Protein / target

C-C chemokine receptor type 5

Encoded byCCR5P51681Homo sapiensSwiss-Prot

UniProt: P51681 Ensembl: ENSG00000160791 HGNC: HGNC:1606 NCBI Gene: 1234

Clinically validated

Therapeutic maturity

Approved medicines

Open Targets target-level

Small-molecule tractable

Druggability

Approved Drug

Research papers

Protein at a glance

Biological role

Phosphatidylinositol-4,5-bisphosphate phospholipase C

Strongest disease association

Diabetes Mellitus, Type 1

Via encoding gene CCR5 · Genetic evidence · score 0.43

Therapeutic position

Established drug target

Small molecules and antibodies

Research activity

Emerging research

8 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

Receptor for a number of inflammatory CC-chemokines including CCL3/MIP-1-alpha, CCL4/MIP-1-beta and RANTES and subsequently transduces a signal by increasing the intracellular calcium ion level.

View complete UniProt function annotation

Receptor for a number of inflammatory CC-chemokines including CCL3/MIP-1-alpha, CCL4/MIP-1-beta and RANTES and subsequently transduces a signal by increasing the intracellular calcium ion level. May play a role in the control of granulocytic lineage proliferation or differentiation. Participates in T-lymphocyte migration to the infection site by acting as a chemotactic receptor (PubMed:30713770)

Subcellular location

Cell membrane

Domains and Gene Ontology detail (32)

Gene Ontology

Ccell surface
Ccytoplasm
Cendosome
Cexternal side of plasma membrane
Cplasma membrane
Factin binding
FC-C chemokine binding
FC-C chemokine receptor activity
Fchemokine (C-C motif) ligand 5 binding
Fchemokine receptor activity
Fcoreceptor activity
Fidentical protein binding

352 aa · 41 kDa

Biological roles

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

Cell migrationGOLipid & lipoprotein metabolismGOImmune signallingGO

View supporting evidence

Cell migration

·cell chemotaxis
·chemotaxis
·dendritic cell chemotaxis

Lipid & lipoprotein metabolism

·response to cholesterol

Immune signalling

·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 CCR5

Gene-level evidence surfaced through the gene CCR5 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.

HIV Infections

0.82Well supported

Clinical evidence dominant · Open Targets 0.70

COVID-19

0.55Moderately supported

Clinical evidence dominant · Open Targets 0.40

Diabetes Mellitus, Type 1

0.50Moderately supported

Genetic evidence dominant · Open Targets 0.29

Virus Diseases

0.48Limited support

Clinical evidence dominant · Open Targets 0.38

Colitis, Ulcerative

0.44Limited support

Genetic evidence dominant · Open Targets 0.26

View evidence synthesis (5)

HIV InfectionsWell supported

0.82

agreement 0.71–0.94

Clinical57%Pathway31%Literature11%RNA expression1%

Open Targets aggregate 0.70 · 4 independent evidence families

COVID-19Moderately supported

0.55

agreement 0.44–0.66

Clinical71%Literature20%Genetic9%

Open Targets aggregate 0.40 · 3 independent evidence families

Diabetes Mellitus, Type 1Moderately supported

0.50

agreement 0.36–0.64

Genetic78%Literature22%

Open Targets aggregate 0.29 · 2 independent evidence families

Virus DiseasesLimited support

0.48

agreement 0.33–0.64

Clinical90%Literature10%

Open Targets aggregate 0.38 · 2 independent evidence families

Colitis, UlcerativeLimited support

0.44

agreement 0.33–0.55

Genetic87%Clinical10%Literature3%

Open Targets aggregate 0.26 · 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

HIV Infections0.70

COVID-190.40

Virus Diseases0.38

Diabetes Mellitus, Type 10.29

Acquired Immunodeficiency Syndrome0.28

Pulmonary Disease, Chronic Obstructive0.28

Pneumonia0.26

Colitis, Ulcerative0.26

Drug development

13 compounds recorded · 1 approved · 12 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)

MARAVIROCApproval

PF-232798Phase 2

BMS-813160Phase 2

HGS-1025Phase 1

AZD5672Phase 2

PF-04634817Phase 2

INCB-9471Phase 2

CCR5MAB004Phase 1

APLAVIROCPhase 3

CENICRIVIROCPhase 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

Small molecules — Strong

Approved Drug and Structure with Ligand support this modality.

Antibodies — Strong

Advanced Clinical and UniProt loc 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 · Approved DrugSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.