Protein / target

C-X-C motif chemokine 10

Encoded byCXCL10P02778Homo sapiensSwiss-Prot

UniProt: P02778 Ensembl: ENSG00000169245 HGNC: HGNC:10637 NCBI Gene: 3627

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

CAMP-dependent protein kinase regulator

Strongest disease association

Arthritis, Rheumatoid

Via encoding gene CXCL10 · Literature evidence · score 0.13

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

7 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

View complete UniProt function annotation

Pro-inflammatory cytokine that is involved in a wide variety of processes such as chemotaxis, differentiation, and activation of peripheral immune cells, regulation of cell growth, apoptosis and modulation of angiostatic effects (PubMed:11157474, PubMed:22652417, PubMed:7540647). Plays thereby an important role during viral infections by stimulating the activation and migration of immune cells to the infected sites (By similarity). Mechanistically, binding of CXCL10 to the CXCR3 receptor activates G protein-mediated signaling and results in downstream activation of phospholipase C-dependent pathway, an increase in intracellular calcium production and actin reorganization (PubMed:12750173, PubMed:19151743). In turn, recruitment of activated Th1 lymphocytes occurs at sites of inflammation (PubMed:12663757, PubMed:12750173). Activation of the CXCL10/CXCR3 axis also plays an important role in neurons in response to brain injury for activating microglia, the resident macrophage population of the central nervous system, and directing them to the lesion site. This recruitment is an essential element for neuronal reorganization (By similarity)

Subcellular location

Secreted

Domains and Gene Ontology detail (41)

Gene Ontology

Cexternal side of plasma membrane
Cextracellular region
Cextracellular space
FcAMP-dependent protein kinase regulator activity
Fchemoattractant activity
Fchemokine activity
FCXCR chemokine receptor binding
FCXCR3 chemokine receptor binding
Fheparin binding
Fsignaling receptor binding
Padenylate cyclase-activating G protein-coupled receptor signaling pathway
Pantiviral innate immune response

98 aa · 11 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

·Pro-inflammatory cytokine that is involved in a wide variety of processes such as chemot…
·chemotaxis
·neutrophil chemotaxis
·positive regulation of monocyte chemotaxis

Cell proliferation & survival

·positive regulation of cell population proliferation
·regulation of cell population proliferation

Immune signalling

·Pro-inflammatory cytokine that is involved in a wide variety of processes such as chemot…
·antiviral innate immune response
·cellular response to interleukin-17
·inflammatory response

G protein-coupled signalling

·adenylate cyclase-activating G protein-coupled receptor signaling pathway
·G protein-coupled receptor signaling pathway

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 CXCL10

Gene-level evidence surfaced through the gene CXCL10 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.

Arthritis, Rheumatoid

0.23Preliminary

Literature evidence dominant · Open Targets 0.13

Lung carcinoma

0.16Preliminary

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

Lupus Erythematosus, Systemic

0.15Preliminary

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

Neoplasms

0.15Preliminary

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

Tuberculosis

0.15Preliminary

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

View evidence synthesis (5)

Arthritis, RheumatoidPreliminary

0.23

agreement 0.10–0.36

Literature57%Clinical37%RNA expression6%

Open Targets aggregate 0.13 · 3 independent evidence families

Lung carcinomaPreliminary

0.16

agreement 0.00–0.35

Literature80%RNA expression21%

Open Targets aggregate 0.11 · 2 independent evidence families · no direct causal or clinical evidence

Lupus Erythematosus, SystemicPreliminary

0.15

agreement 0.00–0.34

Literature91%RNA expression9%

Open Targets aggregate 0.12 · 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

TuberculosisPreliminary

0.15

agreement 0.00–0.42

Literature100%

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

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

Arthritis, Rheumatoid0.13

Neoplasms0.12

Tuberculosis0.12

COVID-190.12

Infections0.12

Lupus Erythematosus, Systemic0.12

Carcinoma, Hepatocellular0.11

Lung carcinoma0.11

Scleroderma, Systemic0.11

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)

NI-0801Phase 2

ELDELUMABPhase 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 UniProt loc high conf support this modality.

View underlying tractability evidence (7)

SM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketAB · Advanced ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMM

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of gene expressionToxCast

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.