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Juan J. Nogueira

Institute for Advanced Medical Research

2 papers in the library · 1 citation · publishing 2023-2026

Papers

Characterization of the Binding Poses of Classical and Photoswitchable Psychedelics Interacting with 5-HT2AR

ChemRxiv February 7, 2023 Vito F. Palmisano, Claudio Agnorelli, David Erritzøe et al. 1 citation

Classic psychedelics target the 5-HT2A serotonin receptor, but their precise mode of action remains unclear. Computational modeling of the receptor's orthosteric binding pocket for several psychedelics—including serotonin, LSD, DMT, and a photoswitchable analog (AzoDMT)—revealed two nearly equivalent binding poses. LSD and serotonin preferred the canonical crystallized pose, whereas DMT and 4-OH-DMT slightly favored a newly identified pose. The cis form of AzoDMT was the most stable, and its azobenzene domain interacted with the same residue (L229) responsible for LSD's extracellular loop closure. These simulations clarify drug–protein interactions and may aid development of new psychedelic compounds.

Rewiring Receptor Activation: Mechanistic Insights into Toggle Switch Modulation by 25CN-NBx Compounds

ACS Chemical Neuroscience February 18, 2026 Vito F. Palmisano, Micaela Vidal−sánchez, Juan J. Nogueira

Bulky substitutions on the N-benzyl ring of 25CN-NBx compounds cause a significant shift in the position of W336, a key toggle switch residue in the 5-HT2A receptor. This shift influences receptor activation and is thought to play a crucial role in mediating psychedelic signaling. Potential of mean force calculations along the toggle switch's dihedral angle confirm this result. End-state free energy calculations show that 25CN-NB-2-OH-3-Me and 25CN-NB-2-OH-5-MeO have the highest and lowest affinities, respectively, for the receptor. When W336 adopts its negative dihedral state, it establishes stronger van der Waals interactions with residues F332 and I163, key players in receptor activation. This framework can extend to other G protein-coupled receptors where the toggle switch is central to signal activation.