Few questions about DXM

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So I find myself wanting to try DXM seriously for the first time. It might sound funny considering that I've been an ex meth and benzo addict and basically tried whatever reached my hand including H plurious times but so far I never tried a decent dose of DXM since it is absolutely unknown as a recreational drug here where I live and I always though of it as a 'cheap' way of getting a 'cheap' high, however after a little bit of reading I changed my mind and I'm planning to give it a try.

I got some questions however that I would like to bring up:

1) How come DXM has such a low bioavailbility? From what I read on wiki only ca. 10% of the substance actually does its job and it seems that DXM itself isn't really the drug but rather a prodrug that turns into dextrorphan which for some reason is listen in schedule I according to american laws (isn't this pretty fucked up?). So does this mean that out of 1000mg of DXM only 10% will be converted into DXO and do its job?

2) Is there any other way you know apart from IV to increase the bioavailability of DXM? I've tried other drugs rectally very few times cuz I stil don't find myself very comfortable with sticking things up my arse, and for now I would like some serious advice before trying to do it with DXM.

3) What's up with DXM always being sold as DXM.HBr? Is it unstable in other acid conjugated forms? This is also pretty annoying since HBr has a MM of about 81 compared to the MM of DXM wich is 271 lowering by far the actual dose of the compound when looking up at the pill box mg content.

Thanx

 

[madswagga]

this is all off the top of my head

1) your body does not get high off dxm, but rather its metabolite DXO. Your body breaks down DXM into DXO naturally. The dosage's everyone has come up with does not deal with DXO, just the dosage of DXM you must put in your body. I am not sure what the conversion ratio is.

2)grapefruit juice, or any other juice that is highly acidic. this improves the conditions of which your body can convert the DXM to DXO, thus giving a better ratio. DONT IV DXM!!! unless you can obtain it from a dealer or extract the dxm and convert it over to a freebase form would i do it any other way than ingesting (which would be snorting).

3) hydrogen bromide is only the cation, you can find DXM HCl or DXM polistrex (delsym)

 

[LawnChairSkank]

You can extract the dxm hbr, and turn it into dxm hcl or dxm citrate. Google a guide for it, its fairly simple. A lot of people don't like high doses of the bromide salt because it causes a histamine release and makes them itch like crazy.

 

[onmyway]

i don't know anything about the pharmacokinetics of DXM, but i think you should refrain from administering it IV. i have never heard of anyone doing that. i'm sure you could find papers where it is given iv to rats (or even people), but that is done under presumably ideal conditions with ideal preparation. unless you research it and find pharmaceutical grade DXM, don't iv it.

 

[melange]

you are wrong - dxm is active in its own right, you are not just "getting high" on dxo - quit spreading misinformation

 

[indelibleface]

Here's an interesting excerpt from the incredibly well researched and entertaining DXM FAQ by William White on Erowid:

Dextrorphan is a metabolite of DXM (i.e., the body converts DXM to dextrorphan). The conversion from DXM to DXO occurs via removal of the methyl group at position 6, a process called "O-demethylation". DXO is very similar chemically to DXM, and reacts with the same receptors in the body, but with a very different spectrum. Whereas DXM is strongest at the PCP2 and sigma receptors, DXO primarily targets the NMDA receptor (see Section 10).

The practical upshot is that the dissociative and intoxicating or "stoning" effects are stronger with DXO, whereas the stimulation, cognitive alterations, delusions, and psychotomimetic (literally, "psychosis-like") effects are stronger with DXM. Most DXM users find some balance between the two to be the most pleasurable. Too much sigma activity is usually regarded as dysphoric (strongly unpleasant) and disturbing, and if prolonged, may be dangerous (101,135).

Fortunately, you don't have to worry about converting DXM to DXO; the body does it for you via an enzyme called P450-2D6 or CYP2D6 (also called debrisoquine 4-hydroxylase). However, between 5 to 10% of the Caucasian population lacks this enzyme (12-15), and in the rest of us it can vary. Many drugs can temporarily block P450-2D6 from working (10-11) and thus alter the balance between DXM and DXO. For a list of these drugs, see Section 15.1.

One of DXM's metabolites, 3-methoxymorphinan, can itself block P450-2D6. As a consequence, taking a second dose some time after the first dose of DXM will probably increase the ratio of DXM to DXO in the bloodstream. Taking the dose all at once, on the other hand, will probably increase the relative amount of DXO. Generally, then, the quicker the dosing, the more DXO and less DXM, and the more NMDA blockade (like ketamine) and the less sigma and PCP2 activity. Subcutaneous injection leads to very little conversion from DXM to DXO.

When discussing effects, this text usually uses "DXM" to refer to both dextromethorphan and its metabolite, DXO. A few people have used DXO specifically; one indicated that it did in fact have fewer cognitive effects than DXM.

If you're planning on venturing into DXM experimentation, the FAQ has pretty much everything you would ever want to know (and makes for quality bathroom reading if you print it out, lol). It's nice, because it contains all sorts of newbie information as well as the advanced chemistry and pharmacology stuff that is more relevant to the ADD crowd.