HTR3A as a Radioligand Therapy Target
HTR3A, 5-hydroxytryptamine receptor 3A, is a cell-surface protein (GPCR). In Human Protein Atlas immunohistochemistry, HTR3A staining is highest in melanoma (25% of samples positive), lymphoma (17% of samples positive) and kidney cancer (9% of samples positive). Evidence on whether HTR3A internalizes is mixed. Clinical status: Clinical-stage (up to phase 3, any modality).
Is HTR3A 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: Low IHC staining in melanoma, 25% of samples positive.
- ⚠️ Internalization: Mixed evidence.
- ✅ 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.
HTR3A expression in cancer
Protein expression of HTR3A 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 | 0.11 | Low | 25% |
| Lymphoma | 0.08 | Low | 17% |
| Kidney Cancer | 0.03 | Low | 9% |
| Pancreatic Cancer | 0.03 | Low | 9% |
| Skin Cancer | 0.03 | Low | 8% |
Not detected by IHC in: colorectal cancer, head and neck cancer, ovarian cancer, breast cancer, thyroid cancer, bladder cancer, neuroendocrine tumors, cervical cancer, lung cancer, prostate cancer, gastric cancer, testicular cancer, endometrial cancer, glioma, liver cancer.
Is HTR3A internalized?
Uncertain. Insufficient literature found.
HTR3A clinical trials
Clinical-stage (up to phase 3, any modality). Nuclens hasn't indexed trials for HTR3A yet. Search ClinicalTrials.gov for HTR3A trials.
HTR3A 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 HTR3A in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
HTR3A gene essentiality (DepMap)
CRISPR knockout effect across 1236 cancer cell lines: 0.15 (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.
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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.