e.g. in the context of conventional beta PRRT (e.g. Lutathera, Lu177 Dotatate) which is based on a somatostatin receptor ‘agonist’ approach, whereas (e.g.) 177Lu Satoreotide is a receptor ‘antagonist’. The differences are quite technical but in the most layman terms, the antagonist has the capability of attaching (binding) to more receptors, including those in a ‘resting’ or ‘inactive’ state, spends more time on the tumor than agonist-based therapies. The result is a higher number of receptor binding sites and greater tumor uptake.
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