theAlkēmist
Alchemist
This is purely speculative and theoretical!!
This is my first post as a full member so thank you Nexus!!
I might have possibly come across information in the journal linked here to explain anecdotal oral activation of ACRB taken whole on its own without MAOIs.
Alongside the MAO we are all familiar with is an enzyme called primary-amine oxidase aka semicarbazide-sensitive amine oxidase (SSAO). This is a new enzyme to me and it seems like there isn’t much research behind it and its role is not fully understood. From my limited understanding it also deanimates short-chain amides just like MAOs via converting primary amides to their corresponding aldehydes, however, it’s speculated it acts by assisting MAO as a ‘scavenger’. MAOIs do not inhibit SSAO.
Several psychoactive compounds are substrates of SSAO (mescaline, tyramine, phenethylamine, etc). Often these compounds are also substrates of MAO-A and MAO-B enzymes.
PRE-NOTE: ACRB contains MAO-B and SSAO Inhibitors. As we know we have to predose with amine oxidase Inhibitors. Hence, eating ACRB just once should not be orally active, you would have to dose twice or three times every half hour.
There are two potent Inhibitors of MAO-B in ACRB. Catechins are fairly insoluble in water and are lipophilic, hence making tea will not extract them.
IC50 = 89μM | (+)(-)catechin
IC50 = 59μM | (-)(-)epicatechin
From all my extensive research tryptamines are equally broken down by MAO-A and MAO-B, so I do not understand why MAO-A is all the fuss. Is DMT different, can anyone provide peer reviewed sources as to why if so?
Five SSAO inhibitors have been isolated from ACRB, these were all myrisetin galloglycosides: EDIT: I’ve found out myrisetin galloglycosides are insoluble in water, hence why anyone who makes a tea without MAOIs reports no effects, and why only reports of eating the bark whole have psychoactive effects.
The two strongest SSAOIs were:
IC50 = 36.16μM | myricetin-3-O-(3″-O-galloyl)-α-rhamnopyranoside-7-methyl ether
IC50 = 39.35μM | myricetin-3-O-(2″,3″-di-O-galloyl)-α-rhamnopyranoside
Followed by:
myricetin-3-O-(2″-O-galloyl)-α-rhamnopyranoside-7-methyl ether
myricetin-3-O-(3″-O-galloyl)-α-rhamnopyranoside
myricetin-3-O-(2″-O-galloyl)-α-rhamnopyranoside
Here is a comprehensive list of SSAOIs
Potent Inhibitors
Geraniin IC50 = 6.58μM (found in Cranesbill, Phyllanthus urinaria L, Geranium maculatum)
Heptylamine IC50 = 7μM
Hexylamine IC50 = 60μM
Nonylamine IC50 = 2nM
Octylamine IC50 = 2μM
Phenylhydrazine IC50 = 30nM
Weak Inhibitors
Butylamine IC50 = 0.1mM
Caffeine IC50 = 0.8 ± 0.3mM
Methylamine IC50 = 1mM
Penthylamine IC50 = 0.1mM
Phenethylamine IC50 = 0.3mM
Tryptamine IC50 = 0.3mM
Inhibitors (Unknown Potency)
Aminoguanidine
B-24
Benserazide
Carbidopa
FLA-336
Galactosamine
Glucosamine
Hydralazine
Hydroxylamine
Iproniazid
MDL-72145
MDL-72974A
Mannosamine
(+)Mexiletine
Phenelzine
Procarbazine
Propargylamine
Pyridoxamine
Semicarbazide
1-(isoquinolin-1-ylcarbonyl)pyrrolidine-2-carboxamide
This is my first post as a full member so thank you Nexus!!
I might have possibly come across information in the journal linked here to explain anecdotal oral activation of ACRB taken whole on its own without MAOIs.
Alongside the MAO we are all familiar with is an enzyme called primary-amine oxidase aka semicarbazide-sensitive amine oxidase (SSAO). This is a new enzyme to me and it seems like there isn’t much research behind it and its role is not fully understood. From my limited understanding it also deanimates short-chain amides just like MAOs via converting primary amides to their corresponding aldehydes, however, it’s speculated it acts by assisting MAO as a ‘scavenger’. MAOIs do not inhibit SSAO.
Several psychoactive compounds are substrates of SSAO (mescaline, tyramine, phenethylamine, etc). Often these compounds are also substrates of MAO-A and MAO-B enzymes.
PRE-NOTE: ACRB contains MAO-B and SSAO Inhibitors. As we know we have to predose with amine oxidase Inhibitors. Hence, eating ACRB just once should not be orally active, you would have to dose twice or three times every half hour.
There are two potent Inhibitors of MAO-B in ACRB. Catechins are fairly insoluble in water and are lipophilic, hence making tea will not extract them.
IC50 = 89μM | (+)(-)catechin
IC50 = 59μM | (-)(-)epicatechin
From all my extensive research tryptamines are equally broken down by MAO-A and MAO-B, so I do not understand why MAO-A is all the fuss. Is DMT different, can anyone provide peer reviewed sources as to why if so?
Five SSAO inhibitors have been isolated from ACRB, these were all myrisetin galloglycosides: EDIT: I’ve found out myrisetin galloglycosides are insoluble in water, hence why anyone who makes a tea without MAOIs reports no effects, and why only reports of eating the bark whole have psychoactive effects.
The two strongest SSAOIs were:
IC50 = 36.16μM | myricetin-3-O-(3″-O-galloyl)-α-rhamnopyranoside-7-methyl ether
IC50 = 39.35μM | myricetin-3-O-(2″,3″-di-O-galloyl)-α-rhamnopyranoside
Followed by:
myricetin-3-O-(2″-O-galloyl)-α-rhamnopyranoside-7-methyl ether
myricetin-3-O-(3″-O-galloyl)-α-rhamnopyranoside
myricetin-3-O-(2″-O-galloyl)-α-rhamnopyranoside
Here is a comprehensive list of SSAOIs
Potent Inhibitors
Geraniin IC50 = 6.58μM (found in Cranesbill, Phyllanthus urinaria L, Geranium maculatum)
Heptylamine IC50 = 7μM
Hexylamine IC50 = 60μM
Nonylamine IC50 = 2nM
Octylamine IC50 = 2μM
Phenylhydrazine IC50 = 30nM
Weak Inhibitors
Butylamine IC50 = 0.1mM
Caffeine IC50 = 0.8 ± 0.3mM
Methylamine IC50 = 1mM
Penthylamine IC50 = 0.1mM
Phenethylamine IC50 = 0.3mM
Tryptamine IC50 = 0.3mM
Inhibitors (Unknown Potency)
Aminoguanidine
B-24
Benserazide
Carbidopa
FLA-336
Galactosamine
Glucosamine
Hydralazine
Hydroxylamine
Iproniazid
MDL-72145
MDL-72974A
Mannosamine
(+)Mexiletine
Phenelzine
Procarbazine
Propargylamine
Pyridoxamine
Semicarbazide
1-(isoquinolin-1-ylcarbonyl)pyrrolidine-2-carboxamide
