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RCs 3F-Phenmetrazine (3-FPM)

(the parent compound apparently has a half life of 16-31 hours if that's anything to go by)
Hey, thanks for the report. Where'd you get that half-life? According to Wikipedia the half-life on phenmetrazine is eight hours.

Edit: Out of curiosity, how hard would it be to get rid of that darn 3-F atom? If I remember correctly, fluorine-carbon bonds are very strong..
 
Yeah, good post furryfreek.

You better get a shower, unless you want people to get unwillingly introduced to 3-FPM-aftereffects-land, just because they were nuzzling on your cozy (but contaminated) fur.
I wouldn't want the saying "died through cuddling a fur" carved onto my tombstone, would you ?
 
See page 2 : http://www.bluelight.org/vb/threads/737012-3F-Phenmetrazine?p=12658377&viewfull=1#post12658377

Apparently someone did a good job in advertising this mediocre, aftereffects-ridden stim. :D

Setting aside the fact that we all could have been duped with some random chemical....

In my personal opinion 3F-P was a solid smooth-functional stimulant & mood booster, and had a present euphoria akin to a non-cracked out amphetamine and an enjoyable burst of energy/creativity. I was also fine interacting with other people while on it and the negative physical effects were minimal. If you're looking for a rush and a good time this drug obviously isn't going to fit the bill; if you define mediocre as not giving you a fat rush and making you want to furiously masturbate then yes, it's mediocre. However personally I did not found it after-effects ridden. The comedown (before the evening when I started using a little MDPV) wasn't hell and while it was a bit compulsive, since it wasn't very amp-y/rush-like it was much easier to control myself.

Obviously to each their own and while I don't recommend buying concentration/study drugs off the interwebz, I feel like this chem is getting a bad rep because it's not amp, or even an amp replacement. It's a very solid stim, gave me a good mood lift and I enjoyed it.
 
Hey, thanks for the report. Where'd you get that half-life? According to Wikipedia the half-life on phenmetrazine is eight hours.

I got that figure from here: http://www.drugbank.ca/drugs/DB00830
Not sure if that's really any more accurate than wiki TBH.. Reading up on half lives can be a bit confusing as some sources seem to take metabolites into account, whereas other don't (this seemed to be the case when I was comparing benzos on wiki a few months back.)

(Unintendedly long) edit:

From my experience so far (20-30mg/day orally for 3 days) I would lean towards a figure slightly greater than the 8hrs reported by wiki (so 25% of it would be in your system after 16hrs). The first day I took 20mg at 9am, re-dosed another 10mg 40 minutes later and couldn't sleep until at least 1am (T+15:00), and that was with the assistance of benzos and at a time when I really should have been pretty tired given how little sleep I've had lately. Unfortunately, I kind of over compensated with the benzos that night, but without them I reckon I would have been up until about 3 or 4 am at least. My benzo of choice for sleep is etizolam but I don't have much of that laying around so I took 2mg of diclazepam instead at 9pm. By 11pm I could feel the diclazepam doing it's thing in terms of motor coordination and stuff, but I was still feeling a pretty wired and not ready to sleep so I took 0.5mg of etizolam which seemed to help far more and got me to sleep by about 1am. The second day I woke up at noon, still really mashed on diclazepam which is itself really long lasting, so I started the day with 20mg of 3-fpm which completely counteracted the drowsiness of the diclazepam, but still left me stumbling around and slurring like a drunk all day. Again I had trouble sleeping at first but 0.5mg of etizolam sorted that out. Today is day three which will probably be my last trial for a while. Woke up at 9am and took 30mg, so nothing more to say yet.

But yeah, this stuff (and/or its metabolites) seem to linger for a long time, even though pleasurable/recreational effects drop off pretty quickly and, admittedly I'm taking relatively small doses and wasn't even expecting any sort of body high or anything, but I did get a mild body high off of it the first couple of days (didn't last so long on the second but I only took 20mg with no re-dose) while today with 30mg those effects are barely noticeable, so tolerance seems to be an issue too.
 
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@furryfreek:
That's quite weird, it seems that Drugbank takes into account the metabolites, while Wikipedia doesn't.. actually, in the Wikipedia article it says that about 70% of the drug is excreted from the body within 24 hours, which quite closely matches the number on Drugbank.
Since 3-FPM is so similar, it could (in my mind, at least) have metabolites that have similar half-life, that is 16-31 hours, but perhaps are more active, which would lead to the long-lasting coffee-like stimulation after the short peak.

Also, Wikipedia says this about phenmetrazine:
In terms of central stimulation however, the dextro isomer is about 4 times as effective in both methods of administration.
Does central stimulation mean that kind of inability to stay still, teeth grinding, etc? I'm thinking 3-FPM could also have this quality to some extent, which could be a reason for the vastly differing opinions about it.. different batches made by different syntheses which lead to different isomers.

