Thanks, thats more useful but how about the mole question?

The molar excess confuses me but mayb its the same as the benzo?

Dingbow. Thanks for thee heads up... but if its basics why have you and sedit given different answers? It makes sense to me now though!
 

dingbow your correct on both fronts, it wasn't just a long day but an early morning at that point . Chilling out with friends till three in the morning getting the spirit in you makes keyboards your enemy.

I asked about this in the monomethylation of amphetamines, but no one answered me so far, so ill ask here

is N-methyl 2-phenethylamine active? I'v read somewhere that the methyl group protects it from monoamine oxidase, but wikipedia didnt give me much to work with.

There's no truth to the ridiculous rumor that the swarm is omniscient, but hope seems to spring eternal among the newbees    The long time member that has posted the synthesis elsewhere doesn't log on here much     The MSDS says that it's toxic, specifically stating it's harmful if swallowed   You're going to have to find that on your own if you want to read it since that MSDS comes from a source    All that was done to find this information was to input the name of the compound into a search engine, which is something you should have done already   

Its IMO more worth searching for potential journal references, via a search engine, and in particular, google scholar, if trying to find out if a known compound is active in that sort of way.

MSDS sheets do not usually, of ones I have seen give data on psychotropic properties. There are exceptions, such as intoxicating industrial solvents sometimes, giving usually hints, reading between the lines, not ofthen that I can recall reading, have I ever seen something more direct. MSDS sheets on DOx amphetamines I have read came up with basically, summed up, data in that particular respect, amounting to 'hazardous by....various routes of exposure'

I would hazard a guess, based on extrapolation from the activity per os of 2,n,n-trimethyltryptamine that it is not impossible that shielding from MAO-a would be accomplished in this manner. 2,n,n-TMT has some pretty similar features, structurally, n,n-DMT of course is inactive by mouth thanks to MAO chopping it a new arse ring fast and efficiently enough to prevent it getting to the brain, Might have been Shulgin you read, if it was 2,n,n-TMT you are thinking about, that is in TIHKAL. Can't remember off the top of my head anything about the amphetamine...

But either way, all three of the major player monoamine neurotransmitters are targeted by MAO-a, although, MAO-a being more selective for adrenaline-like pressors, for tyramine (dietary, also trace amine neurotransmitter, ligand of TAAR subtype something or other I think...not very well up on trace-amine associated receptors and their neuropharmacology though I must confess), and for serotonin, as far as I remember, and MAO-b preferring dopamine and dietary phenethylamine in terms of selectivity.

Now..I must say, you cannot have searched that hard on wikipedia, if you just searched for the compound itself, rather than data on MAO isoforms (in the human there are only two to choose from) and drug user forums of note, such as bluelight, drugs forum to name the main two I know of, and in one case am a member of under another handle, monoamine oxidase inhibitors, to see if anybody had put to test, despite potential danger of hypertensive crisis in the case of a fuckup or unpredictable dangers aside from the known possibilities of interactions of monoamine releasers with MAOIs of other sorts, the thought to test either an inhibitor of MAO-a, or MAO-b with phenethylamine as a substrate, given the very easy access to phenethylamine and lack of legal 'control' of it.

That would help figure out weather blocking either enzyme might render PHE an active psychostimulant, and takes, knowing what needs blocking to protect the target molecule, and that there are only two subtype being, if you didn't already know, no specialist pharmacology knowledge to go and look how many there are one might have to boil it down to to figure out deductively, only logic (i.e, if MAO-a inhibitors are WELL KNOWN for being potentially lethal with stimulants, and the older irreversible inhibitors of MAO-a used as antidepressants, now one of the last lines of attack when attempting to remedy treatment-resistant depression, because the well known dietary restrictions, which are always mentioned in any article about MAOI antidepressants or drug user discussion on ayahuasca, or oral DMT in other settings, any of the articles on somewhere like wikipedia, pubmed, medline, etc, inform that a 'cheese reaction' as its often referred colloquially to, in the case of those older MAOIs, phenelzine, tranylcypromine etc. wasn't just much much more likely with a much smaller amount of tyramine-containing food, and pretty damn certain if adrenergic pressors, or noradrenergic/serotonergic releasers, but its pretty easy for it to prove fatal also. Which should disqualify searching for MAO-a as the responsible enzyme and have one look towards the other isoform, MAO-b, because if somebody tried testing either sort of MAOI against a MAO-substrate and reported success in using it to produce amphetamine like effects, it can only have been a selective MAO-b inhibitor, with a MAO-a inhibitor of any significant efficacy its already well known, and has been for decades, that a MAOa blocker, including reversible (competitive) inhibitors that stimulants would produce a hypertensive crisis and severe, or possibly still in the latter case, fatal nevertheless, MAO-b must be the one to look for data on targeting by the structural modification in question, the 2 position methyl as opposed to the better known alpha substituent.

