Hi....
Well, by old SAR logic and papers, a MeO or HO or amine group or such on the 3 position of the phenyl ring will produce Mu action. Whether or not this action is agonistic or antagonistic or something else has yet to be determined. The MeO group would produce the least affinity, and Hamhurricane reported a friend screening 3-MeO PCP (which we would expect to behave quite similarly to MXE) for MOR agonism and it having none. It is possible MXE is o-demethylated during its metabolism, producing a 3-HO group ,which has been shown via the PCP analog to have a
much higher affinity...whether this is an agonist or antagonist has yet to be determined. At least by me.

I've read some conflicting stuff. And we still don't know its metabolism.
Aaaand, on the subjective front, I spent a good chunk (10 years) of my early life addicted to opioids. I know mu agonism like nothing else

And I've never felt anything remotely resembling any sort of MOR activity with MXE, in doses up to 100mg. Friends report the same. Friends on opioids with varying affinities (heroin, buprenorphine, hydrocodone) report no antagonism either. If MOR activity of any sort is there I think it is insignifigant at the doses people are taking.
Do your self a favor and I.M. ket. That advice
is harm reduction. Reducing the harm caused by underestimating the power and potential of ketamine by taking it intranasally.

Really, it is
profoundly different. That is, if you really like K. if its just a fuck you up party drug for you, don't bother. But if you are after the dissociative-astral-wormhole-rolls royce-psychedelia, you will be amazed. I'm amazed just thinking about it. Seriously, it is easily in the top ten of experiences a human being can have on this planet. And MXE, while not as drastic of a contrast, is also amazingly better via I.M. than any other ROA. Amazingly.
I described intranasal MXE as unpredictable or inefficient because that is what most users are reporting. The N-ethyl group (as opposed to Kets N-Methyl) serves a few purposes. It is most effective for potency (higher than methyl, or just naked, or going the other way to propyl, etc), as can be seen with difference between MXE> K, or PCE > PCP, etc. It also allows the compound to have much higher oral bioavailability, as can also be seen comparing it to ketamine. This N-ethyl group is believed to be cleaved off metabolically, creating the norketamine version of MXE. This nor metabolite is what is believed to be cause the bladder and kidney issues with K, after prolonged periods of mammoth doses. We should expect MXE to behave similarly, but due to its much lower dose, and its self-limiting nature I think we won't see much true cystosis. But we'll see.
Have you tried sublingual dosing? You mention a drip irritating your stomach but you shouldn't get a drip if you are doing it correctly. Not near as much as by intranasal! Well if you don't try it by I.M. , plugging gets very rave reviews, second only to I.M. I've gotten it to go into solution at 100mg/ml without a problem (heating and stirring) but at higher concentrations it precipitated out after it cooled. 50mg/ml works great, and allows for more refined dosing. Lube up that 3ml and start probing the ol' wormhole!
Have fun and be safe
Of course, glad to be of service! Let us know how your MXE experiences go. I've seen your awed mentions of I.M. ket so I'd love to hear your opinion on methoxetamine.
Cheers