VIM as a Radioligand Therapy Target
VIM, vimentin, is a cell-surface protein. In Human Protein Atlas immunohistochemistry, VIM staining is highest in melanoma (100% of samples positive), kidney cancer (100% of samples positive) and thyroid cancer (100% of samples positive). Clinical status: Clinical-stage (up to phase 2, any modality).
Is VIM 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 melanoma, 100% of samples positive.
- ❔ Internalization: Not yet assessed.
- ✅ Clinical precedent: Clinical-stage (up to phase 2, any modality)
- ❔ Shedding: Not yet assessed.
- ❔ Normal-tissue dosimetry: Check kidney, liver, bone marrow and salivary expression in the Human Protein Atlas tissue atlas.
VIM expression in cancer
Protein expression of VIM 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 |
|---|---|---|---|
| Melanoma | 1.00 | High | 100% |
| Kidney Cancer | 1.00 | High | 100% |
| Thyroid Cancer | 1.00 | High | 100% |
| Endometrial Cancer | 0.79 | High | 100% |
| Liver Cancer | 0.79 | High | 100% |
| Head and Neck Cancer | 0.75 | High | 100% |
| Lymphoma | 0.73 | High | 80% |
| Pancreatic Cancer | 0.69 | High | 100% |
| Gastric Cancer | 0.69 | High | 100% |
| Testicular Cancer | 0.67 | High | 92% |
| Lung Cancer | 0.64 | High | 91% |
| Skin Cancer | 0.61 | High | 92% |
| Bladder Cancer | 0.61 | High | 83% |
| Cervical Cancer | 0.47 | Medium | 92% |
| Glioma | 0.44 | Medium | 50% |
| Ovarian Cancer | 0.39 | Medium | 75% |
| Prostate Cancer | 0.19 | Low | 42% |
| Colorectal Cancer | 0.14 | Low | 42% |
| Breast Cancer | 0.03 | Low | 10% |
Not detected by IHC in: neuroendocrine tumors.
Is VIM internalized?
Nuclens has not yet extracted internalization evidence for VIM. Internalization matters for radioligands because an internalizing receptor traps the radionuclide inside the tumor cell. Run a full analysis to pull the latest literature.
VIM clinical trials
Clinical-stage (up to phase 2, any modality). Nuclens hasn't indexed trials for VIM yet. Search ClinicalTrials.gov for VIM trials.
VIM 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 VIM in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
VIM gene essentiality (DepMap)
CRISPR knockout effect across 1258 cancer cell lines: 0.05 (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 melanoma radioligand targets
HER3 (ERBB3) · c-MET (MET) · STEAP2 · SSTR2 · B7-H3 (CD276) · ITGAV · TMEFF2 · FAP
See all radioligand therapy targets in melanoma.
See how VIM ranks against 15,000 targets for your indication.
Run a free analysisData 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.