PDE9A as a Radioligand Therapy Target
PDE9A, phosphodiesterase 9A, is a cell-surface protein. In Human Protein Atlas immunohistochemistry, PDE9A staining is highest in lung cancer (80% of samples positive), bladder cancer (88% of samples positive) and neuroendocrine tumors (75% of samples positive). Clinical status: Clinical-stage (up to phase 2, any modality).
Is PDE9A 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 lung cancer, 80% 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.
PDE9A expression in cancer
Protein expression of PDE9A 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 |
|---|---|---|---|
| Lung Cancer | 0.53 | High | 80% |
| Bladder Cancer | 0.50 | Medium | 88% |
| Neuroendocrine Tumors | 0.50 | Medium | 75% |
| Melanoma | 0.48 | Medium | 82% |
| Endometrial Cancer | 0.48 | Medium | 73% |
| Ovarian Cancer | 0.47 | Medium | 75% |
| Colorectal Cancer | 0.44 | Medium | 83% |
| Glioma | 0.39 | Medium | 58% |
| Pancreatic Cancer | 0.36 | Medium | 73% |
| Cervical Cancer | 0.36 | Medium | 58% |
| Breast Cancer | 0.30 | Medium | 55% |
| Liver Cancer | 0.30 | Medium | 50% |
| Kidney Cancer | 0.19 | Low | 33% |
| Gastric Cancer | 0.17 | Low | 30% |
| Skin Cancer | 0.17 | Low | 25% |
| Prostate Cancer | 0.10 | Low | 20% |
| Thyroid Cancer | 0.08 | Low | 25% |
Not detected by IHC in: head and neck cancer, lymphoma, testicular cancer.
Is PDE9A internalized?
Nuclens has not yet extracted internalization evidence for PDE9A. Internalization matters for radioligands because an internalizing receptor traps the radionuclide inside the tumor cell. Run a full analysis to pull the latest literature.
PDE9A clinical trials
Clinical-stage (up to phase 2, any modality). Nuclens hasn't indexed trials for PDE9A yet. Search ClinicalTrials.gov for PDE9A trials.
PDE9A 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 PDE9A in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
PDE9A gene essentiality (DepMap)
CRISPR knockout effect across 1251 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 lung cancer radioligand targets
EGFR · HER3 (ERBB3) · c-MET (MET) · EPCAM · CEA (CEACAM5) · STEAP2 · B7-H3 (CD276) · Mesothelin (MSLN)
See all radioligand therapy targets in lung cancer.
See how PDE9A 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.