RCs 2-FMA (2-Fluoromethamphetamine) - Megathread

[smashpast]

Ordered some from my vendor for a friend. Just talked to him and he said, he took 1g with a friend last night, leaving them disappointed. Cannot be the genuine substance, does it?

 

[Quiglesigles]

I can see how it may have left them disappointed. It could have been genuine 2-FMA but if they used 1 gram in a night, they definitely would have felt something. It just doesn't have much euphoria compared to other amphetamines.

 

[Shpongleton]

Just wanted to share that I can confirm the kidney pain as others have mentioned. I have only taken small doses 20-30 mg with at least a week between them. The pain is sort of a quick piercing pain which only lasts a few seconds but it has me very very worried about this stuff. Does anyone know what the cause of this could be and how dangerous a threat it poses? Otherwise this substance is wonderful, just as euphoric at times as 4-FA but not pushy at all.

 

[21p]

Clearly, this stuff tests negative for amphetamines on Marquis Reagent. Interesting info for those out walking around with a baggie of it. %)

partial affinity would cause a tan discoloration, which makes sense if you think about the structure of the chemicals. The substituted flourine creates steric hindrance around the enzyme/tweek active site and doesn't grab the marquis for an eight hour fuck session like meth does. Random thought but your logic makes sense to me.

Just wanted to share that I can confirm the kidney pain as others have mentioned.

I found the drug to be vasoconstrictive in moderate/heavy dosages (giving mgs is pointless with these drugs for a number of physiological and social variables).
Binging on this chemical could be worse than adderall (d/l amp) or dex, as it seems to stimulate the release of more norepinephrine than epinephrine. Nor-epi binds better with the receptors responsible for peripheral vasoconstriction and has less attraction to the receptors that get you hiiiigghhh... which fits in with the collective clinical experiences people are reporting.

What does all this scientific garbage mean? -- I think the drug can cause hypertension in some people more readily than other amps, which explains the kidney pain. By default, this would mean extended use could lead to pulmonary hypertension, ventricular hypertrophy, pulmonary embolism, heart attack, death, and even worse - a stroke. Your blood is pumping through your system on a shorter race track, you're not pissing out any fluid, and your muscles are being deprived of oxygen. If you're experiencing any of these symptoms, I strongly suggest you rethink daily use. If you have a history of heart problems or high blood pressure in your family I would recommend skipping the substituted amphetamines altogether.

Not trying to scare/impress, but I'm paying 40k a year to study this shit so I might as well use it to help people out. If you like this chem, get it while you can because it won't be around long.

 

[Shpongleton]

Yea well I get strong hypertension when I drink a cup of coffee too. I quit all caffeine several months ago because I couldn't take the dizziness and jitters at the dosage necessary to keep me energized working at my very physically and mentally draining job. I have only had a curiosity in other stimulants since then, nothing more than that. I think it's important to find the kind of dosage that is acceptable and safe on the human body regardless of the effects and then assess the risks going beyond that with respect to potentially desirable effects.

And remember, caffeine is lethal in easily obtained doses. Amphetamine is handed out to millions every year. I don't want to sound like I am trying to defend this new substance but I think it's important to keep an open mind. It could be useful to people. We simply need to know more about this substance before deciding it's no good.

Edit: 21p you seem to be knowledgeable about these substituted amphetamines. Do you have any opinion on 4-FA?

 

[21p]

Hahaha, well thanks man, but I'm far from being an expert. 4-fa is serotonergic compared to 2-fma, so that's a huge red flag for daily use. As far as cardiac issues, I have no first hand experience and haven't read enough reports to get an idea of which receptors the chemical might also hit (aside from what's obvious).

The real danger of hypertension whilst taking these types of chems vs. 4 hour energy or a red bull is the possibility of vasospasm induced arrhythmia progressing to acute myocardial infarction. Most users probably aren't over 30-35 yoa, so the chances of these types of problems are significantly lower.

