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Oral metabolism of methoxetamine.

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Methoxetamine:
220px-Methoxetamine.png


Ketamine is subject to a high rate of n-demethylation in the liver leading many users to shun oral use to avoid the first pass from the stomach.

Methoxetamine has an n-ethyl group instead. Would this be subject to the same dealkylation levels?

What is it that makes ketamine's methyl group so easy to remove compared to say, MDMA?
 
It's just the shape of the moledule and how your liver enzymes hit it.

I'd expect N-dealkylation to nor-MXE, oxidisation to 6-hydroxy MXE (and 6-OH-nor-MXE) and maybe O-demethylation. Same as ketamine. I haven't heard of people eating MXE orally, I think sublingual/snorted is going to be the most effective.
 
I don't think it will dealkylate at even nearly the same rate as a methyl. i believe it'd b something similar to o-demethylation, exchanging the methyl on the hydroxy group for ethyl or whatever greatly inhibits it's metabolism. But I'd bet MXE is subject to o-demethylation as well to what i guess u could call hydroxetamine? <-which is probly much more opiate like
 
I don't think it will dealkylate at even nearly the same rate as a methyl. i believe it'd b something similar to o-demethylation, exchanging the methyl on the hydroxy group for ethyl or whatever greatly inhibits it's metabolism. But I'd bet MXE is subject to o-demethylation as well to what i guess u could call hydroxetamine? <-which is probly much more opiate like.

I believe N-ethylation increases the duration by altering kinetics and affinity for NMDA not by preventing metabolism. There are plenty of studies on the metabolism of tiletamine and they all show N-dealkyaltion as one of the primary routes followed by hydroxylation of the ketone and conjugation with glucuronic acid.
 
ulcerative cystitis

Well, 3-methoxylation does not seem to have much effect on duration, if anything it decreases it. So I think the N-ethyl is the best candidate for explaining why MXE lasts as long as it does. Although it is not necessarily one or the other. Here is my question regarding MXE metabolites:

It is common BL lore that ketamine's toxicity to the urinary bladder is the result of norketamine. Often F&B will say something, which may have simply been speculation on his part, and it gets repeated so often that it becomes a fact. Is there any reason to say that norketamine specifically is responsible for ketamine induced ulcerative cystitis? I understand that less than 5% of the drug is excreted unchanged, but there are a half dozen other metabolites that could end up in the urinary bladder: dehydronorketamine, dehydroketamine(?), and whatever conjugates, correct?
 
I believe it's probably an acidic metabolite like 6-hydroxynorketamine that causes ketamine bladder damage.
 
well would this metabolite also be a damaging factor of methoxetamine? I know it wouldn't be the same chemical but would there be something similar?
 
Well that sucks! But I guess it's not really taken orally anyway so it's not a big deal. But still:(
 
Either way it would get metabolized. the doses are much lower with MxE so I duno if it'd be a problem.
 
Yeah, the nice thing about increasing potency is that, as pointed out by Shulgin, you lower the repercussions of metabolic toxicity. This is especially true in the case of things like N-fluoroethyl-nor-LSD, which by all rights really ought to be metabolized to fluoroacetate, but with a dose of about 200 micrograms being metabolized to no more than 30 micrograms of fluoroacetate it doesn't come within 1% of the lethal dose and isn't even close to being concerning.
 
I'm not sure why you attached that link, it does not mention norketamine or other metabolites a single time.
 
I've been getting decent effects off of 20mgs of capped mxe.

I haven't compared it much to sublingual, but it definitely works.

So far it's all been people saying to avoid oral due to ketamine's poor oral uptake, but has anyone else tried it before deciding it was a poor roa?
 
Seems like a number of people in the discussion threads are also saying that oral metabolism has no subjective differences from snorting, so I think there may well be some merit in the idea that it's much less subject to breakdown than ketamine.
 
a number of people have reported that its stronger when taken sublingual or oral as opposed to insufflation.

i have found this to be true but swallowing it has at times led to nausea
 
i have found very little difference between oral, sublingual and insufflated.
 
Hmmm.........can't contribute anythng of substance.......but it seems as though there is a large amount of interest in this compound. I almost feel obliged to test it; purely in name of science.......
 
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