It is the result of O-demethylation of the prodrug by several enzymatic systems, although it is chiefly a product of the Cytochrome P450 IID6 (CYP2D6) pathway.
Pharmacology
Dextrorphan is structurally similar to dextromethorphan, and has an affinity for the same receptors in the central nervous system, although with a slight difference in selectivity. While dextromethorphan is a weak non-competitive NMDA receptor antagonist, dextrorphan is a more potent antagonist[1].
It should be noted, however, that due to its potency as an NMDA receptor antagonist, as well as the fact that it is produced as a by-product of DXM metabolization in the body, DXO is thought to be largely responsible for the psychological side-effects that occur at high doses of DXM. These side-effects can include alteration of consciousness, or "cognitive dissociation", which are characteristic of NMDA blockade and which have afforded DXM its potential for use as a recreational drug.