potent dopaminergics prolintane & amfonelic acid

[asecin]

so i finally found sources for those two potent dopaminergics but im hesitant to acquire them now since reports are scarce and im not really sure of their toxicological report being hard to find research chemicals. i would really appreciate some information and if they are worthy of try. for example, prolintane is compared to "bath salts" and we all know how nasty those are BUT it does mention the effect is much shorter and doesnt interfere with sleep so thats actually a good thing. on the other hand, some mixed reports on amfonelic acid being quite potent and lasting up to 12 hours or more which is a huge turn off i think. its still very difficult to discern and choose properly any help would be so appreciated!

 

[serotonin2A]

I would stay clear of amfonelic acid.

http://www.chemedx.org/pick/sad-pink-monkey-blues-hamilton-morris

 

[asecin]

yikes! only negative things i read before were the very long half life of 12 hours and lots of jitters and what not also of course its addictive nature. i assume this stuff must be real damn good if professional scientists abused it wow its actually making it more enticing now than anything. from what i have seen, there were no reported cases of death from using it tho, unlike "bath salts" which brings me to ask if anything more is available on prolintane...

 

[Nagelfar]

from what i have seen, there were no reported cases of death from using it tho, unlike "bath salts" which brings me to ask if anything more is available on prolintane...

"Bath salts" aren't a distinct IUPAC proper categorization of any sort. Look at the actual compound, slang assignations don't convey a proper safety profile, whether mislabeled grey-market, or illicit black market of drugs.

 

[palmanita]

Prolintane has been sold OTC for many years in some countries like Germany, as a mild stimulant with good safety profile. Seeing the similarly with a-PVP, this is very probably a matter of dosage. Needless to say, it has been withdrawn because of abuse (sadly, was the only OTC stimulant left). Never had the chance to try though.

Amfonelic acid on the other side appears to be an evil one with very narrow dose range. And I've developed a skin rash when titrating, before reaching an active level (that was before I knew of the dangers), the first time ever I had an allergic reaction to a drug, so gladly I stopped.

 

[asecin]

im going to be focused on prolintane then. ill see how many more reports ill get but i already know a source

 

[clubcard]

Prolintane is very mild, Not unpleasant, but it's cLogP is decent so it will accumulate in the brain, it's just not that active. Amfonelic acid is a bad idea because usage is going to cause antibiotic resistance. I really think that AA is a bad idea, it really could indirectly harm a lot of people.

 

[DotChem]

Amfonelic acid is a quinolone antibiotic and the antibacterial dose (200-500mg) is way higher than the stim dose and amfonelic acid is reportedly extremely addictive. So sub-antibacterial doses (ie normal stim dose 50mg or less) will lead to building up of bacterial-drug resistance VERY QUICKLY and increase susceptibility to infection sharply. A simple kitchen might lead to infection that could potentially kill Plus it is extremely expensive due to complicated synthesis. Not worth it ..

Selective dopamine reuptake inhibitors alternative to amfonelic acid would be 3C-PEP. Couldn't find much information about this compound besides the wiki entry and one reference cited there. It is reportedly 10,000 times more than cocaine as as DRI in vitro. I guess cut with inositol 100x would make pretty nice stim. Generally piperazines also makes "safer" drugs with less off-target side-effects!

https://en.wikipedia.org/wiki/1-(3-Chlorophenyl)-4-(2-phenylethyl)piperazine

3C-PEP is one of the most potent dopamine transporter (DAT) ligand reported to date. It is highly selective for the dopamine transporter (DAT dissociation constant K_i = 0.04 nM) with relatively low affinity for the closely related Norepinephrine transporter NET (K_i = 1107 nM ) and the Serotonin Transporter SERT (K_i = 802 nM). In addition, the compound has little or no affinity for D2-like receptor (K_i = 327 nM), Serotonin 5-HT2 receptor (K_i = 53 nM) Opioid receptor (K_i>10000 nM) and the PCP/NMDA receptor (K_i>10000 nM).^[2]

With a DAT dissociation constant K_i of 0.04 nM, 3C-PEP is one of the most potent dopamine transporter ligand described to date in the literature. In comparison, cocaine which is a prototypical DAT ligand and reuptake inhibitor has a dissociation constant K_i of 435 nM thus making 3C-PEP about 10,000 times more potent than cocaine as a dopamine transporter inhibitor in vitro.^[2]

 

[serotonin2A]

^ In general, the piperazine-type DAT inhibitors lack cocaine-like effects because they don't act as DAT "inverse-agonists". As an example, vanoxerine (GBR-12909) produced sedation when it was tested in clinical trials.

 

[Pomzazed]

^

But that molecules metabolize to m-CPP, an unselective serotonin agent, and 3C doesnt dound good.

