Protein / target

E-selectin

Encoded bySELEP16581Homo sapiensSwiss-Prot

UniProt: P16581 Ensembl: ENSG00000007908 HGNC: HGNC:10718 NCBI Gene: 6401

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Advanced Clinical

Research papers

Protein at a glance

Biological role

Transmembrane signaling receptor

Strongest disease association

Venous Thrombosis

Via encoding gene SELE · Genetic evidence · score 0.44

Therapeutic position

Clinically advancing target

Small molecules and antibodies

Research activity

Emerging research

1 papers · latest 2022

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

Cell-surface glycoprotein having a role in immunoadhesion.

View complete UniProt function annotation

Cell-surface glycoprotein having a role in immunoadhesion. Mediates in the adhesion of blood neutrophils in cytokine-activated endothelium through interaction with SELPLG/PSGL1. May have a role in capillary morphogenesis

Subcellular location

Cell membrane

Domains and Gene Ontology detail (36)

Domains & features

C-type lectinEGF-likeSushi 1Sushi 2Sushi 3Sushi 4Sushi 5Sushi 6

Gene Ontology

Ccaveola
Cclathrin-coated pit
Ccortical cytoskeleton
Cexternal side of plasma membrane
Cextracellular space
Cmembrane raft
Cperinuclear region of cytoplasm
Cplasma membrane
Fmetal ion binding
Foligosaccharide binding
Fphospholipase binding
Fsialic acid binding

610 aa · 67 kDa

Biological roles

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

Immune signallingUniProt · GOCell adhesionGO

View supporting evidence

Immune signalling

·Cell-surface glycoprotein having a role in immunoadhesion. Mediates in the adhesion of b…
·inflammatory response
·leukocyte migration involved in inflammatory response
·regulation of inflammatory response

Cell adhesion

·heterophilic cell-cell adhesion
·leukocyte cell-cell adhesion

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 SELE

Gene-level evidence surfaced through the gene SELE 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.

Venous Thrombosis

0.53Moderately supported

Genetic evidence dominant · Open Targets 0.30

Leukemia, Myeloid, Acute

0.48Limited support

Clinical evidence dominant · Open Targets 0.36

Asthma

0.37Limited support

Clinical evidence dominant · Open Targets 0.28

Neoplasms

0.14Preliminary

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

Autoimmune disorder of central nervous system

0.10Preliminary

Pathway evidence dominant · Open Targets 0.16 · no direct causal or clinical evidence

View evidence synthesis (5)

Venous ThrombosisModerately supported

0.53

agreement 0.43–0.64

Genetic73%Literature16%Clinical11%

Open Targets aggregate 0.30 · 3 independent evidence families

Leukemia, Myeloid, AcuteLimited support

0.48

agreement 0.33–0.64

Clinical75%Literature25%

Open Targets aggregate 0.36 · 2 independent evidence families

AsthmaLimited support

0.37

agreement 0.21–0.52

Clinical90%Literature10%

Open Targets aggregate 0.28 · 2 independent evidence families

NeoplasmsPreliminary

0.14

agreement 0.00–0.42

Literature100%

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

Autoimmune disorder of central nervous systemPreliminary

0.10

agreement 0.00–0.33

Pathway100%

Open Targets aggregate 0.16 · 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

Leukemia, Myeloid, Acute0.36

Venous Thrombosis0.30

Asthma0.28

Autoimmune disorder of central nervous system0.16

Neoplasms0.12

Drug development

4 compounds recorded · 4 in clinical development

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

View all recorded compounds (4)

UPROLESELANPhase 3

RIVIPANSELPhase 3

BIMOSIAMOSEPhase 2

CDP-850Phase 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 — Strong

Advanced Clinical and Structure with Ligand support this modality.

Antibodies — Supported

Phase 1 Clinical and UniProt loc high conf support this modality.

Protein degraders — Emerging

Feasibility evidence (database ubiquitination and small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (10)

SM · Advanced ClinicalSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · Phase 1 ClinicalAB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Small Molecule Binder

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.

Research activity

1 papers · to 2022

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

Most cited

Whole-genome sequencing reveals host factors underlying critical COVID-19.270 cites

Kousathanas A · Nature · 2022

Recent

Whole-genome sequencing reveals host factors underlying critical COVID-19.

Kousathanas A · Nature · 2022

Europe PMC papers linked directly to this protein.