 

[tweex]

I found the drug to be vasoconstrictive in moderate/heavy dosages (giving mgs is pointless with these drugs for a number of physiological and social variables).
Binging on this chemical could be worse than adderall (d/l amp) or dex, as it seems to stimulate the release of more norepinephrine than epinephrine. Nor-epi binds better with the receptors responsible for peripheral vasoconstriction and has less attraction to the receptors that get you hiiiigghhh... which fits in with the collective clinical experiences people are reporting.

What does all this scientific garbage mean? -- I think the drug can cause hypertension in some people more readily than other amps, which explains the kidney pain. By default, this would mean extended use could lead to pulmonary hypertension, ventricular hypertrophy, pulmonary embolism, heart attack, death, and even worse - a stroke. Your blood is pumping through your system on a shorter race track, you're not pissing out any fluid, and your muscles are being deprived of oxygen. If you're experiencing any of these symptoms, I strongly suggest you rethink daily use. If you have a history of heart problems or high blood pressure in your family I would recommend skipping the substituted amphetamines altogether.

Not trying to scare/impress, but I'm paying 40k a year to study this shit so I might as well use it to help people out. If you like this chem, get it while you can because it won't be around long.

Anecdotal evidence isn't the best, but I took 50mg today (first time in quite a while). I took a set of baseline vitals before - BP 96/72 HR of 48 (I'm working out again, if you haven't guessed from my Hannibal Lectorian vitals ). Then again at t+1hr on 2-FMA, BP 108/82 HR of 56.

Elevated my BP? Sure did. Am I afraid of a stroke? I'm still f***in bradycardic! Maybe if my roommate decides to inject me with a gallon of PCP http://www.youtube.com/watch?v=Ah7ApyeyneY

Next up? I'm going to try a dual panel AMP/MAMP urine screen at t+8 hours and see if I piss hot, this might shed a tiny bit of light on what (if anything) is happening to 2-FMA in-vivo. I'm still trying to get a friend of mine to run GC/MS on some 2-FMA piss for more rigorous results.

Edit: Please still do exercise a lot of caution if you do have any risk factors for cardiovascular/cerebrovascular incidents, I should point out I'm a trained lab rat with a case of athletic bradycardia. The last thing you want is to be lying on the table getting an emergency AAA repair when you're half brain dead already

Maybe someone who has reported kidney pain could try taking their BP before and while on 2-FMA? Perhaps try taking a low dose of Clonidine first, and see what effect this has?

I might try with 50mcg clonidine and see if it effects my vitals next time, but there aren't any side effects in me for it to alleviate... (other than bruxism)

 

[tweex]

Reporting back in, the plot thickens.

Urine taken at t+8h after ingestion of 50mg of 2-FMA produced a clearly negative test on the amphetamine immunoassay, but an ambiguous result on mAMP (an extremely faint line, you can barely see it). Repeating the same test on 2-FMA dissolved in water yielded a clear positive for mAMP, and still negative for AMP.

These results interestingly conflict with the supposedly high cross-reactivity to amphetamine immunoassay reported in one of the few studies of 2-FMA: http://bitnest.ca/external.php?id=%7DbxUgY%5CC%40%1BR%2B8%3CW%5C%0E%05%15%1CVIv%7C%7E%14TwxGD

This is the same batch of 2-FMA that I tested with Marquis, so I can rule out contamination with actual meth.

So what to make of this? Well nothing is certain. However here is what I'm thinking...
-Previous (very silly) claims that the fluorine is magically stripped off of 2-FMA to yield methamphetamine are clearly debunked, as meth would have started metabolizing into amphetamine, leading to an AMP positive. I mean who the hell believed that?
-Clearly neither amphetamine or methamphetine are major metabolites of 2-FMA, as the latter decomposes into the former via further metabolism, and the former is not being detected.
-2-FA may be a metabolite. I have no idea how 2-FA reacts to the immunoassay.
-The possibility that 2-FMA is excreted by the kidneys intact is still there, and perhaps the most plausible. This would explain basically the same reaction between post-2-FMA urine and 2-FMA dissolved in water to the AMP/mAMP dual panel, excluding differences in concentration. Confirmation of this without GC/MS would require determining specific 2-FMA concentrations that cause a positive/negative screen for mAMP on the brand of test I'm using via binary search, followed by repeated collection of urine into a large container and subsequent systematic dilution until a negative test is obtained to figure out the concentration of 2-FMA, and thus see if the detected concentration matches up to the initial dose over some long period. This should theoretically be a way of confirming that either 2-FMA or something that reacts to the test in an identical way is being excreted in the exact same concentration that is being ingested. Of course if elimination methods other than renal exist, this seriously complicates things.

