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Radioligand therapy target profile

CEA (CEACAM5) as a Radioligand Therapy Target

CEA cell adhesion molecule 5 · Ensembl ENSG00000105388 · Data updated 2026-08-01

CEA (CEACAM5), CEA cell adhesion molecule 5, is a cell-surface protein. In Human Protein Atlas immunohistochemistry, CEA staining is highest in colorectal cancer (100% of samples positive), gastric cancer (91% of samples positive) and lung cancer (91% of samples positive). Clinical status: Clinical-stage (up to phase 3, any modality).

LocalizationCell-Surface
Top cancer (IHC)Colorectal Cancer
InternalizationNot assessed
Clinical stageClinical-stage (up to phase 3, any modality)
Active trialsSee ClinicalTrials.gov
Cancer association (Open Targets)0.56

Is CEA a good radioligand therapy target?

Scored against the six criteria that decide whether a protein can become a radioligand therapy:

CEA expression in cancer

Protein expression of CEA across 20 cancer types from Human Protein Atlas immunohistochemistry. The score is a weighted staining intensity from 0 to 1; "% positive" is the share of patient samples with detectable staining.

Cancer typeIHC scoreLevel% positive
Colorectal Cancer0.87High100%
Gastric Cancer0.73High91%
Lung Cancer0.67High91%
Pancreatic Cancer0.64High91%
Cervical Cancer0.58High91%
Bladder Cancer0.44Medium67%
Head and Neck Cancer0.42Medium75%
Endometrial Cancer0.30Medium56%
Liver Cancer0.19Low29%
Ovarian Cancer0.17Low30%
Skin Cancer0.09Low27%

Not detected by IHC in: lymphoma, breast cancer, melanoma, kidney cancer, thyroid cancer, neuroendocrine tumors, prostate cancer, testicular cancer, glioma.

Is CEA internalized?

Nuclens has not yet extracted internalization evidence for CEA. Internalization matters for radioligands because an internalizing receptor traps the radionuclide inside the tumor cell. Run a full analysis to pull the latest literature.

CEA clinical trials

Clinical-stage (up to phase 3, any modality). Nuclens hasn't indexed trials for CEA yet. Search ClinicalTrials.gov for CEA trials.

CEA normal tissue expression

Normal-tissue expression in dose-limiting organs (kidney, liver, bone marrow, salivary glands) drives radioligand dosimetry risk. Nuclens is re-validating its normal-tissue values, so they are not shown here yet. See CEA in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.

CEA gene essentiality (DepMap)

CRISPR knockout effect across 1245 cancer cell lines: 0.06 (not essential). Radioligands kill by radiation, not by blocking the target, so essentiality matters less than for inhibitors. A non-essential target can still be an excellent radioligand target.

Related colorectal cancer radioligand targets

c-MET (MET) · HER3 (ERBB3) · FAP · EGFR · EPCAM · SSTR2 · STEAP2 · HER2 (ERBB2)

See all radioligand therapy targets in colorectal cancer.

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Data sources

Subcellular localization: UniProt via Open Targets (CC BY 4.0 / CC0). Tumor immunohistochemistry: Human Protein Atlas (CC BY-SA 4.0). Clinical trials: ClinicalTrials.gov (public domain). Gene essentiality: DepMap (CC BY 4.0). Internalization and shedding: AI-extracted from PubMed abstracts, so verify against the cited papers before relying on them. Nuclens is a first-pass triage layer, not a substitute for wet-lab validation or clinical dosimetry. Derived expression data on this page is shared under CC BY-SA 4.0.