M6PR as a Radioligand Therapy Target
M6PR, mannose-6-phosphate receptor, cation dependent, is a cell-surface protein (membrane receptor). In Human Protein Atlas immunohistochemistry, M6PR staining is highest in thyroid cancer (100% of samples positive), kidney cancer (100% of samples positive) and testicular cancer (100% of samples positive). Published literature reports that M6PR internalizes after ligand binding, which helps retain a radionuclide inside tumor cells. Clinical status: Discovery-stage (no clinical drug program).
Is M6PR a good radioligand therapy target?
Scored against the six criteria that decide whether a protein can become a radioligand therapy:
- ✅ Cell-surface accessibility: Localized to the cell surface, so a radioligand can reach it from circulation.
- ✅ Tumor expression: High IHC staining in thyroid cancer, 100% of samples positive.
- ✅ Internalization: Reported to internalize, which favors radionuclide retention.
- ⚠️ Clinical precedent: Discovery-stage (no clinical drug program)
- ❔ Shedding: Not yet assessed.
- ❔ Normal-tissue dosimetry: Check kidney, liver, bone marrow and salivary expression in the Human Protein Atlas tissue atlas.
M6PR expression in cancer
Protein expression of M6PR 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 type | IHC score | Level | % positive |
|---|---|---|---|
| Thyroid Cancer | 0.92 | High | 100% |
| Kidney Cancer | 0.89 | High | 100% |
| Testicular Cancer | 0.87 | High | 100% |
| Colorectal Cancer | 0.86 | High | 100% |
| Prostate Cancer | 0.81 | High | 100% |
| Liver Cancer | 0.81 | High | 100% |
| Endometrial Cancer | 0.78 | High | 100% |
| Breast Cancer | 0.77 | High | 100% |
| Lymphoma | 0.73 | High | 100% |
| Bladder Cancer | 0.72 | High | 100% |
| Cervical Cancer | 0.69 | High | 100% |
| Head and Neck Cancer | 0.67 | High | 100% |
| Ovarian Cancer | 0.67 | High | 100% |
| Neuroendocrine Tumors | 0.67 | High | 100% |
| Lung Cancer | 0.64 | High | 100% |
| Pancreatic Cancer | 0.64 | High | 100% |
| Gastric Cancer | 0.64 | High | 100% |
| Melanoma | 0.56 | High | 100% |
| Glioma | 0.55 | High | 91% |
| Skin Cancer | 0.25 | Medium | 50% |
Is M6PR internalized?
Yes. These bifunctional molecules link a target protein to a lysosome targeting receptor (LTR), forming a ternary complex that drives internalization.
Sources: PMID 42298978 · PMID 41605838 · PMID 41509342 · PMID 40929815 · PMID 39434219. AI-extracted from abstracts, so verify before citing.
M6PR clinical trials
Discovery-stage (no clinical drug program). Nuclens hasn't indexed trials for M6PR yet. Search ClinicalTrials.gov for M6PR trials.
M6PR 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 M6PR in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
M6PR gene essentiality (DepMap)
CRISPR knockout effect across 1258 cancer cell lines: -0.02 (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 thyroid cancer radioligand targets
c-MET (MET) · HER3 (ERBB3) · EPCAM · SSTR2 · EGFR · ITGAV · STEAP2 · FAP
See all radioligand therapy targets in thyroid cancer.
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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.