• N&PD Moderators: Skorpio | thegreenhand

Novel cathinone ethyl-hexedrone

I have never tried coke so I cant compare but nasally 10-20mg I like. Lasts about 3 hours and crash comes with fatigue. It is moreish while it's working but not too badly.
Can you sleep when crash comes, I dont know, I sleep with quetiapine. One afternoon I had a little binge on it and I dosed several times, eyeballed 10's mg's. It is mildly painful when snorted but pain subsides after 30sec. But it still irritates nose. When on binge then runny nose is for couple of days. It dilates pupils and blushes face. Heartrate and bodytemp raises. If taken too much then anxiety kicks in and silence is preferred to music. Just now I tried about 10mg sublingually. It numbs mouth about for 20 minutes, no change in mood. BUT !, area under my tongue and tip of my tongue is partly covered with small blisters, most of them are filled with blood, so don't do it sublingually ! I have done about 10 different stimulants and this one is acceptable in my opinion.
 
So how is this has anyone sampled it. Is it anything like mephedrone or at least as good as 3mmc?
 
Had this from a big EU vendor, bright white crystalline powder, but stopped at <10mg because I got tachycardia together with slight heart pain (I am very sensitized to this since I overdid things years ago, not in terms of dose but prolonged daily use. I can still use the better ones in moderation like IPPD, PVP and even good coke without problems though. So it's a definite warning for me, but can't say of what, vasoconstriction?)

So my 2 cents are that it has potent peripheral activity which probably isn't what you want. 3-mmc was at least a dirty but strong stimulant in lowish doses for me, while this felt even stronger physically with less central activity.
 
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Single dose is better than redosing. It damages nasal canals a bit. Days after use when I blow my nose there are blood in mucus. Herb oil based nose spray really soothes nose back up after use.
 
So this stuff is not very water soluble? Would only order it for the purpose of IV injections...
 
it is the result of a great deal of work elucidating the quantitative structure–activity relationship of the scaffold. The team looked for the key moieties which resulted in creating a compound which acts as NDRI(norepinephrine-dopamine reuptake inhibitor) with higher selectivity for dopamine transporter than norepinephrine transporter).

Yeah, well, they've overdone themselves this time for sure!
 
Had 2 batches of this stuff, Batch 1 was tiny white/transparent crystals. Effects from 30-50mg were just as good as good cocaine. But you only got one, maybe 2 redoses before it stopped working. Duration was 1-2h per dose.

Batch 2 was a brownish powder with some stimulant effects but really nothing special.
 
I kept it going overnight and the second full day - however my nasal canals are so seriously covered in polyps i can hardly breathe and insufflation is no longer viable. Is anything known about whether the ethyl group lends itself to causticity? All oral when i come back to this one. Nooo thank you to how irritating this feels. Maybe consumed 500mg over 30 hours, but rails stopped working around 15. Shoulda known better.
 
There are definitely different batches going around with so greatly differing effects that an analysis would be really interesting.

Got a chance to try these transparent-white little shards (no smell and painless insufflation) now and it's a very different experience than what I've sampled before. It is just a first impression now but it feels like a true winner, might even be the best pure stimulant (without 5-HT effects etc) I had up to now. Appears to go straight into the CNS with little peripheral side effects; there is an overall increase of energy, physically as well as mentally, but no tachycardia or jitteriness (when dosing conservative). And it's a social one, at least more so than IPH.

And it has legs. I'm up for 36 hours now (skipping nights is not exactly easy for me usually) and I don't feel any negatives from it besides tiredness coming up now, but also I've been out for a long walk in the hills today. Just by taking a bump of hex-en every now and then (5-10mg per dose, intervals varying up to 4 hours or so), truly unexpected.

So a real upside of this compound is that it doesn't build up nasty metabolites like many cathinones do. (Could anyone shed some light into the metabolism of hex-en, is it inactive metabolites or rapid excretion, or something else?)

This leads to the thought of a 3- or 4-methyl hex-en - would this even be active?
Unfortunate that we only have one pure serotonin releaser (MDAI) if I'm right, and no isolated SERT inverse agonist (yet) to combine.

Might be a decent ADHD tool too.
 
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Lefetamine I think is going to be more than a stimulant, its known to have moderate opioid and dissociative effects isn't it? diphenidine and methoxphenidine are diphenidine analogs and I can feel the opioid signature of it even through my tolerance to opioids, and those two are STRONGLY dissociative, especially methoxphenidine, and especially via the IV route, although solubility is better than diphenidine its still crap. Lefetamine has been on my to-synth list for a while, but not got round to to it yet, as there have been other things that are higher priorities. But even relatively weak dissociative/opioid effects on a primarily stimulant drug would make it reinforcing as hell.
Love those two analogs of it myself, diphenidine especially. lower non-hole doses are REALLY moreish once it fades, only moderated by its longish action.

To the poster who commented on lefetamine-have you tried it?
 
I'm particularly wondering about fencamfamine (that, if wikipedia is correct, still gets used by some rare cases against daytime fatigue) and its supposed opioid mechanism...

and also to opioid receptors in the reinforcement produced by fencamfamine, as place preference was blocked by the selective dopamine D1 antagonist SCH 23390 and by the opioid antagonist naloxone.[5] A similar place preference, which was blocked by naloxone and by SCH 23390 and by raclopride, has been seen in a study on rats with drinking water. Animals treated with naloxone before the conditioning sessions showed a place aversion instead of the place preference found in saline-treated animals. Naloxone also reduced drinking. It was proposed that naloxone induced a state of frustrative nonreward. It was suggested that both dopamine and (endogenous) opioids are important for water-induced reinforcement. Possible interactions between these two neurotransmitter systems were discussed.
I could be wrong, but if naloxone alone induces frustration and blocks the reward circuits, then it's not exactly the best tool to check whether something is opioid- or dopamine mediated?

