<unk>  is a potent serotonin reuptake inhibitor, but does not affect the reuptake of dopamine. Unlike ibogaine,<unk>  does not bind to the sigma-2 receptor. Similarly to ibogaine,<unk>  acts as a weak NMDA receptor antagonist and binds to opioid receptors. It has greater affinity for each of the opioid receptors than does ibogaine.<unk>  is a hERG inhibitor and appears at least as potent as ibogaine. The inhibition of the hERG potassium channel delays the repolarization of cardiac action potentials, resulting in QT interval prolongation and, subsequently, in arrhythmias and sudden cardiac arrest. κ-Opioid receptor<unk>  has been determined to act as a biased agonist of the κ-opioid receptor (KOR). It activates the G protein (GDP-GTP exchange) signaling pathway with 75% the efficacy of dynorphin A (EC50 = 9 μM), but it is only 12% as efficacious at activating the β-arrestin pathway. Moreover, due to its very low efficacy on the β-arrestin pathway,<unk>  blocked dynorphin A activation of the pathway (IC50 = 1 μM) and hence functioned as an antagonist of it. The β-arrestin pathway is thought to be responsible for the dysphoric and aversive effects of KOR activation, and its lack of activation by<unk>  may be the reason for the lack of dysphoric effects of the drug. This biased agonist/antagonist action of<unk>  at the KOR is unique to it relative to other iboga alkaloids and related compounds such as ibogaine and 18-methoxycoronaridine (18-MC). Moreover, it has been hypothesized that it may give<unk>  unique properties such that it may have the analgesic and antiaddictive effects of KOR agonists without the anxiogenic, dysphoric, or anhedonic effects that are typical of them.
Noribogaine
Oxybuprocaine
Proxymetacaine
Ibogaine
Tetracaine
Levobupivacaine
Procaine
Iontocaine