ACP3 as a Radioligand Therapy Target
ACP3, acid phosphatase 3, is a cell-surface protein. In Human Protein Atlas immunohistochemistry, ACP3 staining is highest in prostate cancer (100% of samples positive), pancreatic cancer (17% of samples positive) and ovarian cancer (9% of samples positive). Clinical status: Discovery-stage (no clinical drug program).
Is ACP3 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 prostate cancer, 100% of samples positive.
- ❔ Internalization: Not yet assessed.
- ⚠️ 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.
ACP3 expression in cancer
Protein expression of ACP3 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 |
|---|---|---|---|
| Prostate Cancer | 1.00 | High | 100% |
| Pancreatic Cancer | 0.06 | Low | 17% |
| Ovarian Cancer | 0.03 | Low | 9% |
| Skin Cancer | 0.03 | Low | 8% |
Not detected by IHC in: colorectal cancer, head and neck cancer, lymphoma, breast cancer, melanoma, kidney cancer, thyroid cancer, bladder cancer, neuroendocrine tumors, cervical cancer, lung cancer, gastric cancer, testicular cancer, endometrial cancer, glioma, liver cancer.
Is ACP3 internalized?
Nuclens has not yet extracted internalization evidence for ACP3. Internalization matters for radioligands because an internalizing receptor traps the radionuclide inside the tumor cell. Run a full analysis to pull the latest literature.
ACP3 clinical trials
Discovery-stage (no clinical drug program). Nuclens hasn't indexed trials for ACP3 yet. Search ClinicalTrials.gov for ACP3 trials.
ACP3 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 ACP3 in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
ACP3 gene essentiality (DepMap)
CRISPR knockout effect across 1250 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 prostate cancer radioligand targets
PSMA (FOLH1) · HER3 (ERBB3) · c-MET (MET) · EGFR · EPCAM · FAP · B7-H3 (CD276) · STEAP2
See all radioligand therapy targets in prostate cancer.
See how ACP3 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.