 

[asecin]

Amfonelic acid is a quinolone antibiotic and the antibacterial dose (200-500mg) is way higher than the stim dose and amfonelic acid is reportedly extremely addictive. So sub-antibacterial doses (ie normal stim dose 50mg or less) will lead to building up of bacterial-drug resistance VERY QUICKLY and increase susceptibility to infection sharply. A simple kitchen might lead to infection that could potentially kill Plus it is extremely expensive due to complicated synthesis. Not worth it ..

Selective dopamine reuptake inhibitors alternative to amfonelic acid would be 3C-PEP. Couldn't find much information about this compound besides the wiki entry and one reference cited there. It is reportedly 10,000 times more than cocaine as as DRI in vitro. I guess cut with inositol 100x would make pretty nice stim. Generally piperazines also makes "safer" drugs with less off-target side-effects!

https://en.wikipedia.org/wiki/1-(3-Chlorophenyl)-4-(2-phenylethyl)piperazine

ive never heard of that one but reading about it makes me all wet and excited. each time i see some new stuff out there being compared to cocaine with potency of 10,000 i get the shivers instantly. now, i doubt anyone has ever tried it so they can report anything which sucks, but i might have a huge problem finding a source for that one!

so until then, is prolintane really crap or what? what im seeking is some dopamine boost type of coke high, does prolintane even have a slight imitation effect at least?
the reason im so hung up on it now is because i have a source, its not expensive and its the only thing to get thus far compared to the more interesting but difficult obscure stuff so...

 

[palmanita]

Maybe you want to try this ethyl-hexedrone, don't know how legit these statements are but it got repeated positive reports about coke-like dopaminergic euphoria. At least it's very probably safer than amfonelic acid and doesn't have such insane potency ... (I do understand the excitement but reading things like 10,000 times the potency gives me rather creepy shivers and thoughts of super-fentanyl like chemical warfare stuff)

 

[asecin]

im sure they exaggerate this, the way it sounds it could be quite dangerious but i didnt find any such report. i will be quite satisfied if i can find one damn substance that at least mimics coke and not being few times better or not. and this one, ethyl-hexedrone, quite obscure just like the previously mentioned 3c-pep. not sure why pharmaceutical companies dont try new type of antidepressants that actually work on dopamine similar to stimulants but with less side effects and stimulation (perhaps some sedating quality add on) and hopefully much less inhibition of norepenephrine

 

[sekio]

not sure why pharmaceutical companies dont try new type of antidepressants that actually work on dopamine similar to stimulants but with less side effects and stimulation

even selective D1/2 receptor direct agonist cmpds are stimulating, it is effectively impossible to isolate the focus-improving/reward-inducing/wakefulness promoting effects from each other.

imo ethyl hexedrone is overhyped bull crap, weaker than mdpv

prolintane is weaker still with ~20mg hcl orally being about equivalent to ~100mg oral caffeine
Hollister, L. E.; Gillespie, H. K. (1970). "A new stimulant, prolintane hydrochloride, compared with dextroamphetamine in fatigued volunteers". The Journal of Clinical Pharmacology 10 (2): 103–109. doi:10.1177/009127007001000205. PMID 4392006.

 

[asecin]

so prolintane is comparable to caffeine? does it actually give a nice boost in dopamine or it doesnt? i am still confused as to what people describe it as, like just a stimulant or a stimulant that might give euphoria?

also i have nicergoline, does it work well on dopamine? i know a lot of those ergoids are d1/2 agonists and i dont care for some of the side effects, do they actually boost dopamine and give probable euphoria or not?

 

[sekio]

caffeine can be plenty euphoric given the right set & setting, so YMMV?

 

[DotChem]

^ In general, the piperazine-type DAT inhibitors lack cocaine-like effects because they don't act as DAT "inverse-agonists". As an example, vanoxerine (GBR-12909) produced sedation when it was tested in clinical trials.

vanoxerine and similar piperazines are extremely lipophilic (done by design) so they wont give a rush anywhere like coke. sedation is probably due to off-target effect: I wouldn't be surprised if they are sedating (or at least some of their metabolites) since they look pretty similar to diaryl antihistaminics piperazines .
But less lipophilic DRI piperazines like the one mentioned may have be quite different profile.. similar to coke who knows? .. probably like BZP but Dopamine-selective benzylpiperazines... pure dopaminergic.. but who knows?

@Pomazazed But that molecules metabolize to m-CPP, an unselective serotonin agent, and 3C doesnt dound good.

If the Ki of 0.04nM reported for 3C-PEP DAT inhibition is correct, the m-CPP potential metabolite which is non-selective serotonergic may not be an issue since its concentration will be extremely low to see anything (ie the stim doses will be way much lower than the mCPP doses required to elicit any serotonergic!)