Are these theories just a non-logical product of my stoned brains or do they sound plausible to some of the people here who actually know something about chemistry? :)
 
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Does central stimulation mean that kind of inability to stay still, teeth grinding, etc? I'm thinking 3-FPM could also have this quality to some extent, which could be a reason for the vastly differing opinions about it.. different batches made by different syntheses which lead to different isomers.

Are these theories just a non-logical product of my stoned brains or do they sound plausible to some of the people here who actually know something about chemistry? :)
Well, central is just referring to the central nervous system here.
 
I'd imagine the racemate is what is on the market - enantiometric separation is a costly process.
 
Well, central is just referring to the central nervous system here.
Oh, of course :)

I'd imagine the racemate is what is on the market - enantiometric separation is a costly process.
What I meant with that was if there'd be two different syntheses in use each producing either levo- or dextro- enantiomers, some sold from some vendors, and the other through others, it could've been partly the reason people have about 3-FPM. But I know almost nothing about chemistry, so I really have no idea whether this even could be true.
Kinda like methamphetamine; the levorotary enantiomer, levomethamphetamine, is an OTC cold medicine, and non-abusable, while the dextro is pretty much USA's favourite drug (don't see that much meth in Europe.)
 
3FPM is so much better than 4MPM. I like that 3FPM isn't as harsh on the nose as EPH. I found 4MPM to be harsher than 3FPM nasally. I could take 3FPM all day by nose and not have issues where EPH, and 4-MPM to a lesser degree, were both very hard on the tissue. Had 100mg of 4MPM and found it gave some stimulation, but not as good as 3FPM. Doses of 4MPM felt like they would be fairly close to 3FPM but I started very small with the 4MPM and worked up slowly so there were no larger trials. All 100mg was taken spread out over a full day to no ill effect. Given the current price situation and effects, 3FPM is the winner hands down. I like a combo of both EPH & 3FPM. EPH Orally, 3FPM nasally.
 
I would be *shocked* if this were the case LeeviON, stereospecific syntheses are much more costly and not economical in this market as customers do not pay proportionally more.
 
I would be *shocked* if this were the case LeeviON, stereospecific syntheses are much more costly and not economical in this market as customers do not pay proportionally more.

Thank you, Transform, for expressing that point far more eloquently than I.
 
Dont know if it is mentioned anywhere but this substance is a reuptake inhibitor no? Not a releaser...
 
Considering that phenmetrazine is a releasing agent I think it's fair to assume that this would be too.
 
Pretty sure, that it is a releasing agent with a higher relative affinity for dopamine neurons than other monamine neurons. We should allow bets for those speculations. =D
 
Considering that phenmetrazine is a releasing agent...

I first thought same when had checked Wikipedia. But here what DrugBank says:

Phenmetrazine is thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron leading to an increase in the release of these monoamines into the extraneuronal space.
[...]
Phenmetrazine also acts as a monoamine oxidase inhibitor.

Hm? :\ So it's like amphetamine in some way (as expected), no?

ps: O Canada... :)
 
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Phenmetrazine is thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron leading to an increase in the release of these monoamines into the extraneuronal space.
Does that make sense? I mean when transporters are blocked less monoamines end up inside the cells. How exactly does that cause more to be released, when there's a lack of monoamine inside the cell to begin with? Doesn't eqilibrium play some role here? It has been my understanding that the postsynaptic neurons are desensitized due to the excess monoamine (How? Downregulation? Phsphorylation? I have no idea). Well, I mean it would obviously make sense that the cell starts producing more of the respective monoamine because it is tricked into thinking there is too little of it, but that would take a few days, right? It sure shouldn't cause a "rush" as one or two people have claimed can be experienced when smoking or injecting the substance intravenously.

I really know next to nothing about reuptake inhibitors, but that quote sounds very confusing. If the authors were as confused as I am now, it's probably not a very reliable source... ;) However, like I said before, structural modifications can indeed cause a releaser to become a reuptake inhibitor. The Fluor group shouldn't have that big an effect though, should it??

I could even imagine it doing both btw. Just look at how complex the pharmacodynamics of amphetamine are and it becomes apparent that it is not always as simple as classifying drugs into two categories.