Anyway, food for thought. I'm still trying to get GC/MS done on my piss to solve this once and for all.

 

[21p]

Tweek, here are a few thoughts I had while reading your post:

1. Very creative approach, but a GC/MS on your urine won't be accurate for excretion unless you are John Nash's understudy. You will be able to test for the presence of 2-f and metabolites, but don't expect anything more. Way too many variables to control for and the kidney is not an accurate barometer of what the body does consistently over short periods. Any 2fma metabolites present may have gone through several rounds of decay/enzymatic manipulation at unknown rates.

2. You will learn the most useful information about the drug by nabbing blood glucose, aldosterone, and hormone panels timed specifically to 2fma's observed duration of action. Although the chemical is novel, it isn't new. We know what catecholamines and sympathomimetics do (for the most part) and know what to look for when we piece together symptoms as part of a 'constellation dx.' I will be very surprised if the chem degrades much at all.

What I think we'll see after some research on 2fma:
1. greater activity on alpha-1 adrenergic receptors in the peripheral vasculature when compared to adderall/dex (explains vasoconstriction)
2. decreased duration of binding/affinity to inactive sites caused by steric hindrance, similar to MDPV. (explains marquis)
3. Increased risk of pulmonary htn (medium to long run)
4. Increased risk of CHF/D (long run)
5. Several absolute CIs related to 1-4,

One last point: I dunno if it's a good idea to post anything that could be misinterpreted as medical advice on bluelight unless you're 100% sure you're correct or the risks of being silent are too high. No disrespect, but about half of the last post was inaccurate (even the bradycardia comment, I'm afraid... which sucks bc you bolded it hahaha. been there, done that. Will probably do it again a few more times today...

 

[tweex]

One last point: I dunno if it's a good idea to post anything that could be misinterpreted as medical advice on bluelight unless you're 100% sure you're correct or the risks of being silent are too high. No disrespect, but about half of the last post was inaccurate (even the bradycardia comment, I'm afraid... which sucks bc you bolded it hahaha. been there, done that. Will probably do it again a few more times today...

Huh? I'm fairly sure bradycardia is defined as a heart rate of below 60. Does it have any clinical significance if it is athletic bradycardia? no, but bradycardia none the less. My bodyfat is a bit high ( 15% ), but I'm in the best shape I've been since high school. I just did my first sub-minute 400m (while off any drugs) in years, granted my heart rate was in the neighborhood of 200 at the end

Edit: Tried 2-FMA with clonidine today. Baseline vitals were BP104/76 52HR. Administered 100mcg clonidine at t=0. Vitals taken again at t+1h, BP88/70 46HR and 50mg 2-FMA administered. Vitals at t+2h BP 100/74 56HR.

So it appears for me at least, 100mcg of clonidine roughly negates the hypertensive effects 50mg of 2-FMA. Again, not that I seem to be someone with a tremendous amount to worry about in the hypertension department to start with...

 

[21p]

I took a set of baseline vitals before - BP 96/72 HR of 48 (I'm working out again, if you haven't guessed from my Hannibal Lectorian vitals ). Then again at t+1hr on 2-FMA, BP 108/82 HR of 56.

Athletic left ventricular hypertrophy is still the subject of debate in the medical community, especially in pathology. If you have vascular issues as the cardiac muscle fibers begin to expand, ischemia and heart attack can follow in theory. The diagnosis is being re-studied bc doctors and medical examiners historically assumed the dead track star's valvular dysfunction was the primary cause of death, not compensatory hypertrophy leading to valvular prolapse. There are so many parallel processes occurring it usually confounds the diagnosis, kind of a chicken or egg thing most ER docs naturally don't give a shit about because like 2% of Americans exercise that frequently or strenuously.

