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Natural MAO-B inhibitors?

Ham-milton

Ham-milton

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Jul 20, 2007
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I was wondering if anyone was familiar with any natural MAO-B inhibitors, especially any reversible MAOB inhibitors (are there any?) with shortish half lives.

Does Harmine have any MAO-B inhibition?
 
Like I had mentioned in the PEA thread, the kavalactones (especially methysticin) are reversible MAO-B inhibitors. Also, I think I had read that an alkaloid (or perhaps an analogue of an alkaloid) in the Australian Willow was a selective MAO-B inhibitor, but I will have to see if I can remember the name (geip...something).

Also, supposedly the fugus Cordyceps sinensis may be an MAO-B inhibitor, but I can't find anything to substantiate this...

^^Edit^^: The full-text of http://www.ncbi.nlm.nih.gov/pubmed/9764768?dopt=Citation cites cordyceps sinensis as an MAO-B inhibitor...
 
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Okay, I'll have to look into it more.

Unfortunately kavalactones are out, I vomited blood both times I used it, and ended up in the ER one of those time.
 
out of curiosity, are you just looking for MAO-B inhibitors to potentiate dopaminergic activity from other compounds?
 
Ham-milton said:
Does Harmine have any MAO-B inhibition?
Click to expand...


I've wondered the same thing; harmine and related alkloids are contraindicated for use with any phenethylamines, leading me to think there must be some MAO-B inhibition....
 
That was my suspectation.

What would you reccomend for trying to get PEA to be orally active.
 
Fo-ti (He Shou Wu) is widely touted as a MAO-B. Not sure about reversibility or not.

Note that it also seems to be fairly estrogenic and the emodin can cause diarrhea.
 
Took a look at emodin. I think the ki value was 35ug/m, which was the best out of a series of compounds tested (for MAO-B)
 
Tobbacco definitely contains MAO-B inhibitors that I believe are reversible, but I can't name any specific ones off the top of my head.
 
Emodin is weird stuff, I have quite a lot of it but have been scared to take any large amount because of estrogenic, nephrotoxic and gastrointestinal effects (it is a great inducer of diarrhea!).

The anthraquinone derivative Emodin ameliorates neurobehavioral deficits of a rodent model for schizophrenia.
M Mizuno, H Kawamura, N Takei, H Nawa
Center for Transdisciplinary Research, Niigata University, Niigata, Japan.
Abnormality in cytokine signaling is implicated in the neuropathology of schizophrenia. Previously, we established an animal model for schizophrenia by administering epidermal growth factor (EGF) to neonatal rats. Here we investigated effects of the anthraquinone derivatives emodin (3-methyl-1,6,8-trihydroxyanthraquinone) and sennoside (bis-[D: -glucopyranosyl-oxy]-tetrahydro-4,4'-dihydroxy-dioxo[bianthracene]-2,2'-dicarboxylic acid) on behaviors of this model and EGF signaling. Subchronic oral administration of emodin (50 mg/kg) suppressed acoustic startle responses and abolished prepulse inhibition (PPI) deficits in this rodent model. ANCOVA revealed that emodin had distinct effects on PPI and startle responses. In contrast, sennoside (50 mg/kg) had no effects. Emodin attenuated weight gain initially during treatment but had no apparent effect on weight gain and locomotor activity thereafter. Application of emodin to neocortical cultures attenuated the phosphorylation of ErbB1 and ErbB2. We conclude that emodin can both attenuate EGF receptor signaling and ameliorate behavioral deficits. Therefore, emodin might be a novel class of a pro-drug for anti-psychotic medication.
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http://lib.bioinfo.pl/pmid:18301953

The inhibition of emodin on MAO B was of mixed type with the K(i) and K(I) data of 15.1 and 22.9 microM, respectively. [2004]
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http://www.ncbi.nlm.nih.gov/pubmed/15120460
 
It seems to be in a number of plants, like aloe vera (hence the sale as a laxative). Are there related compounds? Interesting to think that aloe inhibits MAO-B.
 
Ham-milton said:
That was my suspectation.

What would you reccomend for trying to get PEA to be orally active.
Click to expand...

Taking a high dose will make it active. 500-1,500 mg works in most people.

Some quotes from other forums.

We've had enough of this testimonials lark & until you actually cite a peer reviewed journal reference for just one of your claims (although most would be rather nice...), the future will be orange!
 
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^^^Goddamn, that testimonial sounds hArDcOrE!

Note:
If you want to be taken seriously, perhaps reply to the following thread:questo
 
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^He's a doctor*, he doesn't care if he's taken seriously as long as he SAVES LIVES! That said, it doesn't appear he cares for that too.

LuxEtVeritas said:
common harmaloids do not have significant MAOB inhibitory properties
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Well, thats kinda what I was saying. Why is phenethylamine contraindicated with ayahuasca if there is no MAO-B inhibition? As we know, proper ayahuasca (b. caapi) ony contains plant based beta-carbolines of the harmala family, which should only be MAO-A inhibitors.

I thought the pricniple MAOi in tobacco was actually harmine....?


*?
 
I just thought of a neat experiment: combine phenethylamine with emodin acutely and concurrently and see if you achieve the 'amphetamine effect'. Emodin is very cheaply and freely available (large amounts are contained in the extract of Japanese Knotweed).
 
nuke said:
I just thought of a neat experiment: combine phenethylamine with emodin acutely and concurrently and see if you achieve the 'amphetamine effect'. Emodin is very cheaply and freely available (large amounts are contained in the extract of Japanese Knotweed).
Click to expand...

Soon to be branded& sold as...

POWER BURN 4000 =D:p
 
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