• N&PD Moderators: Skorpio | thegreenhand

Oral metabolism of methoxetamine.

This stuff is absolutely active orally(and great by the way). I've taken it a few dozen times, and recently I noticed that if I take it orally it hits quicker (effects in 10-15 minutes as opposed to 30 min nasally). Also, it's more potent - for me 20mg oral is = to 30mg nasal.

Sublingual I don't have much experience with.
 
I have found mxe to be totally diff orally compared to bumping, bumping had very poor effects, however sublingual was like a diff substance alltogether, deff oral is the way to go imo.
Far less edgy much more positive body effects,music etc
 
Probably not terribly helpful in the discussion of metabolites, but i've found oral to be subjectively more pleasant & roughly equipotent with insufflation.
 
Is it possible that people are finding oral dosing to work better because they are getting MXE freebase. I ordered two chems 4-Aco-DMT Furmarate and Methoxetamine. Since the 4-Aco-DMT had the Furmarate at the end and the MXE didn't have a binding acid I realized the MXE we ordered was probably freebase and not in salt form making it nasally less active if not inactive. I also noted that my friend who snorted it said she got the drip way before she had any effects making me believe that it had to drip into her digestive system before being absorbed into the blood. So I decided to take mine orally, 80mg, and got so much more out of it than my friends even though they snorted like 2-3 times as much. So i had like a 80mg shock to the system where they had 200mg slowly dripping into their system. I feel like one large dose of any drug shocking the system always gets you better than redosing, so much that I never redose anything, if i do, I usually end up chasing a high that I just can't achieve. I just take what I'm doing and ride it out.

Not sure why sublingual or buccal would work better unless freebase drugs flow through those membranes easier than the nasal.
 
I don't think you really have MXE free-base

Is it possible that people are finding oral dosing to work better because they are getting MXE freebase. ...

Since the 4-Aco-DMT had the Furmarate at the end and the MXE didn't have a binding acid I realized the MXE we ordered was probably freebase and not in salt form making it nasally less active if not inactive.

Not to sound disrespectful, but I can say with near absolute surety that you in fact do not have the free-base form of MXE.

* Free-base MXE is usually not a solid, it is a clear to slightly yellowed oil with a thick viscosity.

* No vendor/supplier is currently listing the counter-ion to the MXE cation, so just because your MXE doesn't list the other half of the salt doesn't mean it isn't there. In fact, most 2C-X compounds do not have the salt counter-ion listed either, but that doesn't mean that everyone talking about 2C-C or 2C-P has the free-base form.

* The counter-ion for 4-Aco-DMT is usually listed so that researchers can distinguish between the more stable fumarate and the less stable hydrochloride forms.

* If you ate (oral ROA) MXE free-base the acid in your stomach would immediately protonate the MXE to produce the salt form (MXE pKa probably around 10-11), there would be no difference between MXE free-base and MXE salt via the oral route.

Unfortunately my dedicated thread to MXE free-base was deleted by mods for some reason that I am currently trying to determine, but in the meantime, if you would like to read particulars on the free-base form, please look to Jbrandon's post where he quotes the bulk of the pertinent components of my thread:

http://www.bluelight.ru/vb/threads/...seriously)?p=10114588&viewfull=1#post10114588
 
I believe most MXE is sold as the hydrochloride; indeed this is the route that I have seen e.g. 4-Meo-PCP, tiletamine, and ketamine sold as commercially.

I also think MXE forms hydrated salts, but cannot confirm this.
 
I am currently using methoxetamine as an anti-depressant & have just switched from nasal to oral dosing.

Apart from daily nasal administration destroying your nose/mucus membranes, it is also a poor ROA in terms of bioavailability & duration on onset.

Snorting little white lines of anything is an addiction in itself, hence why it has taken me until now to make the change to oral dosing.

The suggestion that sublingual/buccolingual dosing affects the taste buds & diminishes one's sense of taste completely put me off that ROA. I like to taste my food when I eat so I want my taste buds fully functional! %)

Also, the above-mentioned dose equivelance of 30mg nasal = 20mg oral seems about right.
 
Just to reinforce what others have said, I do find oral dosing of MXE to be very similar in potency as compared to insufflation.

It's interesting that tiletamine is subject to N-dealkylation as a primary means of metabolism - this surely suggests MXE shares a similar fate. Perhaps methoxetamine's primary amine is still an active dissociative? :?

Either way, as an opioid addict several years in remission, I do *subjectively* feel as if oral MXE is a 'warmer' experience - which to me implies at least some O-demethylation to the corresponding 3-HO, 2-Keto PCE.
 
Ketamine is metabolised primarily by N-dealkylation to norketamine via the liver enzyme CYP2B6, and cyclohexyl ring hydroxylation/dehydration to dehydro(nor)ketamine and hydroxy(nor)ketamines. In addition it seems the phenyl ring may be hydroxylated in some individuals, like with PCP->4-HO-PCP.

ISibs.png


Primary urinary metabolites are norketamine and dehydroketamine. Hydroxylated components are usually conjugated. Only norketamine shows activity as a dissociative still. (I assume the phenyl-hydroxylated ketamine metabolites show it too but those are present in vanishingly small amounts).

I expect methoxetamine to follow a similar metabolic fate. Dealkylation to normethoxetamine & dehydration. Nor-methoxetamine is very much still an active dissociative, all of the primary phenylcyclohexylamines should be. I expect it is responsible for the different "feel" of oral vs insufflated vs sublingual admin.

I still have my doubts about ring demethylation to 3'-HO-methoxetamine. 3'-HO-PCP was apparently frighteningly strong as an opioid ligand, & methoxetamine has enough FX at dopamine receptors it would be unusual if it did not produce a "warm glow" (Opioids are fairly strong dopamine releasers, at least in the reward centres IIRC). Also, to the best of my knowledge, it has been shown that ketamine has affinity but no activity at mu-opioid. It deos, strangely, have fx @ the kappa opioid receptor as an agonist, but I'm basing that off a reference guide for medical use.

Refs for metabolism
 
I tried oral dosing ~10mg less MXE than I usually insufflate, and it produced almost zero psychedelic effects. It was much more like an opioid in it's effects instead. Someone I know tried this as well with a tiny dose of kratom and was nodding very hard.

I should note that I was on piracetam as well though.
 
Oral is indeed slightly different effects-wise and defo one hell of a good ROA.
 
Ketamine is metabolised primarily by N-dealkylation to norketamine....I expect methoxetamine to follow a similar metabolic fate. Dealkylation to normethoxetamine & dehydration. Nor-methoxetamine is very much still an active dissociative, all of the primary phenylcyclohexylamines should be. I expect it is responsible for the different "feel" of oral vs insufflated vs sublingual admin.

Since methoxetamine is N-ethyl, would this nor-methoxetamine be N-methyl, or would it reduce it to the primary amine?
 
I tried oral dosing ~10mg less MXE than I usually insufflate, and it produced almost zero psychedelic effects. It was much more like an opioid in it's effects instead. Someone I know tried this as well with a tiny dose of kratom and was nodding very hard.

I should note that I was on piracetam as well though.

piracetam pretty much kills the dissociation effects for you too right? or is it just me?(tried with dmt, mxe, and k)


also anyone able to compare the difference between oral and sublingual? usually sublingual it, but sometimes end up swallowing some in the end anyhow depending on dose.
Is oral "smoother" than sublingual?
 
Nor-MXE would be a primary amine, the liver does not remove single carbon atoms (i.e. convert ethyl->methyl) very well.
 
Top