This could be bradycardia, but normal limits are situational in real life. An old woman or small, physically fit male could easily be considered within normal limits with those numbers, but a 6'3" man would be headed for disaster. If he's African American, the scenario changes again. Often times, these patients are asymptomatic.

You also have clonidine on hand, which means you either sought it out or it was prescribed to you. This is the first thing I'd note if I was taking your history as it potentially skews your statistics. Clonidine isn't well tolerated in a significant minority of people because it can cause reflex tachycardia and palpitations. You also have to ween yourself off of the drug if you take it regularly. If a kid started self-medicating with clonidine to offset potentially non-existent hypertension, there could be a megashitfuckton of problems when he/she ran out and didn't know better. In general, you break a cardinal rule when you suggest a treatment before knowing the cause of the ailment. Many cardiac drugs are receptor-specific and could be life threatening when taken without appropriate testing. I didn't want to go nitty-gritty because these types of conversations are not the most interesting reads, and besides... everybody here just wants to get hiiggghhh. sooo higghhh.

Anecdote:
Oddly, I learned this stuff before med school. An eighteen year old football player died under my palms one night in the trauma bay. I cut his shoulder pads off and traded CPR rounds while the trauma team tried to chemically resuscitate him. Autopsy just showed ischemia and 'athletic heart' hypertrophy, no congenital or valvular abnormalities. His family let the issue go, but you should have seen the resident pre-round discussion the next morning. I've never seen a room full of surgeons so confused and argumentative, as they tend to be more self-assured and obsessed with pecking order than other specialties. He probably should have gone directly to the ER, but the two departments were standoffish when I was wiping butts there... which is a reality check on health care best reserved for when I don't have so much stuff to study.

You seem like a smart guy and you're pretty insightful for not having been through three years of hell. I only know this stuff because it was shoved down my throat with a ram-rod.

 

[Lady Codone]

Thank you doctor-like people for the information! It's virtually all that exists about this compound.

2-FMA doesn't speed up my pulse as much as 4-FA. I've taken my bp on both drugs and it was within the normal range every time (albeit approaching the borderline for Stage I hypertension once on a ton of 4-FA). These aren't occasional use drugs for me, it's pretty much a daily thing (yes I know it's no bueno).

In my years of RC stimulant use, here's what I've found helpful:

*If you're gonna take any stimulant regularly, you need to drink more water than usual and adjust your lifestyle to help prevent cardiovascular problems. Remember that many things can affect bp and heartrate, such as excess sodium and even stress. Make adjustments to help offset the amphetamine-induced changes. If you're experiencing vasoconstriction (cold extremities, discoloration in the knees, headache, etc), take a warm shower or chew some ginger root.

*Stimulants can cause dehydration by increasing urine output. Mild dehydration can cause many vague symptoms, such as fatigue, dry mouth, dizziness, dry skin and headache, so drink plenty of water or electrolyte drinks. Soda, coffee and other caffeinated drinks are like consuming NEGATIVE fluids since they increase urine output. Avoid them.

*Eat right, exercise (but NOT while on stimulants) and get plenty of sleep. Exercising on stimulants is very dangerous because both exercise and stims raise bp and heartrate. Brush your teeth every single day and floss nightly. Dry mouth = more cavities.

Common sense stuff mostly, but I felt like typing :D

 

[tweex]

Athletic left ventricular hypertrophy is still the subject of debate in the medical community, especially in pathology. If you have vascular issues as the cardiac muscle fibers begin to expand, ischemia and heart attack can follow in theory. The diagnosis is being re-studied bc doctors and medical examiners historically assumed the dead track star's valvular dysfunction was the primary cause of death, not compensatory hypertrophy leading to valvular prolapse. There are so many parallel processes occurring it usually confounds the diagnosis, kind of a chicken or egg thing most ER docs naturally don't give a shit about because like 2% of Americans exercise that frequently or strenuously.

