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Ethcathinone

fastandbulbous said:
^ Not the same thing, ther's no keto group in ethylamphetamine (& it's a very, very nice stimulant on a par with amphetamine potency wise, but much smoother (a bit like meth, but without the crazy potential - the euphoria wasn't as pronounced as with methamphetamine, but it was plentiful enough)
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Do you have any theories for why ethylamphetamine is subjectively smoother than amphetamine?
 
I'd venture to say that it might be higher rate of BBB crossing, thereby reducing its effects in the PNS.

But don't take my word for it... if anyone is an expert on this, its definitely F&B :D
 
Hey, shouldn't it be easy to make 3-ethyl-2-phenylmorpholine (phenmetrazine 4 carbon analogue)? Unscheduled I think...
 
haribo1 said:
I'm someone else who finds MDPV unpleasent. I much preferred desoxypipradrol (in spite of it's wicked 1/2 life).
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Haribo, I asked you a question regarding how you obtained M1, years ago. You still haven't answered. Here's the link. http://www.bluelight.ru/vb/showthread.php?t=305427

and my post:

Quote:
Originally Posted by haribo1
No mate, Gruntenthal used Sigma-Aldrich material for some reason. Now you know HOW I 'aquired' it.


But you claimed to have ordered it from Sigma Aldrich (you even said the price), and you also said you stole it from Gruenthal when they left out the vials. No offence, but I'm curious what your going to say next

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haribo1
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I've tried desmethyl tramadol from Sigma-Aldrich. It's more or less half way between morphine & codeine. Snorted it kicks in at about 3 minutes. Very euphoric and long-lasting. It caused me some hyperthermia but that was the only side-effect off 100mg of the HCl salt.

haribo1
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This is going back a decade! 1g was about $200. Yes it was freebase but that's hardly difficult to sort out.
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PS: no offence, but I want to make sure I am chatting with honest people. Sure you can clear this all up. Tnx, and please don't be angry, but please do reply this time.
 
fastandbulbous said:
I got some many, many years ago from Aldrich's catalogue of rare chemicals (don't worry it's not a source, since they joined with Sigma they wont do buisness with anyone without university or similar affiliation - or several notes from your mother!) as it's an active metabolite of diethylpropion (Tenuate Dospan or chalkies/tombstones in hip parlance =D), which is alright as a stimulant, but nothing to get too excited about. 50mg will produce reasonable CNS stimulation, but you'll not be eating anything for 18 hours afterwards
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Interesting
why would the N-ethyl (metabolite) be longer acting than the N,N-diethyl as I thought Diethylproprion is required to take multiple times per day thus in no way having a 18hr duration and thus reason for creating the CR drug form
 
N-ethylcathinone is the active species responsible for the effects of diethylpropion. In order to obtain ethylcathinone, however, diethylpropion has to undergo 1st pass metabolism. The tertiary nitrogen is definitely not the only target of reduction--the ketone is also reduced, yielding (d)- and (l)-diethyl-cathine. I'm gonna bet these both suck as stimulants and sympathomimetics. Thus, perhaps people who take diethylpropion only end up with a little bit of the active ethylcathinone. Maybe taking (S)-ethylcathinone straight-up is 5-10 times more potent on a mg-for-mg level than diethylpropion. Hence, it was that much more tweaking. Also, people have different responses to amphetamines--I never get anorectic effect, nor have I ever.

As for the extended release version of diethylpropion, I suspect that it is just another example of a pharmaceutical company scramble to monopolize a chemical for as long as possible. Whether or not the drug actually needed that extended release is not their concern. It's all about the coldhard.
 
LuxEtVeritas said:
Interesting
why would the N-ethyl (metabolite) be longer acting than the N,N-diethyl as I thought Diethylproprion is required to take multiple times per day thus in no way having a 18hr duration and thus reason for creating the CR drug form
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Ah, maybe it's just me, but diethylpropion would make my stomach feel iffy for a full day afterwards, killing the desire to eat. This is different to the centrally mediated appetite supression (which only lasts 4-5 hours for both) and is paralelled by the locomotor stimulant activity.

Basically, it made my guts churn for a fair while after the desirable effects had vanished
 
Jamshyd said:
I'd venture to say that it might be higher rate of BBB crossing, thereby reducing its effects in the PNS.

But don't take my word for it... if anyone is an expert on this, its definitely F&B :D
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It's also to do with it's effects on the serotonogic system - a fraction of the activity of methamphetamine, but still greater than that of plain ol' amphetamine. Serotonogic efflux/reuptake inhibition seems to reduce the edgyness that is seen with amphetamine
 
fastandbulbous said:
Ah, maybe it's just me, but diethylpropion would make my stomach feel iffy for a full day afterwards, killing the desire to eat. This is different to the centrally mediated appetite supression (which only lasts 4-5 hours for both) and is paralelled by the locomotor stimulant activity.

