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What are "Low dosages" of PEA? - A problem with the second passage of the article[edit]

The very second passage of the article ends with the sentence: "however, orally ingested phenethylamine experiences extensive first-pass metabolism by monoamine oxidase B (MAO-B), which turns it into phenylacetic acid. This prevents significant concentrations from reaching the brain when taken in low doses.[4][5]".

Indeed - A clarification is needed: What are these "Low doses" the article mention? I don't have an access to the listed articles from the PC (and seemingly won't have easy access anyhow in the next weeks), But someone who can should take care of this asap.

Another thing that should be clarified is if very similar molecules (like Phentermine for example), goes through the same metabolic processes... Thanks, Ben-Natan (talk) 01:08, 3 December 2014 (UTC)

We're actually not supposed to specify a specific dose in articles per WP:MEDMOS, but to answer your question here: the paper linked in the section above this lightly covers the neuropsychological effects of oral PEA in humans. The psychoactive dose of PEA varies by individual - mostly due to individual differences in MAO-B expression/activity; it can enter the brain since it's quite plasma-soluble and easily crosses the blood-brain barrier (and membranes in general). In individuals with no drug tolerance to TAAR1 agonists, the above ref notes that 500 mg can induce noticeable cognitive effects in some people, though I imagine for others it might be on the order of 1-2 grams (re: MAO-B variability). PEA is regulated as a dietary supplement and sold commercially (e.g., Amazon's search results), so you can technically see for yourself if you're not convinced. It's more potent than amphetamine at modulating dopamine neurotransmission, so a psychoactive dose will induce a blatantly obvious effect (e.g., euphoria, motivated behavior, increased arousal, etc), despite being rather transient due to the half-life.
W.r.t. the second question, α-methylated PEA derivatives (amphetamine - i.e., α-methylphenethylamine - is the parent of these; phentermine is amphetamine with an additional α-methylation - i.e., α,α-dimethylphenethylamine) are quite robust to metabolism by MAO-B (see Phenylpropanolamine#Chemistry for more on the structure-activity relationship of some PEA substitutions). In contrast to PEA, substituted amphetamines generally are metabolized primarily by CYP2D6. The other methylphenethylamines (and some of their derivates) are all metabolized by MAO-B, similar to PEA. Seppi333 (Insert  | Maintained) 06:52, 3 December 2014 (UTC)

I'm sort of chemistry illiterate, so...[edit]

@DMacks: Did I say anything stupid in this edit? Seppi333 (Insert  | Maintained) 11:49, 10 March 2015 (UTC)

Looks fine. That specific example comes from the cited ref. And this method is not one of the "Alternative syntheses are outlined in the footnotes" of the OrgSyn ref. With so many different methods available, probably should have some criteria for deciding what to illustrate. For example, being an OrgSyn prep is a pretty strong assertion of value, rather than just being a primary scientific-lit ref. DMacks (talk) 12:01, 10 March 2015 (UTC)
Ah. I merely included it because it's the only usable synthesis diagram on Commons for enwiki... and I felt like the phys/chem section could use a little expansion since it's dwarfed by the pharmacology section. Seppi333 (Insert  | Maintained) 13:35, 10 March 2015 (UTC)
I'll work on some synth diagrams. Definitely will do OrgSynth (a gold-standard for synth). Others seem merely mechanistic studies, making this among many other similar compounds to demonstrate a certain new reaction (for example, the JACS ref for LiAlH4), rather than as a citedly valuable route for this particular chemical. A useful one would be if there is a most recent discussion in secondary lit, or the current commercially- or illicitly-used routes. PiKHAL mentions reduction of benzyl cyanide and decarboxylation of phenylalanine as the two major industrial routes (without comment about what reagents are used). DMacks (talk) 18:56, 11 March 2015 (UTC)

Legal status UK[edit]

It must be a mistake that the legal status of phenethylamine is "Class A" in the UK. Or is chocolate now illegal in the UK?!?
If it would be true, then the next step would be a ban on phenylalanine, because of being a precursor of phenethylamine -> phenylalanine is an essential amino acid => no phenylalanine, no human life possible

Regards, Stefan --Stefan Bach7777 (talk) 21:05, 16 April 2015 (UTC)

Drugs controlled by the UK Misuse of Drugs Act#Class A drugs says compounds "structurally derived from phenethylamine" are banned but it doesn't say anything about phenethylamine itself. I'll change this. Sizeofint (talk) 23:44, 16 April 2015 (UTC)

Legal Status in NZ[edit]

Hi guys,

There seems to be some issues with the footnote for whether this compound is legal in NZ. Firstly, the reference isn't the correct way of referencing legislation or schedules within. Secondly, the reference may be out of date or incorrect as a search of that piece of legislation reveals no mention of it anywhere. Could someone please look into this? — Preceding unsigned comment added by ClubmanGT (talkcontribs) 22:11, 15 April 2016 (UTC)

Phenethylamine monographs[edit]

There is a LOT of content from these sources that needs to be added to the article. Seppi333 (Insert ) 21:32, 20 September 2016 (UTC)

Phenethylamine monographs


  1. ^ "2-PHENYLETHYLAMINE". United States National Library of Medicine – Toxicology Data Network. Hazardous Substances Data Bank. Retrieved 20 September 2016. 
  2. ^ "Phenethylamine". United States National Library of Medicine – National Center for Biotechnology Information. PubChem Compound. Retrieved 20 September 2016. 
  3. ^ "Phenylethylamine". HMDB Version 3.6. Human Metabolome Database. 11 February 2016. Retrieved 20 September 2016. 

New review to add[edit]

  • [1] - probably worth adding content from tables 3+4 and the article text. Seppi333 (Insert ) 19:57, 30 January 2017 (UTC)


  1. ^ Khan MZ, Nawaz W (October 2016). "The emerging roles of human trace amines and human trace amine-associated receptors (hTAARs) in central nervous system". Biomed. Pharmacother. 83: 439–449. doi:10.1016/j.biopha.2016.07.002. PMID 27424325.