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Protein / target

Cytidine deaminase

Encoded byCDAP32320Homo sapiensSwiss-Prot
UniProt: P32320Ensembl: ENSG00000158825HGNC: HGNC:1712NCBI Gene: 978
Clinically validated
Therapeutic maturity
1
Approved medicines
Open Targets target-level
Small-molecule tractable
Druggability
Approved Drug
2
Research papers

Protein at a glance

Biological role

Protein homodimerization

Strongest disease association

Atrioventricular Block

Via encoding gene CDA · Genetic evidence · score 0.43

Therapeutic position

Established drug target

Small molecules

Research activity

Emerging research

2 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

This enzyme scavenges exogenous and endogenous cytidine and 2'-deoxycytidine for UMP synthesis

Domains and Gene Ontology detail (17)

Domains & features

CMP/dCMP-type deaminase

Gene Ontology

  • Ccytosol
  • Cextracellular region
  • Cficolin-1-rich granule lumen
  • Csecretory granule lumen
  • Ctertiary granule lumen
  • Fcytidine deaminase activity
  • Fidentical protein binding
  • Fnucleoside binding
  • Fprotein homodimerization activity
  • Fzinc ion binding
  • Pcellular response to external biotic stimulus
  • PCMP catabolic process

146 aa · 16 kDa

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 CDA

Gene-level evidence surfaced through the gene CDAthat 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.

Myelodysplastic syndrome
0.65Moderately supported

Clinical evidence dominant · Open Targets 0.51

Leukemia, Myeloid, Acute
0.49Limited support

Clinical evidence dominant · Open Targets 0.38

Leukemia, Myeloid
0.49Limited support

Clinical evidence dominant · Open Targets 0.39

Atrioventricular Block
0.43Limited support

Genetic evidence dominant · Open Targets 0.26

Chronic myelomonocytic leukemia
0.42Limited support

Clinical evidence dominant · Open Targets 0.34

View evidence synthesis (5)
Myelodysplastic syndromeModerately supported
0.65
agreement 0.49–0.80
Clinical86%Literature14%

Open Targets aggregate 0.51 · 2 independent evidence families

Leukemia, Myeloid, AcuteLimited support
0.49
agreement 0.34–0.65
Clinical84%Literature16%

Open Targets aggregate 0.38 · 2 independent evidence families

Leukemia, MyeloidLimited support
0.49
agreement 0.33–0.64
Clinical99%Literature1%

Open Targets aggregate 0.39 · 2 independent evidence families

Atrioventricular BlockLimited support
0.43
agreement 0.31–0.55
Genetic100%

Open Targets aggregate 0.26 · 1 independent evidence family

Chronic myelomonocytic leukemiaLimited support
0.42
agreement 0.27–0.58
Clinical98%Literature2%

Open Targets aggregate 0.34 · 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
Myelodysplastic syndrome0.51
Leukemia, Myeloid0.39
Leukemia, Myeloid, Acute0.38
Chronic myelomonocytic leukemia0.34
Neurodegenerative Diseases0.32
chronic myelogenous leukemia, BCR-ABL1 positive0.30
Atrioventricular Block0.26
Neoplasms0.11

Drug development

1 compounds recorded · 1 approved

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

View all recorded compounds (1)
CEDAZURIDINEApproval

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

Approved Drug and Structure with Ligand support this modality.

Antibodies — Emerging

Feasibility evidence (go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

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

View underlying tractability evidence (7)
SM · Approved DrugSM · Structure with LigandSM · High-Quality LigandSM · Druggable FamilyAB · GO CC high confPR · Database UbiquitinationPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

levels of toxicityClinPGxsurvival timeClinPGxclearance of gemcitabineClinPGxhyperbilirubinemiaClinPGxnauseaClinPGxneutropeniaClinPGxdeathClinPGxdiarrhea or dehydrationClinPGxincidence of adverse events, hand-foot syndromeClinPGxdrug toxicityClinPGxgrade 3 hand-foot syndromeClinPGxNeutropeniaClinPGx

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

2 papers · to 2024

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

Most cited

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance.76 cites

Caswell DR · Nature genetics · 2024

Targeted C•G-to-T•A base editing with TALE-cytosine deaminases in plants.12 cites

Zhang D · BMC biology · 2024

Recent

The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance.

Caswell DR · Nature genetics · 2024

Targeted C•G-to-T•A base editing with TALE-cytosine deaminases in plants.

Zhang D · BMC biology · 2024

Europe PMC papers linked directly to this protein.