Basically, it made my guts churn for a fair while after the desirable effects had vanished
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Gotcha...that makes sense...possibly a more individual GI reaction, not anything to do with some extended half-life or such

thx
 
Ethylcathinon could easily have a longer half-life than Diethylpropion. Sometimes Metabolites have this property.Well,just to point out that metabolites aren't necessarily of shorter action by definition,don't know the half-lifes of these two though.
 
hugo24 said:
Ethylcathinon could easily have a longer half-life than Diethylpropion. Sometimes Metabolites have this property.Well,just to point out that metabolites aren't necessarily of shorter action by definition,don't know the half-lifes of these two though.
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true in one regard that metabolites certainly can have a longer active life than the parent, but specifically here since Ethcath is a major active metabolite it would be odd to be significantly longer then the pro-drug which largely is causing a delayed release of the active metabolite itself.

such as sibutramine is mostly active due to its long acting metabolites, but those metabolites do not have a longer overall duration than the 'pro-drug' itself

sibutramine itself before being degraded into its desmethyl and didesmethyl metabolites has only about a 1 hour half-life and thus is simply more or less a pro-drug for the two metabolites that have half-lifes of around 16 hours or so

anyway as we see he noted it was not a true CNS based effect but an individual response side effect that had a prolonged activity far greater than the active duration of the drug itself on the CNS
 
nuke said:
Hey, shouldn't it be easy to make 3-ethyl-2-phenylmorpholine (phenmetrazine 4 carbon analogue)? Unscheduled I think...
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i was just thinking this, but as you refer to it as an analogue of phenmetrazine which is sched 2 than by analogue law, in US at least, it is sched

now if you do this to diphenmetrazine that is sched 3 than i guess it is not controlled in the US

silly freakin way to make laws, which are BS in the first place of course in a country based on liberty
 
ethcathinone is a strange one, has euphoric properties once you understand the action after sampling a few times,, it is compulsivly addictive ,,
 
mal hyde: How would you describe this "clearer view" of it's action after getting used to it and sampling it a few times? What qualities do you feel are hidden in the compound?
 
I've been wondering in what way ethcathinone affects the brain, if it's a releaser and reuptake inhibitor like plain cathinone and methcathinone seem to be or if it's mainly a reuptake inhibitor, like wikipedia seems to suggest? As a novice, I don't really believe that sticking one extra CH2 at the methyl destroy's the releasing properties of MCAT.

I UTFSE, but I couldn't find any conclusive data.

Also, does anyone know how it compares to modafinil, desoxypipradrol, caffeine, cocaine and amphetamine sulfate in terms of (neuro)toxicity? Especially at the low end of the dosage range, to just make your mind a little bit brighter to study and socialize after a bit too little sleep.

Thanks in advance.
 
bob_arctor said:
mal hyde: How would you describe this "clearer view" of it's action after getting used to it and sampling it a few times? What qualities do you feel are hidden in the compound?
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he is er, unlikely to answer you, the clue being the line thru his name and the title ex bluelighter.
 
immad said:
I've been wondering in what way ethcathinone affects the brain, if it's a releaser and reuptake inhibitor like plain cathinone and methcathinone seem to be or if it's mainly a reuptake inhibitor, like wikipedia seems to suggest? As a novice, I don't really believe that sticking one extra CH2 at the methyl destroy's the releasing properties of MCAT.

I UTFSE, but I couldn't find any conclusive data.

Also, does anyone know how it compares to modafinil, desoxypipradrol, caffeine, cocaine and amphetamine sulfate in terms of (neuro)toxicity? Especially at the low end of the dosage range, to just make your mind a little bit brighter to study and socialize after a bit too little sleep.

Thanks in advance.
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Methcathinone isn't a DA releaser, it's a simple DARI.

So, I guess you're right, the extra carbon doesn't destroy the releasing properties that weren't there ;)
 
Thanks for clearing that up.

How (neuro)toxic is Ethcat in comparison to modafinil, desoxypipradrol, caffeine, cocaine and amphetamine sulfate? I was under the impression that plain reuptake inhibitors are less detrimental to the brain than releasers/reuptake inhibitors, is that incorrect too? ;)
 
MCAT is not just a pure dopamine uptake inhibitor--certainly it is more of a reuptake inhibitor than methamphetamine, but it is still a DAT, NET and SERT substrate (more so than an inhibitor). EthCAT is probably more of an inhibitor because of the bulky N-linked alkyl chain. But I would still bet it has more substrate-y properties than say, methylphenidate or the pyrovalerones.

MCAT is probably less neurotoxic than methamp, but more toxic than regular amphetamine.

If I had to bet, here is how I would rank the PEA substrate stimulants in terms of neurotoxic potential, from highest to lowest:

PCA >> MDA, PMA > MDMA > MDEA, Methylone, Methamp > MCAT > EthCAT > ethylamp > (d)-amph, cathinone
 
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