Protein / target

Stromal cell-derived factor 1

Encoded byCXCL12P48061Homo sapiensSwiss-Prot

UniProt: P48061 Ensembl: ENSG00000107562 HGNC: HGNC:10672 NCBI Gene: 6387

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

CXCR chemokine receptor binding

Strongest disease association

Coronary Artery Disease

Via encoding gene CXCL12 · Genetic evidence · score 0.64

Therapeutic position

Clinically advancing target

Research activity

Emerging research

6 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

Chemoattractant active on T-lymphocytes and monocytes but not neutrophils.

View complete UniProt function annotation

Chemoattractant active on T-lymphocytes and monocytes but not neutrophils (PubMed:18802065, PubMed:39093700). Activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis (PubMed:8752281, PubMed:18802065, PubMed:39093700). Also binds to atypical chemokine receptor ACKR3, which activates the beta-arrestin pathway and acts as a scavenger receptor for CXCL12/SDF-1 (PubMed:16107333, PubMed:19255243). Binds to the allosteric site (site 2) of integrins and activates integrins ITGAV:ITGB3, ITGA4:ITGB1 and ITGA5:ITGB1 in a CXCR4-independent manner (PubMed:29301984). Acts as a positive regulator of monocyte migration and a negative regulator of monocyte adhesion via the LYN kinase (PubMed:18802065). Stimulates migration of monocytes and T-lymphocytes through its receptors, CXCR4 and ACKR3, and decreases monocyte adherence to surfaces coated with ICAM-1, a ligand for beta-2 integrins (PubMed:16107333, PubMed:18802065, PubMed:19255243, PubMed:39093700). CXCR4 signaling axis inhibits beta-2 integrin LFA-1 mediated adhesion of monocytes to ICAM-1 through LYN kinase (PubMed:18802065). Inhibits CXCR4-mediated infection by T-cell line-adapted HIV-1 (PubMed:8752281). Plays a protective role after myocardial infarction. Induces down-regulation and internalization of ACKR3 expressed in various cells. Has several critical functions during embryonic development; required for B-cell lymphopoiesis, myelopoiesis in bone marrow and heart ventricular septum formation (By similarity). Stimulates the proliferation of bone marrow-derived B-cell progenitors in the presence of IL7 as well as growth of stromal cell-dependent pre-B-cells (By similarity)

Subcellular location

Secreted

Domains and Gene Ontology detail (52)

Gene Ontology

Cexternal side of plasma membrane
Cextracellular exosome
Cextracellular matrix
Cextracellular region
Cextracellular space
Cmembrane
Fchemokine activity
Fchemokine receptor binding
FCXCR chemokine receptor binding
Fgrowth factor activity
Fintegrin binding
Fsignaling receptor binding

93 aa · 11 kDa · 7 isoforms

Biological roles

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

Cell migrationUniProt · GOCell adhesionGOImmune signallingGO

View supporting evidence

Cell migration

·Chemoattractant active on T-lymphocytes and monocytes but not neutrophils (PubMed:188020…
·cell chemotaxis
·chemotaxis
·induction of positive chemotaxis

Cell adhesion

·extracellular matrix
·cell adhesion
·positive regulation of cell adhesion

Immune signalling

·immune response
·positive regulation of T cell migration

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 CXCL12

Gene-level evidence surfaced through the gene CXCL12 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.

Coronary Artery Disease

0.69Moderately supported

Genetic evidence dominant · Open Targets 0.42

Myocardial Infarction

0.66Moderately supported

Genetic evidence dominant · Open Targets 0.40

Myocardial Ischemia

0.62Moderately supported

Genetic evidence dominant · Open Targets 0.37

Angina Pectoris

0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

View evidence synthesis (4)

Coronary Artery DiseaseModerately supported

0.69

agreement 0.55–0.83

Genetic83%Literature17%

Open Targets aggregate 0.42 · 2 independent evidence families

Myocardial InfarctionModerately supported

0.66

agreement 0.52–0.80

Genetic83%Literature17%

Open Targets aggregate 0.40 · 2 independent evidence families

Myocardial IschemiaModerately supported

0.62

agreement 0.48–0.76

Genetic91%Literature9%

Open Targets aggregate 0.37 · 2 independent evidence families

Angina PectorisModerately supported

0.55

agreement 0.41–0.69

Genetic96%Literature4%

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

Coronary Artery Disease0.42

Myocardial Infarction0.40

Myocardial Ischemia0.37

Angina Pectoris0.33

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)

OLAPTESED PEGOLPhase 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 — 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.

Other modalities — Strong

Advanced Clinical support this modality.

View underlying tractability evidence (7)

SM · Structure with LigandSM · High-Quality LigandAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Small Molecule BinderOC · Advanced Clinical

Raw Open Targets tractability assessment buckets, by modality.