716). Involved in the homeostatic wound healing response to tissue injury, a multistep cascade that guides neutrophil migration to necrotic sites while avoiding collateral damage of healthy tissues. Signals intravascular neutrophil chemotaxis to the injury site

Subcellular location

Cell membrane

Domains and Gene Ontology detail (29)

Gene Ontology

Ccell surface
Cexternal side of plasma membrane
Cmast cell granule
Cmembrane
Cplasma membrane
Csecretory granule membrane
FC-C chemokine binding
FC-C chemokine receptor activity
FC-X-C chemokine receptor activity
FG protein-coupled receptor activity
Finterleukin-8 binding
Finterleukin-8 receptor activity

360 aa · 41 kDa

Biological roles

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

Cell migrationUniProt · GOCell proliferation & survivalGOImmune signallingUniProt · GOG protein-coupled signallingGO

View supporting evidence

Cell migration

·Receptor for interleukin-8 which is a powerful neutrophil chemotactic factor (PubMed:189…
·chemotaxis
·dendritic cell chemotaxis
·neutrophil chemotaxis

Cell proliferation & survival

·positive regulation of cell population proliferation

Immune signalling

·Receptor for interleukin-8 which is a powerful neutrophil chemotactic factor (PubMed:189…
·mast cell granule
·interleukin-8 binding
·interleukin-8 receptor activity

G protein-coupled signalling

·G protein-coupled receptor activity
·G protein-coupled receptor signaling pathway
·phospholipase C-activating G protein-coupled receptor signaling pathway

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

Drugs targeting this protein

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.

Reparixin

Narrow target profilePhase 3Modulator

Interleukin-8 receptor B modulator

Direct interaction with this protein · 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 CXCR2

Gene-level evidence surfaced through the gene CXCR2 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.

Colitis, Ulcerative

0.84Well supported

Genetic evidence dominant · Open Targets 0.52

Inflammatory Bowel Diseases

0.74Moderately supported

Genetic evidence dominant · Open Targets 0.44

Psoriasis

0.61Moderately supported

Genetic evidence dominant · Open Targets 0.35

Crohn's Disease

0.59Moderately supported

Genetic evidence dominant · Open Targets 0.34

Cholangitis, Sclerosing

0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

View evidence synthesis (5)

Colitis, UlcerativeWell supported

0.84

agreement 0.74–0.94

Genetic79%Clinical12%RNA expression7%Literature1%

Open Targets aggregate 0.52 · 4 independent evidence families

Inflammatory Bowel DiseasesModerately supported

0.74

agreement 0.63–0.84

Genetic76%Clinical13%Literature11%RNA expression1%

Open Targets aggregate 0.44 · 4 independent evidence families

PsoriasisModerately supported

0.61

agreement 0.51–0.72

Genetic77%Clinical13%RNA expression7%Literature3%

Open Targets aggregate 0.35 · 4 independent evidence families

Crohn's DiseaseModerately supported

0.59

agreement 0.46–0.71

Genetic86%RNA expression12%Literature2%

Open Targets aggregate 0.34 · 3 independent evidence families

Cholangitis, SclerosingModerately supported

0.55

agreement 0.41–0.69

Genetic100%Literature1%

Open Targets aggregate 0.33 · 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

Colitis, Ulcerative0.52

Inflammatory Bowel Diseases0.44

Psoriasis0.35

Crohn's Disease0.34

Cholangitis, Sclerosing0.33

Spondylitis, Ankylosing0.33

Diabetes Mellitus, Type 10.30

COVID-190.15

Drug development

7 compounds recorded · 7 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 (7)

NAVARIXIN ANHYDROUSPhase 2

REPARIXINPhase 3

NAVARIXINPhase 2

LADARIXINPhase 2

SX-682Phase 2

ELUBRIXINPhase 2

DANIRIXINPhase 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 — Strong

Advanced Clinical and Structure with Ligand support this modality.

Antibodies — Emerging

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

Protein degraders — Emerging

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

View underlying tractability evidence (8)

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

Raw Open Targets tractability assessment buckets, by modality.

Clinical trials

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.

Phase II Study of Reparixin in Patients With Myelofibrosis Myeloproliferative Neoplasms Research Consortium [MPN-RC 120]PHASE2

RECRUITING · via Reparixin · NCT05835466

Reparixin 1200 mg TID as add-on to SoC to Limit Disease Progression in Hospitalised Patients With COVID-19 and Other Community-Acquired Pneumonia. A Multicentre, Randomized, Double-blinded, Placebo-controlled, Phase III Trial (REPAVID-22)PHASE3

TERMINATED · via Reparixin · NCT05254990

A Phase 3, Double-blind, Randomized, Placebo-controlled, Multicenter Study on the Efficacy and Safety of Reparixin in the Treatment of Hospitalized Patients With Severe COVID-19 PneumoniaPHASE3

COMPLETED · via Reparixin · NCT04878055

Study on the Efficacy and Safety of Reparixin in the Treatment of Hospitalized Patients With COVID-19 PneumoniaPHASE2/PHASE3

TERMINATED · via Reparixin · NCT04794803

View all trials (8)

A Phase 2/3, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel Assignment Study to Assess the Efficacy and Safety of Reparixin in Pancreatic Islet Auto-transplantationPHASE2/PHASE3

COMPLETED · via Reparixin · NCT01967888

A Phase 3, Multicenter, Randomized, Double-blind, Parallel Assignment Study to Assess the Efficacy and Safety of Reparixin in Pancreatic Islet TransplantationPHASE3