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Radioactive decay is a spontaneous physical process by which an unstable atomic nucleus loses energy by emitting ionizing radiation, such as alpha or beta particles and gamma rays. In a pharmacological context, it is not a biological target (e.g., a receptor or enzyme) but rather a mechanism used by radiopharmaceuticals to deliver cytotoxic energy to specific sites, such as tumor cells. Radiotherapeutic agents like Lutetium-177 or Iodine-131 leverage this process to induce lethal DNA damage and oxidative stress, leading to the destruction of targeted cells. Because radioactive decay is an intrinsic physical property of certain isotopes, it cannot be modulated or inhibited by traditional biochemical drug-receptor interactions. In therapeutic development, the biological 'target' is usually a specific surface antigen (e.g., PSMA or somatostatin receptors) to which the radioactive isotope is conjugated, while the decay itself serves as the payload's effector mechanism.
Emission of ionizing radiation (alpha particles, beta particles, or gamma rays) from unstable nuclei leading to DNA double-strand breaks and the generation of reactive oxygen species.
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