Back to discover

Protein / target

C-C chemokine receptor type 2

Encoded byCCR2P41597Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
10
Clinical candidates
Small-molecule tractable
Druggability
Advanced Clinical
9
Research papers

Protein at a glance

Biological role

Chemokine (C-C motif) ligand 12 binding

Strongest disease association

Celiac Disease

Via encoding gene CCR2 · Genetic evidence · score 0.54

Therapeutic position

Clinically advancing target

Small molecules and antibodies

Research activity

Emerging research

9 papers · latest 2024

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

Key functional receptor for CCL2 but can also bind CCL7, and CCL12.

View complete UniProt function annotation

Key functional receptor for CCL2 but can also bind CCL7, and CCL12 (PubMed:23408426, PubMed:38157855, PubMed:8048929, PubMed:8146186). Also transduces signaling mediated by CCL13 (PubMed:38157855). Its binding with CCL2 on monocytes and macrophages mediates chemotaxis and migration induction through the activation of the PI3K cascade, the small G protein Rac and lamellipodium protrusion (PubMed:38157855). Also acts as a receptor for the beta-defensin DEFB106A/DEFB106B (PubMed:23938203). Regulates the expression of T-cell inflammatory cytokines and T-cell differentiation, promoting the differentiation of T-cells into T-helper 17 cells (Th17) during inflammation (By similarity). Facilitates the export of mature thymocytes by enhancing directional movement of thymocytes to sphingosine-1-phosphate stimulation and up-regulation of S1P1R expression; signals through the JAK-STAT pathway to regulate FOXO1 activity leading to an increased expression of S1P1R (By similarity). Plays an important role in mediating peripheral nerve injury-induced neuropathic pain (By similarity). Increases NMDA-mediated synaptic transmission in both dopamine D1 and D2 receptor-containing neurons, which may be caused by MAPK/ERK-dependent phosphorylation of GRIN2B/NMDAR2B (By similarity). Mediates the recruitment of macrophages and monocytes to the injury site following brain injury (By similarity)

Subcellular location

Cell membrane
Domains and Gene Ontology detail (62)

Gene Ontology

  • Ccytoplasm
  • Cdendrite
  • Cexternal side of plasma membrane
  • Cmembrane
  • Cneuronal cell body
  • Cperikaryon
  • Cperinuclear region of cytoplasm
  • Cplasma membrane
  • FC-C chemokine binding
  • FC-C chemokine receptor activity
  • FCCR2 chemokine receptor binding
  • Fchemokine (C-C motif) ligand 12 binding

374 aa · 42 kDa · 2 isoforms

Biological roles

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

Cell migrationUniProt · GOExcitatory neurotransmissionGOImmune signallingUniProt · GO
View supporting evidence

Cell migration

  • ·Key functional receptor for CCL2 but can also bind CCL7, and CCL12 (PubMed:23408426, Pub…
  • ·cell chemotaxis
  • ·chemotaxis
  • ·dendritic cell chemotaxis

Excitatory neurotransmission

  • ·positive regulation of synaptic transmission, glutamatergic

Immune signalling

  • ·Key functional receptor for CCL2 but can also bind CCL7, and CCL12 (PubMed:23408426, Pub…
  • ·cytokine-mediated signaling pathway
  • ·immune response
  • ·inflammatory response

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 CCR2

Gene-level evidence surfaced through the gene CCR2 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.

COVID-19
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.36

Celiac Disease
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

Arthritis, Rheumatoid
0.46Limited support

Genetic evidence dominant · Open Targets 0.26

Alcohol drinking
0.36Limited support

Genetic evidence dominant · Open Targets 0.22

Lupus Erythematosus, Systemic
0.27Limited support

Genetic evidence dominant · Open Targets 0.14

View evidence synthesis (5)
COVID-19Moderately supported
0.68
agreement 0.570.79
Genetic48%Clinical39%Literature13%

Open Targets aggregate 0.36 · 3 independent evidence families

Celiac DiseaseModerately supported
0.55
agreement 0.410.69
Genetic97%Literature3%

Open Targets aggregate 0.33 · 2 independent evidence families

Arthritis, RheumatoidLimited support
0.46
agreement 0.340.59
Genetic75%Literature23%RNA expression3%

Open Targets aggregate 0.26 · 3 independent evidence families

Alcohol drinkingLimited support
0.36
agreement 0.220.50
Genetic97%Literature3%

Open Targets aggregate 0.22 · 2 independent evidence families

Lupus Erythematosus, SystemicLimited support
0.27
agreement 0.130.41
Genetic68%Literature32%

Open Targets aggregate 0.14 · 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
COVID-190.36
Celiac Disease0.33
Arthritis, Rheumatoid0.26
Alcohol drinking0.22
Lupus Erythematosus, Systemic0.14

Drug development

10 compounds recorded · 10 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (10)
CENICRIVIROCPhase 3
AZD2423Phase 2
MK-0812Phase 2
ILACIRNONPhase 2
PF-04634817Phase 2
PF-4136309Phase 2
BMS-741672Phase 2
JNJ-41443532Phase 2
PLOZALIZUMABPhase 2
BMS-813160Phase 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 moleculesStrong

Advanced Clinical and Structure with Ligand support this modality.

AntibodiesStrong

Advanced Clinical and UniProt loc high conf support this modality.

Protein degradersEmerging

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

Other modalitiesStrong

Advanced Clinical support this modality.

View underlying tractability evidence (12)
SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · Half-life DataPR · Small Molecule BinderOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.

Research activity

9 papers · to 2024

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Weisberg SP · The Journal of clinical investigation · 2006

Pairo-Castineira E · Nature · 2021

Recent

Europe PMC papers linked directly to this protein.