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Protein / target

Carboxypeptidase E

Encoded byCPEP16870Homo sapiensSwiss-Prot
UniProt: P16870Ensembl: ENSG00000109472HGNC: HGNC:2303NCBI Gene: 1363
Antibody-tractable
Druggability
GO CC high conf
1
Research papers

Protein at a glance

Biological role

Metallocarboxypeptidase

Strongest disease association

Genetic Diseases, Inborn

Via encoding gene CPE · Genetic evidence · score 0.68

Research activity

Emerging research

1 papers · latest 2023

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

Sorting receptor that directs prohormones to the regulated secretory pathway.

View complete UniProt function annotation

Sorting receptor that directs prohormones to the regulated secretory pathway. Also acts as a prohormone processing enzyme in neuro/endocrine cells, removing dibasic residues from the C-terminal end of peptide hormone precursors after initial endoprotease cleavage

Subcellular location

Cytoplasmic vesicle, secretory vesicleCytoplasmic vesicle, secretory vesicle membraneSecreted
Domains and Gene Ontology detail (19)

Domains & features

Peptidase M14

Gene Ontology

  • Cextracellular exosome
  • Cextracellular space
  • CGolgi apparatus
  • Cplasma membrane
  • Csecretory granule membrane
  • Ctransport vesicle membrane
  • Fcarboxypeptidase activity
  • Fcell adhesion molecule binding
  • Fmetallocarboxypeptidase activity
  • Fneurexin family protein binding
  • Fzinc ion binding
  • Pcardiac left ventricle morphogenesis

476 aa · 53 kDa · 2 isoforms

Biological roles

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

ProteolysisUniProt · GO
View supporting evidence

Proteolysis

  • ·Sorting receptor that directs prohormones to the regulated secretory pathway. Also acts…
  • ·carboxypeptidase activity
  • ·metallocarboxypeptidase activity

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 CPE

Gene-level evidence surfaced through the gene CPE 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.

Genetic Diseases, Inborn
0.68Moderately supported

Genetic evidence dominant · Open Targets 0.41

Eye Diseases
0.44Limited support

Genetic evidence dominant · Open Targets 0.27

Dermatitis, Atopic
0.43Limited support

Genetic evidence dominant · Open Targets 0.26

Idiopathic Pulmonary Fibrosis
0.41Limited support

Genetic evidence dominant · Open Targets 0.25

Neurodegenerative Diseases
0.21Preliminary

Pathway evidence dominant · Open Targets 0.31 · no direct causal or clinical evidence

View evidence synthesis (5)
Genetic Diseases, InbornModerately supported
0.68
agreement 0.54–0.82
Genetic100%Literature0%

Open Targets aggregate 0.41 · 2 independent evidence families

Eye DiseasesLimited support
0.44
agreement 0.32–0.56
Genetic100%

Open Targets aggregate 0.27 · 1 independent evidence family

Dermatitis, AtopicLimited support
0.43
agreement 0.29–0.56
Genetic99%RNA expression1%

Open Targets aggregate 0.26 · 2 independent evidence families

Idiopathic Pulmonary FibrosisLimited support
0.41
agreement 0.29–0.53
Genetic100%

Open Targets aggregate 0.25 · 1 independent evidence family

Neurodegenerative DiseasesPreliminary
0.21
agreement 0.03–0.39
Pathway99%Literature1%

Open Targets aggregate 0.31 · 2 independent evidence families · 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
Genetic Diseases, Inborn0.41
Neurodegenerative Diseases0.31
Eye Diseases0.27
Dermatitis, Atopic0.26
Idiopathic Pulmonary Fibrosis0.25

Tractability

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 (database ubiquitination and half-life data) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (5)
AB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2023

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

Most cited

Hippocampal delivery of neurotrophic factor-α1/carboxypeptidase E gene prevents neurodegeneration, amyloidosis, memory loss in Alzheimer's Disease male mice.28 cites

Xiao L · Molecular psychiatry · 2023

Recent

Hippocampal delivery of neurotrophic factor-α1/carboxypeptidase E gene prevents neurodegeneration, amyloidosis, memory loss in Alzheimer's Disease male mice.

Xiao L · Molecular psychiatry · 2023

Europe PMC papers linked directly to this protein.