VIPR2 as a Radioligand Therapy Target
VIPR2, vasoactive intestinal peptide receptor 2, is a cell-surface protein (GPCR). In Human Protein Atlas immunohistochemistry, VIPR2 staining is highest in head and neck cancer (100% of samples positive), skin cancer (92% of samples positive) and kidney cancer (83% of samples positive). Published literature reports that VIPR2 internalizes after ligand binding, which helps retain a radionuclide inside tumor cells. Clinical status: Discovery-stage (no clinical drug program).
Is VIPR2 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 head and neck 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.
VIPR2 expression in cancer
Protein expression of VIPR2 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 |
|---|---|---|---|
| Head and Neck Cancer | 0.89 | High | 100% |
| Skin Cancer | 0.61 | High | 92% |
| Kidney Cancer | 0.47 | Medium | 83% |
| Thyroid Cancer | 0.44 | Medium | 67% |
| Cervical Cancer | 0.39 | Medium | 75% |
| Melanoma | 0.39 | Medium | 67% |
| Lung Cancer | 0.36 | Medium | 64% |
| Bladder Cancer | 0.33 | Medium | 58% |
| Ovarian Cancer | 0.19 | Low | 33% |
| Pancreatic Cancer | 0.17 | Low | 33% |
| Liver Cancer | 0.10 | Low | 10% |
| Testicular Cancer | 0.08 | Low | 25% |
| Glioma | 0.04 | Low | 11% |
| Gastric Cancer | 0.03 | Low | 9% |
Not detected by IHC in: colorectal cancer, lymphoma, breast cancer, neuroendocrine tumors, prostate cancer, endometrial cancer.
Is VIPR2 internalized?
Yes. The PACAP-induced pERK was inhibited by the clathrin inhibitor Pitstop2 to block receptor internalization and endosomal signaling.
Sources: PMID 27194157. AI-extracted from abstracts, so verify before citing.
VIPR2 clinical trials
Discovery-stage (no clinical drug program). Nuclens hasn't indexed trials for VIPR2 yet. Search ClinicalTrials.gov for VIPR2 trials.
VIPR2 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 VIPR2 in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
VIPR2 gene essentiality (DepMap)
CRISPR knockout effect across 1239 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 head and neck cancer radioligand targets
EGFR · c-MET (MET) · HER3 (ERBB3) · ITGAV · SSTR2 · B7-H3 (CD276) · STEAP2 · Mesothelin (MSLN)
See all radioligand therapy targets in head and neck cancer.
See how VIPR2 ranks against 15,000 targets for your indication.
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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.