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    Oral metabolism of methoxetamine. 
    #1
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    Methoxetamine:


    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?
     

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    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.
     

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    #3
    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
     

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    #4
    why would hydroxetamine be more opiate like?
     

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    #5
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    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.
     

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    #6
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    I haven't heard of oral administration either... yet.
    http://www.bluelight.ru/vb/showpost....17&postcount=2 scroll up a little, there's a report there.
    That report also says that n-ethyl increases potency, but he reports it had no effect on duration.
     

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    ulcerative cystitis 
    #7
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    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?
     

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    I believe it's probably an acidic metabolite like 6-hydroxynorketamine that causes ketamine bladder damage.
     

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    #9
    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?
     

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    There's no reason to think there wouldn't be.
     

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    #11
    Well that sucks! But I guess it's not really taken orally anyway so it's not a big deal. But still
     

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    #12
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    Either way it would get metabolized. the doses are much lower with MxE so I duno if it'd be a problem.
     

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    #13
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    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.
     

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    #14
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    It is common BL lore that ketamine's toxicity to the urinary bladder is the result of norketamine.
    http://www.erowid.org/chemicals/keta...article1.shtml
     

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    #15
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    I'm not sure why you attached that link, it does not mention norketamine or other metabolites a single time.
     

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    #16
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    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?
     

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    #17
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    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.
     

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    #18
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    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
     

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    i have found very little difference between oral, sublingual and insufflated.
     

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    #20
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    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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    #21
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    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.
     

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    #22
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    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
     

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    #23
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    Probably not terribly helpful in the discussion of metabolites, but i've found oral to be subjectively more pleasant & roughly equipotent with insufflation.
     

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    #24
    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.
     

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    I don't think you really have MXE free-base 
    #25
    Quote Originally Posted by Robf11 View Post
    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/5...1#post10114588
     

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