MAO-a is present in the periphery, whereas MAO-b is the one found in the brain. I think the question would be solved, if you were to find out (go search those journals, as I said...I've been doing that since 4am last night, with one break for a meal for someone, if something is important enough to need to know, it is important enough to do one's best to find out..I'm using my pharmacology knowledge to help with a potential idea of what to look for, and why, I don't know myself though if MAO-b will be inhibited by this modification)

Here is my logic on thinking it might be what would give a good suggestion of possible, or indeed probable activity:

MAO-a is present peripherally, this definately chews up DMT, and unless given via smoking, rectally, insufflation, or parenterally then it never gets to the brain before its destroyed, thus it must be MAO-a (backed up by the MAO-a selective monoamine oxidase inhibitors, the harmala alkaloids, and by moclobemide, a pharmaceutical competitive inhibitor of MAO-a also being the ones that get used successfully in ayahuasca and various derivatives on that theme that permit an orally inactive tryptamine to become orally active)

An alpha-methyl on either phenethylamine, or tryptamine is definately well known to render both active orally, and in the case of phenethylamine, it has been used as a stimulant by the use of a MAO-b inhibitor, to prevent its degredation too quickly to be of use, I believe the one people tried and reported success doing so  on bluelight was selegiline (which however does cross over into MAO-a inhibition above a certain dose threshold, and in light of this, it was directly stated on bluelight, and I believe more than once, that if it was to be tried at all, selegiline must be dosed at a level which avoids inhibiting MAO-a)

So...look for structurally similar MAO substrates, ones that have a 2-carbon sidechain coming off the ring, that the amine is located on in a similar, or if nothing better can be found, which is unlikely, the next closest positions on a straight chain should be evaluated, and which bear, ortho to the aminoalkyl chain, a methyl group.

And search by topic, as well as likely molecular structures, google scholar is a good place for all sorts of articles, might have to request some articles of interest from those who do have access, if you haven't or can't find it uploaded somewhere already.

I honestly have no idea, weather the docking site between ligand and MAO-b is of the right topology to fit, and just have poor efficacy in the case of AMT. Wikipedia states that dopamine is equally broken down by both isoforms, but, I still think MAO-b protection is whats needed, given a MAO-b inhibitor HAS worked to twist the arm of phenethylamine (this requires great care of course),

But protecting the drug from metabolism, rather than blocking the metabolic machinery from acting by targeting IT, is a great deal safer in many cases...there are exceptions, that is not a rule, acetylcholine receptor mimics, have some pretty bloody lethal toxins on both sides, enzyme inhibitors (nerve agents) or (especially nicotinic types) cholinergic agonists (compounds that act either to irreversibly activate neuromuscular junctions and cause rigid paralysis and suffocation, such as the cyanobacterial anatoxin-A, otherwise known by the nickname 'very fast death factor',

And some that merely continuously cause depolarisation via allosteric binding to the neuromuscular junction type AChR and allow for a non-rigid hypertonic paralysis being that its acetylcholine doing the actual activating of muscular firing, which IS damn quickly, and efficiently removed by acetylcholinesterase, but drugs but are too slowly broken down by the slower-acting butyrylcholinesterase to be removed quickly enough to prevent, after an initial successive, repetitive firing then subsequent exhaustion of the capacity to repolarise (the depolarising neuromuscular blocking agents, such as succinylcholine, used for its rapid onset and short duration of effect for some surgical procedures, notably intubating a critical patient) or antagonists (non-depolarising neuromuscular blockers agents like curare)

So, always do your research, accidents happen, its true, like the case of that poor bastard Kidston, with his botched meperidine analog run that resulted with MPTP, which causes irreversible and very, very severe parkinson's disease, but not doing one's research, in this sort of hobby, thats what is likely to get you killed if sheer blind luck (for the person not putting sufficient effort into the research phase, good luck for other people, either customers if the person is selling also or giving away, sharing, or just in general to people who don't like sharing the better end of the gene pool with something that could have used every bit of chlorine the combined history of chemical warfare, electrolysis and toilet maintainance practises has to offer)

By that, I mean an egregious, persistent moron, that knowing the risks, is sufficiently stupid to ignore them. I am not directing the insult at you yourself.

It works as advertised

re:1-phenyl-1,2-propane dione?

Started by XuTai10

Yes you are right , Reductive amination of Phenylpropane dione with Raney nickel, al/hg, platinum etc will lead to racemic ephedrine not the diol(different conditions)!
If you had the choice of using  this or l-pac you would  go the already stereospecific route of course.

After the MM benzo wacker and various washes what colour should the raw ketone be? I am talking about just before vacuum distillation?

Thanks for that once again! I was a bit worried as it's quite black with green tones, I was under the impression that there would be a much cleaner solution after all the washes... off to the vacco!

The mm wacker suggests distiling the post extraction dcm off with condensors etc, is this really required? I'm thinking an open vessel in warm h2o bath would suffice and be faster?