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Radioligand therapy target profile

c-MET (MET) as a Radioligand Therapy Target

MET proto-oncogene, receptor tyrosine kinase · Ensembl ENSG00000105976 · Data updated 2026-09-28

c-MET (MET), MET proto-oncogene, receptor tyrosine kinase, is a cell-surface protein (RTK). In Human Protein Atlas immunohistochemistry, c-MET staining is highest in colorectal cancer (100% of samples positive), thyroid cancer (100% of samples positive) and head and neck cancer (100% of samples positive). Published literature reports that c-MET internalizes after ligand binding, which helps retain a radionuclide inside tumor cells. Clinical status: Clinical-stage (up to phase 3, any modality), with 97 active clinical trials.

LocalizationCell-Surface
Top cancer (IHC)Colorectal Cancer
InternalizationYes
Clinical stageClinical-stage (up to phase 3, any modality)
Active trials97
Cancer association (Open Targets)0.93

Is c-MET a good radioligand therapy target?

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

c-MET expression in cancer

Protein expression of c-MET 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 Cancer0.86High100%
Thyroid Cancer0.83High100%
Head and Neck Cancer0.75High100%
Ovarian Cancer0.72High100%
Kidney Cancer0.72High100%
Cervical Cancer0.72High100%
Melanoma0.67High100%
Pancreatic Cancer0.67High100%
Endometrial Cancer0.67High100%
Bladder Cancer0.64High100%
Gastric Cancer0.64High100%
Liver Cancer0.60High100%
Skin Cancer0.58High100%
Neuroendocrine Tumors0.58High100%
Breast Cancer0.58High100%
Testicular Cancer0.52High100%
Prostate Cancer0.47Medium100%
Lymphoma0.47Medium92%
Glioma0.42Medium100%
Lung Cancer0.42Medium91%

Is c-MET internalized?

Yes. The review mentions 'internalization-dependent killing' which implies that MET undergoes internalization upon activation, particularly in the context of antibody-drug conjugates.

Sources: PMID 42352921 · PMID 42323111 · PMID 42207299 · PMID 42145655 · PMID 41880505. AI-extracted from abstracts, so verify before citing.

c-MET clinical trials

Clinical-stage (up to phase 3, any modality). 97 active trials reference c-MET (ClinicalTrials.gov, accessed 2026-09-28).

NCT07842835 · NCT05789303 · NCT07605416 · NCT07692529 · NCT02693535 · NCT03899155 · NCT04661137 · NCT03793179 · NCT04923893 · NCT06452277 · NCT07100080 · NCT06717347

c-MET 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 c-MET in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.

c-MET gene essentiality (DepMap)

CRISPR knockout effect across 1258 cancer cell lines: -0.04 (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

HER3 (ERBB3) · FAP · EGFR · CEA (CEACAM5) · 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.