As with all GPCRs, the 5HT2C receptor can detect extracellular effector molecules to activate intracellular responses. An intracellular signaling pathways that are commonly exploited to measure 5HT2C activation is β-arrestin signaling. It was important for us to demonstrate that the installed photocages effectively diminished the binding capacity of both pharmacophores beyond any physiologically relevant concentration. So, we reasoned that if we could confirm activity by the parent pharmacophores and inactivity of the caged drugs through β-arrestin signaling pathways, it was reasonable to believe that the caged drugs did not act as ligands for the 5HT2C receptor.