The dopaminergic part of amphetamine effects as far as I understand them:
- Competitive inhibition of dopamine transporters since amphetamine docks to it the same way dopamine does
- Binding to TAAr-1 (trace amine associated receptor) ---> Here it activates enzymes which phosphorylate DAT's (the dopamine transporter that sits inside the cell membrane)
----> phosphorylated DAT's are internalized, can't transport dopamine anymore
- Binding of amphetamine to VMAT2 (vesicular monoamine transporter) in which it replaces dopamine and therefore causes it's release from VMAT2 vesicles
----> The dopamine is then released and so is the amphetamine

Anyway, you can see both reuptake inhibition as well as release play a large role in what effects amphetamine elicits. It is a very simplified version and doesnt take into account the noradrenergic neurons and the interactions between the two systems.
 
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Phenmetrazine is thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron leading to an increase in the release of these monoamines into the extraneuronal space.

From a simplistic point of view I would assume, that the organism counts every neurotransmitter, that has been emitted and demands the synapse to get it taken up on the other side in a determined time window. If you ingest a compound, that inhibits the reuptake, it is likely, that the body releases more of the expected neurotransmitter in order to get the amount at the other side to recommended levels. It seems like pretty simple logic, at least if you consider the system as detached from the rest of the neuronal network.
 
So.. is it safe to combo with ethylphenidate?
Edit: or MPA?
 
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From a simplistic point of view I would assume, that the organism counts every neurotransmitter, that has been emitted and demands the synapse to get it taken up on the other side in a determined time window. If you ingest a compound, that inhibits the reuptake, it is likely, that the body releases more of the expected neurotransmitter in order to get the amount at the other side to recommended levels. It seems like pretty simple logic, at least if you consider the system as detached from the rest of the neuronal network.
But that's just not how our cells usually work. It's usually about reaching an equilibrium with some sort of negative feedback. When little neurotransmitter is in the cell, there is no reason to assume it has become lost, quite on the contrary. Besides, DrugBank says "it is thought" to be a reuptake inhibitor. Like I explained on the example amphetamine, things just are rarely that simple. Sometimes it's important to take a reductionist view on things, but when it comes to the exact pharmacodynamics, it won't get us anywhere.

I really don't have time to look properly, but here is a piece of more trustworthy information than DrugBank:
http://www.ncbi.nlm.nih.gov/pubmed/19151247 said:
The present study examined the effects of the releasers benzylpiperazine, (+)phenmetrazine, and 4-benzylpiperidine, which have 20- to 48-fold selectivity in vitro for releasing dopamine versus serotonin.
Searching for phenmetrazine with A reuptake, B DRI, C NRI, D DNRI, E DAT yields no results on pubmed. It's pretty clear this isn't (primarily!) a reuptake inhibitor.

I would be *shocked* if this were the case LeeviON, stereospecific syntheses are much more costly and not economical in this market as customers do not pay proportionally more.
Well, I would be shocked, too. However in many cases you wouldn't be using stereoselective synthesis, but instead do an enantiomeric separation after the racemate has been synthesized. Check this patent for example: http://www.freepatentsonline.com/6040479.html

It's not expensive and can be done at home, in case anyone is ever curious about R-ketamine... :D

I'm pretty sure that's not how chinese drug manufacturers roll though.

Oh and btw, to whomever asked, it's not a different synthesis really, you just use the respective isomers of some reagents instead of their racemic versions (an even mixture of all isomers).


http://www.drugbank.ca/drugs/DB00830 said:
Adult monkeys have an LD50 of 15 to 20 mg/kg, whereas for young monkeys the LD50 is only 5 mg/kg. Symptoms of overdose include acute central nervous system stimulation, cardiotoxicity causing tachycardia, arrhythmias, hypertension, and cardiovascular collapse. Whilst some patients show signs of toxicity at blood concentrations of 20 µg/L, chronic abusers of amphetamine have been known to have blood concentration of up to 3000 µg/L.
Has this even been mentioned before? I'm not sure if this might give the wrong idea. They are talking about amphetamine tolerant users on one hand, and drug naive ones on the other.

However it should be taken seriously. Remember the substance is not all located in the blood, so multiplicating the figured by 5 or 6 won't yield a dosage, nothing even close. It varies from substance to substance how high it's concentration in the different types of tissue is, sometimes a huge amount could be located e.g. in fatty tissue or in the cns. Phendimetrazine definitely caused a few deaths despite never being very popular afaik.
 
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That is some valuable info crOOk. Thanks for that.

If 3F-PM has a remotely comparable LD50 (I guess, that Phenmetrazine itself is superior as a functional stim by a huge margin compared to the racemic 3F-PM, if the anecdotes are true), then it must have one of the lowest therapeutic indices of all stims. Then it would not only suck in vivo for me, but also on paper :D

@Leevion

I'd say, that neither of the mentioned compounds are safe (I dislike all 3 of them, but YMMV) taken solo. So the probability, that they are safe, taken in any permutation, is rather low.
 
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