Psilocybin, a novel therapeutic, is metabolized to psilocin, which alters brain function by engaging serotonin receptors. In fifteen healthy individuals, a psychoactive dose (0.2-0.3 mg/kg) reduced the integrity and segregation of brain networks, including the default mode network, while increasing connectivity between networks like the executive control and dorsal attention networks. These changes correlated with plasma psilocin levels and subjective drug intensity. The findings link psilocin's time course to shifts in brain functional architecture and subjective experience, offering insight into the neurobiological mechanisms of psychedelic effects and consciousness.
Bromo-dragonfly, a potent and long-acting hallucinogen linked to severe vasoconstriction and fatal intoxications, was not metabolized in human liver microsomes, cytosol, or recombinant enzyme systems, unlike its analogue 2C-B-fly, which underwent monohydroxylation and N-acetylation via CYP2D6 and MAO-A. Bromo-dragonfly competitively inhibited monoamine oxidase A (MAO-A) with a Ki of 0.352 μM, and its IC50 suggested clinically relevant MAO-A inhibition, though further data are needed to assess its impact on serotonin levels in the body. Protein binding and pharmacokinetic parameters were also investigated.