I found it always interesting that naltrexone should be inactive in people without opioid dependence when it binds strong enough to block endorphins. Shouldn't it then be a truly depression inducing drug?
 
It all depends on the dose, at low doses antagonistic effect is not strong enough to be much uncomfortable but can induce some endorphine release as a result of feedback (weak blockade - decreased opioidergic neurotransmission - release some endorphins, I guess), but at high doses I bet opioid antagonists are unpleasant as long as they work even if you're not dependent on agonists. Low-dose naltrexone works by increasing endorphin release as far as I know, high-dose naltrexone is exclusively used to physically block binding of opioid agonists at opioid receptors.
 
diphenidine and methoxphenidine are diphenidine analogs and I can feel the opioid signature of it even through my tolerance to opioids...

Neither diphenidine nor methoxphenidine are opioid agonists, so you are not picking up opioid effects.

Low-dose naltrexone works by increasing endorphin release as far as I know

That would be a strange MOA because naltrexone would block the effects of endorphin at opioid receptors. Obviously, the dose of naltrexone is high enough to occupy some of the receptors, otherwise it wouldn't be producing an effect.

Wouldn't it make more sense to think that mu receptors normally produce some constitutive inhibition of immune cells, and low-dose naltrexone works by acting as an inverse agonist?
 
Wouldn't it make more sense to think that mu receptors normally produce some constitutive inhibition of immune cells, and low-dose naltrexone works by acting as an inverse agonist?

But how would this relate to a mood boost some people with no past of opioid use report?

Edit: Guys, just look how we managed to change the topic from N-ethylnorhexedrone via lefetamine to naltrexone

palmanita said:
So a real upside of this compound is that it doesn't build up nasty metabolites like many cathinones do. (Could anyone shed some light into the metabolism of hex-en, is it inactive metabolites or rapid excretion, or something else?)

Well, N-ethylnorhexedrone is a cathinone derivative after all and it's going to be metabolized in the same way all cathinones are if they bear no substituents on the aromatic ring. What nasty metabolites do cathinones build up though? You mean norephedrine and ephedrine analogues? This one will be metabolized into beta-hydroxy analogue too, perhaps it's even excreted more slowly due to higher lipophilicity, but I'm not sure if it's going to produce less peripheral side effects, maybe it does being more lipophilic. Looking at the structure there's really nothing about this compound that would make it much different from other cathinones except for increased lipophilicity (I guess high potency per weight is also due to a much better BBB penetration compared to methcathinone or buphedrone).

Though I must say it's not the first positive opinion about this compound that I'm reading. On the other hand I've also read some positive comments on ephylone (N-ethylpentylone!). It looks like they really may have overdone themselves this time! =D Scrupulous research combined with thoughtful analysis of the SAR pays off, it seems.
 
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But how would this relate to a mood boost some people with no past of opioid use report?
It doesn't make much sense to ascribe such an effect to endorphins because naltrexone tends to block their effects. One possible mechanism could be blockade of dynorphin effects on kappa receptors, which is partially responsible for the dysphoric effects of stress.
 
Interested due to coke comparisons floating around. First dab with 15 mg insufflated. Some initial burn more similar to caths than coke, alleviated by the numbness it generates in about 10 seconds. Clean stimulation, not much to report at this dose but definitely feeling more focused.

Edit: Even apparent from this small of a dose, this will be quite caustic for coke like consumption. I'd ponder 3-5 ~40mg lines would take your nose out of commission for a few days.
 
On a sidenote: I did inject 100mg of this and ha a rush, but nothing worth writing home about. Since I generally require relatively large doses to experience a full-fledged rush (100mg cocaine, 500mg 3FPM, 80mg MDMA) and am even then often underwhelmed, I imagine the rush could be noteworthy at 200mg. However I missed the following shots and felt so fucking shitty after what ended to be another 200mg injected subcutaneously that I have not felt any desire to do a 200mg shot. I've just always hated cocaine and this is not very different. Regarding solubility, since I did not findd any information on this, I used 1.5ml (15 units) of water per 100mg of substance. I think 1ml would be enough with some heat applied and given enough time to dissolve, but that's about it.
but at high doses I bet opioid antagonists are unpleasant as long as they work even if you're not dependent on agonists. Low-dose naltrexone works by increasing endorphin release as far as I know, high-dose naltrexone is exclusively used to physically block binding of opioid agonists at opioid receptors.
I've been on naltrexone for addiction treatment (can't remember the dose, but higher than a micro-dose for preventing tolerance) and felt like complete and utter shit. Like shit. The bad kind of shit.
 
Interested due to coke comparisons floating around. First dab with 15 mg insufflated. Some initial burn more similar to caths than coke, alleviated by the numbness it generates in about 10 seconds. Clean stimulation, not much to report at this dose but definitely feeling more focused.

People compared mephedrone to coke and I know for a fact that both mephedrone and 3-MMC used to be sold as cocaine (often mixed with lidocaine or benzocaine for the numbing effect), considering they were sold at 4-6 times the price of cathinone themselves, it must have been a good business, yet the effects are clearly so different.

Anyway, it may not be that striking this is so potent and strong if you consider long alpha-chain cathinones are primarily reuptake inhibitors and apart from pyrrolidinyl analogues, one other tertiary amine analogue (N,N-dimethyl) was fairly potent as well according to one study (google "deconstruction of MDPV" and you'll find it). Perhaps for those cathinones analogues that act as reuptake inhibitors longer alkyl chains on the amine are actually beneficial for their potency. Yet, I'm not sure if it is really that similar to cocaine, the difference between MDPV and cocaine is huge in my experience, I can't imagine N-ethylnorhexedrone to be much like cocaine.
 
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