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Is bk-MBDB neurotoxic?

DL's post was by me, I forgot to switch accounts.

As to the above poster, you are correct. MBDB compared to MDMA has less DA release and higher NE release, chuck a beta ketone on there and you will increase the NE release.

Potentially BK-PMMA looks dangerous as it's non bk cousin is a strong SE releaser and MAOI, I have a friend that has taken loads and noticed no temperature or blood pressure issues beyond a normal stimulant. There is a report on bluelight where the user wore a bp monitor and regularly recorded body temp and it seemed benign. However, till there are many more reports/studies I would advise caution.

I wonder if the beta ketone (same place as the beta hydroxyl in E/NE) makes it easier for MAO A to break down.
 
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Well cathinones last a shorter amount of time than their amphetamine cousins.

Résumé / Abstract
Twenty-nine arylisopropylamines, substituted at the β-position of their side chain by an oxo, hydroxy, or methoxy group, were evaluated in vitro as MAO-A and MAO-B inhibitors. The oxo derivatives ('cathinones') were in general less active as MAO-A inhibitors than the corresponding arylisopropylamines, but exhibited an interesting MAO-B inhibiting activity, which was absent in the hydroxy, methoxy, and β-unsubstituted analogues. These results suggest that selective affinity for the two MAO isoforms in this family of compounds is modulated not only by the aryl substitution pattern but also by the side-chain substituents on the aryl-alkylamine scaffold.
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Cathinones are less active at MAO-A than their amp cousins (MAO-A being responsible for E, NE, SE, and DA) but more affective at MAO-B inhibition (Dopamine and phenethylamine), meaning there would be a higher DA level, but far less SE. This in theory means there is a far far lower risk of serotonin syndrome, especially as the SE release of the bk's will be far lower than their infamous PMA, PMMA and 4 MTA non bk's.

Still, be very careful with experimenting.
 
If the metabolite neurotoxicity theory of MDMA is correct, then couldn't it be likely bk-mbdb could also form toxic metabolites? Irrelevant of dopamine activity, sufficient buildup of a toxic metabolite could be reuptaken into the SE axons and damage them at high enough concentrations. I do understand the hyperthermia is an important factor to neurotoxicity with these compounds, so maybe this is bk-mbdb's saving grace.
 
Hammilton said:
And no: there is no single published study of pCA in humans. If it's ever happened, and it seems especially unlikely since there's no record of it, the only conspiracy theory would have to be Army / CIA studies. There's a lot known about MK-ULTRA now, and pCA has never been mentioned, though.
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Actually...

http://jcp.sagepub.com/content/13/1/3.short
http://www.springerlink.com/content/p326g68700v84032/

The former shows that PCA was tested on humans as a potential antidepressant, and functioned as such.
The latter explains why PCA, and n-methyl-PCA, got past animal trials. It seems that the researchers interpreted depleted 5HT concentrations as simply the result of 5HT release and subsequent degradation, a good sign for antidepressant efficacy. They had no idea that it was largely permanent, toxic damage.
How ironic...
 
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