Receptor binding profile suggests multiple mechanisms of action are responsible for ibogaine's putative anti-addictive activity.
Level 5 - mechanism / opinion, no new human data
In vitro bench pharmacology study
PubMed 7568622 · doi:10.1007/BF02245936
What was done
Radioligand binding assays across more than 50 distinct neurotransmitter receptors, ion channels, and select second messenger systems were performed in vitro to characterize the pharmacological binding profile of ibogaine.
What was found
Ibogaine demonstrated binding interactions across multiple targets at concentrations ranging from 1 to 100 μM. Identified targets included mu, delta, and kappa opioid receptors; 5-HT2 and 5-HT3 serotonin receptors; muscarinic M1 and M2 receptors; dopamine, norepinephrine, and serotonin uptake sites; NMDA-associated ion channels (inhibition of [3H]MK-801 binding); and sodium ion channels (inhibition of [3H]batrachotoxin A 20-alpha-benzoate binding). Specific affinity numbers for individual sites were not reported in the abstract.
Why it matters
These findings suggest that ibogaine's putative anti-addictive actions likely involve polypharmacology across multiple receptor systems rather than a single distinct target.
Limits
The study consists entirely of in vitro binding assays, which do not assess downstream functional activity (agonism versus antagonism) or in vivo relevance. Quantitative affinity metrics for individual targets were not provided in the abstract.
Cited by
- supports Ibogaine interacts broadly with essentially all neurotransmitter systems.