 

[serotonin2A]

vanoxerine and similar piperazines are extremely lipophilic (done by design) so they wont give a rush anywhere like coke. sedation is probably due to off-target effect: I wouldn't be surprised if they are sedating (or at least some of their metabolites) since they look pretty similar to diaryl antihistaminics piperazines .
But less lipophilic DRI piperazines like the one mentioned may have be quite different profile.. similar to coke who knows? .. probably like BZP but Dopamine-selective benzylpiperazines... pure dopaminergic.. but who knows?

Not producing a rush and not producing cocaine-like effects are two completely different things. Delayed entry into the brain may reduce the reinforcing effects of stimulants, but it doesn't eliminate their ability to produce stimulation. For example, lisdexamphatamine still produces stimulant effects even though it isn't highly reinforcing; cocaine and methylphenidate still produce stimulant effects when taken orally. Even if GBR-12909 produces sedation due to off-target effects, that doesn't change the fact that even high doses fail to produce stimulant effects.

The argument that some DAT inhibitors lack stimulant effects because they enter the brain too slowly has been discredited:

http://www.sciencedirect.com/science/article/pii/S0028390814002342

"Reverse-dialysis overcomes the problems of absorption, metabolism and the rate and extent of brain penetration. Since access to the site of action in the brain is virtually instantaneous, it provides an opportunity to compare the effects of cocaine and methylphenidate versus competitive DAT inhibitors, eg GBR12909, and competitive DAT substrates, eg d-amphetamine. Nomikos et al 1990 studied the effects of reverse-dialysis of various drugs on dopamine efflux in the striata of freely-moving rats. GBR12909 produced gradual concentration-dependent increases in dopamine efflux. Its maximum effect occurred 30–45 min after the start of reverse-dialysis and as its concentration was increased, a ceiling to its effect at concentrations ≥100 nM was clearly evident. In contrast methylphenidate and d-amphetamine produced rapid increases in extracellular dopamine and the size and speed of onset of the maximum effect became larger as their concentrations were increased. Since these compounds were all applied directly onto dopaminergic nerve terminals, these results demolish the argument that cocaine-like drugs produce rapid increases in dopamine efflux simply as a result of rapid brain penetration. This is clear because instantaneous application of GBR 12909 did not cause it to mimic cocaine's or methylphenidate's effect dopamine efflux; on the contrary, it produced no change or augmentation of its pharmacological effect."

 

[Scuzzy]

I've had both - Prolintane feels just like Adderall to me, but maybe 75% duration and 50% potency. CNSNS ratio is very similar, and I would have a hard time telling them apart in a blind taste test, unless I paid very close attention to the duration. Slightly pro-social, moderately pro-sexual. AA is different and hard to describe. It's very easy to overdue because there is a high ratio of CNSNS effects and the onset is somewhat gradual. At first, it produces a euphoria that is more opiate like than stimulant like. Very relaxed and contented. It's also decently pro-social for me, and I am someone who almost never finds stimulants pro-social unless they have a strong 5-HT component (a la MDMA or bk-MDMA). This positive effect lasts for perhaps 2 or 3 hours and it slowly degenerates into a drained feeling that's almost parkinsonian if you overdo the dose. I noticed significant muscle rigidity, and a general feeling of being depressed and unwell. There is no urge to redose in order to chase any kind of rush, but rather to restore the contented feeling and abolish the feeling of dopamine depletion. This is not advised because the drug actually has a rather long half-life, which is not immediately apparent. Before you know it, you haven't slept in days. It's also very potent - as little as 0.2 grams can have you up for days. I would estimate that it's 4-5X as potent as d-amp, but no more than that. I find it slightly easier to tolerate than any other straight-up stim, but much less forgiving and suited to recreation than most MDXX compounds. It's very unique, but it's not something to get overly excited about either. I did get a lot of work done on it - in very small doses it could be useful for ADHD, but I have not explored that personally.

EDIT: I did not mean 0.2 grams of AA in a single-dose - that would be ridiculous and dangerous. It should be obvious, but I can't risk someone reading this post and thinking that they can take 200mg of AA in one dose without dying - because you would probably projectile vomit, have a seizure and/or worse if you did.

 

[asecin]

dunno sometimes i have wet dreams about stimulants tho their fucking side effects are such a turn off. it is an idea based on their pro-sexual effects, seeing a slim body with big tits rubbing against you only to find out it has a big dick that fucks you up in the ass.

if anyone noticed, i have been here for 11 years trying to find the perfect stim that is ideal for a love affair but with no avail. as a side note, people on here arent very helpful for the past 11 years their biochemistry is so much better than mine and yet they have zero ability to express themselves adequately enough to warrant serious acknowledgement.