LSD pathways and interaction prediction
Notes
Select any concomitant medications and, if relevant, the phenotype of enzymes involved in metabolism. These selections are used to generate the interaction predictions shown below and to check for supporting literature evidence.
Predictions are supportive estimates only and should be interpreted with caution. The underlying evidence base is limited and includes also in vitro and non-human data, with sparse clinical pharmacogenomic evidence. Results depend on curated metabolic pathways, estimated pathway fractions and categorical inhibitor or inducer strength assignments, all of which may be incomplete or uncertain. The model uses simplified static AUCR assumptions and does not capture many clinically relevant factors such as time-dependent effects, organ impairment, active metabolites, most pharmacodynamic interactions or changes in peak concentration. The list of concomitant medications primarily includes medicines known to inhibit or induce enzymes and these are used to predict pharmacokinetic (PK) effects, with the exception of some known potent 5-HT2A antagonists, which are included to indicate pharmacodynamic (PD) effects.
Select any concomitant drugs:
Select phenotype of enzymes:
PK: Metabolic pathways
Mapped metabolic pathways and enzymes for LSD. Information is sourced from the literature, including in vitro studies, which may not accurately reflect the clinically relevant enzymes in humans.
PK: Transporters
Transporters that may affect absorption, distribution or elimination of LSD.
PD: Pharmacological targets
Main binding targets and receptors associated with the effects of LSD.
Note: The predictions are indicative as the presence and magnitude of interactions may vary depending on route of administration, dose, formulation, timing of co-administration and individual patient factors.