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Pharmacology of DOx

Hmmm, that's pretty interesting. From time to time "trip" reports pop up claiming to have experienced central activity from phenethylamine, I always dismissed them as placebo... perhaps those people simply have really low MAO activity compared to the majority of the population, and they just can't metabolize it before it reaches their brain.

(sorry to continue off topic)
 
I think it's more that, by taking a large enough dose, MAO becomes saturated and the remaining PEA can get into the brain. Though that hardly sounds safe...
 
Fagott said:
So, I´ve been wondering a lot about the pharmacology of the psychedelic amphetamines, specificaly the DOx compounds, as I would guess that DOI, DOC, DOM, DOB etc. will more or less share the same mode of action.

This is what Wikipedia had to say about DOM:

"DOM is a selective 5-HT2A, 5-HT2B, and 5-HT2C receptor partial agonist. Its psychedelic effects are mediated by its agonistic properties at the 5-HT2A receptor. Due to its selectivity, DOM is often used in scientific research when studying the 5-HT2 receptor subfamily. DOM is a chiral molecule, and R-(-)-DOM is the more active enantiomer, functioning as a potent agonist of the serotonin 5-HT family of receptors; mainly of the 5-HT2 subtype."

Yeah, well, being a psychedelic this really isn´t that surprising.

What I`m really wondering about is wether any of the DOx are known to release or inhibit reuptake of Dopamine or Norepinephrine. I mean, they are amphetamines, so some kind of shared pharmacology with regular amphetamine wouldn´t really be that odd.......?

The reason I´ve been thinking about this is because basically all of the DOx compounds are known to be very stimulating compared to other psychedelics. Could this stimulating side of of these amphetamines be caused by some kind of shared mode of action with the amphetamine structure in side these compounds?

Do we know anything about this? Hope I´m making sense.

Thanks
Click to expand...

According to my limited literature:

"But at higher doses of 10 to 30mg [DOM], it produces an effect said to be like amphetamine combined with LSD but of much longer duration than either-16 to 25 hours or even longer"

Psychedelic effects tend to lie in the R(-) enantiomer and amphetamine effects in the S-(+) enantiomer. This can be seen in MDA.
MDMA for example still has amphetamine effects and is known to release dopamine and NE, but the N-methyl congener eliminates all or almost all psychedelic effects.

I would infer that the amphetamine like effects and the release of D and NE would be present, but less than that of other amphetamines.
 
I believe I have seen the numbers you wanted here: European Journal of Pharmacology 559 (2007) 132–137. Fumiko Nagai et al. The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain. To think that DOX share some pharmacological similarity with amphetamine is a common misconception among drug users.

Here is a table from the article

 
Erny said:
Do you have any reasons to suspect it'll be very different from that of TMA-2?
Click to expand...

That's what I was thinking, except then I thought about the dosage difference.

Thanks for the table anyway, I always thought 2C-x's had some serotonin increasing effect (I see re-uptake inhibition, although mild).
 
You'll notice scattered tendencies of reuptake inhibition and less often release for various 2C-compounds and TMAs. It is plausible that DOx-series compounds would work similarly. We should note, though, that this is nowhere near 'half way between a stimulant and psychedelic'.

ebola
 
Erny said:
I believe I have seen the numbers you wanted here: European Journal of Pharmacology 559 (2007) 132–137. Fumiko Nagai et al. The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain. To think that DOX share some pharmacological similarity with amphetamine is a common misconception among drug users.

Here is a table from the article

Click to expand...
wow 8o Who would have thought DPT, 5-meo-DIPT and 5-meo-MIPT had NE, D and 5-HT reuptake inhibition. Or am reading that paper right? doesn´t feel like it anyway.
 
Erny said:
I believe I have seen the numbers you wanted here: European Journal of Pharmacology 559 (2007) 132–137. Fumiko Nagai et al. The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain. To think that DOX share some pharmacological similarity with amphetamine is a common misconception among drug users.

Here is a table from the article

Click to expand...

Very nice! AMT seems to be a fairly potent triple reuptake inhibitor as well as a releasing agent, didn't know that.
 
^^ i feel like there's likely more to the story than just that. there's roughly a 5x difference in potency. you know more than i do... would the absence of the oxygen in the para position change the way that DOM binds to the receptor?
 
Fagott said:
wow 8o Who would have thought DPT, 5-meo-DIPT and 5-meo-MIPT had NE, D and 5-HT reuptake inhibition. Or am reading that paper right? doesn´t feel like it anyway.
Click to expand...

It's a pretty tiny amount. 5-MeO-DiPT is a tenth as potent at SERT as is AMT, and the typical dose of foxy is maybe a fourth of an AMT dose. So I doubt monoamine release really factors into most tryptamines' action very much.
 
thenightwatch said:
^^ i feel like there's likely more to the story than just that. there's roughly a 5x difference in potency. you know more than i do... would the absence of the oxygen in the para position change the way that DOM binds to the receptor?
Click to expand...

I think it's a somewhat good explanation, it also explains the difference in duration. TMA-2's an 8 hour type thing.

And yeah, having an big oxygen atom in there would affect the way it binds.
 
^^ it is a good explanation but i doubt that it is that simple. its a factor for sure but i feel like there must be more to it than just that.
 
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