[13] The β-arrestin signaling pathway is hypothesized to be responsible for the anxiogenic, dysphoric, or anhedonic effects of KOR activation.

[14] Attenuation of the β-arrestin pathway by noribogaine may be the reason for the absence of these aversive effects,[13] while retaining analgesic and antiaddictive properties.

This biased KOR activity makes it stand out from the other iboga alkaloids like ibogaine and the derivative 18-methoxycoronaridine (18-MC).

It induces a robust KOR-dependent increase in GDNF protein levels in the ventral tegmental area and medial prefrontal cortex.

After a single dose or short-term treatment, oxa-noribogaine induces long-lasting suppression of opioid drug seeking in rodent relapse models.