Protein / target

Fractalkine

Encoded byCX3CL1P78423Homo sapiensSwiss-Prot

UniProt: P78423 Ensembl: ENSG00000006210 HGNC: HGNC:10647 NCBI Gene: 6376

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

CXCR1 chemokine receptor binding

Strongest disease association

Neurodegenerative Diseases

Via encoding gene CX3CL1 · Pathway evidence · score 0.19

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

5 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

Chemokine that acts as a ligand for both CX3CR1 and integrins ITGAV:ITGB3 and ITGA4:ITGB1.

View complete UniProt function annotation

Chemokine that acts as a ligand for both CX3CR1 and integrins ITGAV:ITGB3 and ITGA4:ITGB1 (PubMed:12055230, PubMed:21829356, PubMed:23125415, PubMed:9782118, PubMed:9931005). The CX3CR1-CX3CL1 signaling exerts distinct functions in different tissue compartments, such as immune response, inflammation, cell adhesion and chemotaxis (PubMed:12055230, PubMed:9024663, PubMed:9177350, PubMed:9782118). Regulates leukocyte adhesion and migration processes at the endothelium (PubMed:9024663, PubMed:9177350). Can activate integrins in both a CX3CR1-dependent and CX3CR1-independent manner (PubMed:23125415, PubMed:24789099). In the presence of CX3CR1, activates integrins by binding to the classical ligand-binding site (site 1) in integrins (PubMed:23125415, PubMed:24789099). In the absence of CX3CR1, binds to a second site (site 2) in integrins which is distinct from site 1 and enhances the binding of other integrin ligands to site 1 (PubMed:23125415, PubMed:24789099)

Subcellular location

Cell membraneSecreted

Domains and Gene Ontology detail (72)

Gene Ontology

Ccell projection
Ccell surface
Cextracellular region
Cextracellular space
Cmembrane
Cneuron projection
Cneuronal cell body
Cperinuclear region of cytoplasm
Cplasma membrane
FCCR chemokine receptor binding
Fchemoattractant activity
Fchemokine activity

397 aa · 42 kDa

Biological roles

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

Cell migrationUniProt · GOSynaptic signallingGOCell proliferation & survivalGOImmune signallingUniProt · GOCell adhesionUniProt · GOApoptosis & cell deathGO

View supporting evidence

Cell migration

·Chemokine that acts as a ligand for both CX3CR1 and integrins ITGAV:ITGB3 and ITGA4:ITGB…
·cell chemotaxis
·chemotaxis
·eosinophil chemotaxis

Synaptic signalling

·synapse pruning

Cell proliferation & survival

·positive regulation of cell population proliferation

Immune signalling

·Chemokine that acts as a ligand for both CX3CR1 and integrins ITGAV:ITGB3 and ITGA4:ITGB…
·antimicrobial humoral immune response mediated by antimicrobial peptide
·cytokine-mediated signaling pathway
·immune response

Cell adhesion

·Chemokine that acts as a ligand for both CX3CR1 and integrins ITGAV:ITGB3 and ITGA4:ITGB…
·cell adhesion
·cell-cell adhesion
·positive regulation of calcium-independent cell-cell adhesion

Apoptosis & cell death

·negative regulation of apoptotic process
·negative regulation of hippocampal neuron apoptotic process

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 CX3CL1

Gene-level evidence surfaced through the gene CX3CL1that 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.

Arthritis, Rheumatoid

0.24Preliminary

Literature evidence dominant · Open Targets 0.13

Neurodegenerative Diseases

0.15Preliminary

Pathway evidence dominant · Open Targets 0.19 · no direct causal or clinical evidence

Neoplasms

0.15Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

Carcinoma, Hepatocellular

0.13Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Lung Diseases, Interstitial

0.13Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

View evidence synthesis (5)

Arthritis, RheumatoidPreliminary

0.24

agreement 0.11–0.38

Literature52%Clinical47%RNA expression1%

Open Targets aggregate 0.13 · 3 independent evidence families

Neurodegenerative DiseasesPreliminary

0.15

agreement 0.00–0.33

Pathway76%Literature24%

Open Targets aggregate 0.19 · 2 independent evidence families · no direct causal or clinical evidence

NeoplasmsPreliminary

0.15

agreement 0.00–0.42

Literature100%

Open Targets aggregate 0.12 · 1 independent evidence family · no direct causal or clinical evidence

Carcinoma, HepatocellularPreliminary

0.13

agreement 0.00–0.41

Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Lung Diseases, InterstitialPreliminary

0.13

agreement 0.00–0.40

Literature100%

Open Targets aggregate 0.10 · 1 independent evidence family · no direct causal or clinical evidence

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. 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

Neurodegenerative Diseases0.19

Arthritis, Rheumatoid0.13

Neoplasms0.12

Carcinoma, Hepatocellular0.11

Lung Diseases, Interstitial0.10

Alzheimer's Disease0.10

Ovarian carcinoma0.10

Parkinson's Disease0.10

Prostate carcinoma0.10

Drug development

1 compounds recorded · 1 in clinical development

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

View all recorded compounds (1)

QUETMOLIMABPhase 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) — no clinical-stage drug of this modality recorded.

Antibodies — Strong

Advanced Clinical and UniProt loc high conf support this modality.

Protein degraders — Emerging

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

View underlying tractability evidence (7)

SM · Structure with LigandAB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMAB · Human Protein Atlas locPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.