Auger-electron therapy
Auger-electron therapy uses radioactive atoms such as iodine-125 or terbium-161 that release cascades of low-energy electrons travelling only nanometres to micrometres, so they kill a cell only if the atom sits on or inside its DNA and spare the neighbours. Terbium-161 can replace lutetium-177 in existing PSMA ligands; true nuclear delivery remains preclinical.
Overview
Auger emitters such as iodine-125, indium-111 and terbium-161 release cascades of low-energy electrons with nanometre to micrometre range. Delivered into the nucleus they are exquisitely cytotoxic and, unlike alpha emitters, spare neighbouring cells almost entirely. Terbium-161 is closest to clinical use because it can be substituted for lutetium-177 in existing PSMA and somatostatin ligands, with first-in-human work reported; strategies that require true nuclear delivery remain preclinical.
How it works
Electron-capture or internal-conversion decay releases multiple very low-energy electrons; energy deposition is confined to a few nanometres, so proximity to DNA determines lethality.
- Single-cell selectivity, well suited to micrometastases
- Minimal crossfire into normal tissue
- Terbium-161 slots into existing ligand chemistry
- Needs delivery into the nucleus for the pure Auger effect
- Isotope supply and short half-lives
- Dosimetry models built for beta emitters do not apply
Latest papers
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