Ibogaine is a very odd duck in the category of psychedelics. Unlike most psychedelics, which bind principally to the 5-ht2a receptor, ibogaine's affinity for this receptor is 16 micromolar, which should make it irrelevant. Its metabolite noribogaine does bind to the kappa-opioid receptor, the primary target of Salvia divinorum, but still with a weak affinity of around 600 nanomolar. The strongest binding site is actually at the nicotine receptor, and the strongest binding site of noribogaine is at the serotonin transporter. These activities usually would not confer psychedelic action.

It's possible the nicotine-like (nicotinic acetylcholine receptors) and antidepressant-like effects of ibogaine act to moderate and stabilize the typically wild and dysphoric effects of the kappa-opioid activity that is characteristic of salvia intoxication. This might be a combination that could be mimicked by hopefully less toxic synthetic analogues. For its part, salvia demonstrates similar anti-addictive effects to ibogaine in animal trials, but people tend to recall a salvia experience as though they had been run over by a car.