Radioligand plus DNA-repair inhibitor combinations
Adding a PARP or ATR inhibitor to a radioactive drug so the tumour cannot repair the damage the radiation causes.
Overview
Radioligand therapy kills by DNA damage, so blocking repair should amplify it. Early-phase studies combine 177Lu-PSMA with olaparib in prostate cancer and 177Lu-DOTATATE with PARP inhibitors in neuroendocrine tumours; the recurring question is whether marrow toxicity rises faster than tumour control. No phase 3 had read out by 2026.
How it works
Beta or alpha decay produces single- and double-strand breaks; PARP or ATR inhibition prevents repair, converting sublethal damage into cell death and lowering the activity required.
- Rational and mechanism-driven
- Both components already approved separately
- Could reduce the number of radioligand cycles
- Overlapping haematologic toxicity
- Optimal sequencing and timing unknown
- No randomised evidence yet
Latest papers
topQuery for this technology: (TITLE:"Radioligand plus DNA-repair inhibitor combinations" OR ABSTRACT:"Radioligand plus DNA-repair inhibitor combinations") AND (radiopharmaceutical OR radioligand OR radionuclide OR theranostic OR "nuclear medicine" OR "molecular imaging" OR radiotracer OR scintigraphy OR cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about Radioligand plus DNA-repair inhibitor combinations, not a curated reading list.
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