KIT as a Radioligand Therapy Target
KIT, KIT proto-oncogene, receptor tyrosine kinase, is a cell-surface protein (RTK). In Human Protein Atlas immunohistochemistry, KIT staining is highest in testicular cancer (50% of samples positive), neuroendocrine tumors (50% of samples positive) and thyroid cancer (25% of samples positive). Published literature suggests KIT does not readily internalize, so radionuclide retention may rely on surface binding. Clinical status: Clinical-stage (up to phase 3, any modality).
Is KIT 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: Medium IHC staining in testicular cancer, 50% of samples positive.
- ❌ Internalization: Reported not to internalize.
- ✅ Clinical precedent: Clinical-stage (up to phase 3, any modality)
- ❔ Shedding: Not yet assessed.
- ❔ Normal-tissue dosimetry: Check kidney, liver, bone marrow and salivary expression in the Human Protein Atlas tissue atlas.
KIT expression in cancer
Protein expression of KIT 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 |
|---|---|---|---|
| Testicular Cancer | 0.39 | Medium | 50% |
| Neuroendocrine Tumors | 0.25 | Medium | 50% |
| Thyroid Cancer | 0.08 | Low | 25% |
| Lung Cancer | 0.06 | Low | 8% |
| Melanoma | 0.03 | Low | 8% |
| Bladder Cancer | 0.03 | Low | 8% |
| Pancreatic Cancer | 0.03 | Low | 8% |
| Glioma | 0.03 | Low | 8% |
Not detected by IHC in: skin cancer, colorectal cancer, head and neck cancer, ovarian cancer, lymphoma, breast cancer, kidney cancer, cervical cancer, prostate cancer, gastric cancer, endometrial cancer, liver cancer.
Is KIT internalized?
No. The results indicate that PKC-iota inhibits lipid raft-mediated EGFR endocytosis and degradation while upregulating EGFR membrane localization.
Sources: PMID 41808706 · PMID 41543895 · PMID 41521708 · PMID 40140922 · PMID 39731471. AI-extracted from abstracts, so verify before citing.
KIT clinical trials
Clinical-stage (up to phase 3, any modality). Nuclens hasn't indexed trials for KIT yet. Search ClinicalTrials.gov for KIT trials.
KIT 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 KIT in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
KIT gene essentiality (DepMap)
CRISPR knockout effect across 1254 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 testicular cancer radioligand targets
HER3 (ERBB3) · c-MET (MET) · STEAP2 · SSTR2 · TMEFF2 · Mesothelin (MSLN) · HER2 (ERBB2) · FAP
See all radioligand therapy targets in testicular 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.