Interesting, so you think working out hard enough that you develop ventricular hypertrophy may actually cause mitral valve prolapse?

This could be bradycardia, but normal limits are situational in real life. An old woman or small, physically fit male could easily be considered within normal limits with those numbers, but a 6'3" man would be headed for disaster. If he's African American, the scenario changes again. Often times, these patients are asymptomatic.

Well, I suppose I'm using the term bradycardia a bit more loosely than you are, simply HR<60. The main reason I qualified it as athletic bradycardia. I'm actually 6'2" 205lbs now, and white (insert joke about amphetamine users here) and I have absolutely no symptoms of poor perfusion aside from the very occasional mild episode of orthostatic hypotension if I stand up quickly after a nap we all get. Actually my baseline HR being out of shape is in the 70s. I was in a nasty skiing accident last winter and got deconditioned, and have just finally been returning to serious athletic activity.

You also have clonidine on hand, which means you either sought it out or it was prescribed to you. This is the first thing I'd note if I was taking your history as it potentially skews your statistics. Clonidine isn't well tolerated in a significant minority of people because it can cause reflex tachycardia and palpitations. You also have to ween yourself off of the drug if you take it regularly. If a kid started self-medicating with clonidine to offset potentially non-existent hypertension, there could be a megashitfuckton of problems when he/she ran out and didn't know better. In general, you break a cardinal rule when you suggest a treatment before knowing the cause of the ailment. Many cardiac drugs are receptor-specific and could be life threatening when taken without appropriate testing. I didn't want to go nitty-gritty because these types of conversations are not the most interesting reads, and besides... everybody here just wants to get hiiggghhh. sooo higghhh.

Sought it out. I actually had a workup from a cardiologist back when I was marathoning seriously a couple years ago. Fortunately I tolerate it quite well, and I use it pretty rarely. I primarily use it to counteract the hypertensive effects of repeated very high oral doses of nicotine, as clonidine reduces catecholamine secretion induced by nicotine. Why I take repeated very high oral doses of nicotine is a much longer story... Although this combination also has the interesting effect of strongly increasing HGH levels

I just decided to see what effect it would have on 2-FMA, as it wouldn't carry any risk of adrenergic storm, unlike say, beta blockers. (Granted this isn't much of a real risk until the doses get insane)

Anecdote:
Oddly, I learned this stuff before med school. An eighteen year old football player died under my palms one night in the trauma bay. I cut his shoulder pads off and traded CPR rounds while the trauma team tried to chemically resuscitate him. Autopsy just showed ischemia and 'athletic heart' hypertrophy, no congenital or valvular abnormalities. His family let the issue go, but you should have seen the resident pre-round discussion the next morning. I've never seen a room full of surgeons so confused and argumentative, as they tend to be more self-assured and obsessed with pecking order than other specialties. He probably should have gone directly to the ER, but the two departments were standoffish when I was wiping butts there... which is a reality check on health care best reserved for when I don't have so much stuff to study.

Could this possibly have been a case of HCM in disguise? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1769182/

I've heard several anecdotes of athletes dropping dead of undiagnosed HCM. Deconditioning obviously does work to differentiate the two. Also he sounds like he would have been a prime case for being resuscitated by ECMO if he got high quality CPR, too bad it is just now starting to see use for out of hospital arrests...

You seem like a smart guy and you're pretty insightful for not having been through three years of hell. I only know this stuff because it was shoved down my throat with a ram-rod.

Hah thanks. I sat many years of engineering school, it requires the ability to absorb a lot of information. I'm in the medical field now, but not in med school. I'm thinking about it though...

 

[21p]

Hah thanks. I sat many years of engineering school, it requires the ability to absorb a lot of information. I'm in the medical field now, but not in med school. I'm thinking about it though...

Waste of time unless you want to spend 90% of your life devoted to your work. I went back at 29 and think it's much easier if you're younger and your body can handle the hours. You will have to ignore the majority of people outside your immediate family (most can't understand until they've done it, which is a weird dilemma) and be forced to interact with people just like yourself... except younger. Hahaha, it's great at times and other times I question the decision.
I don't think I would do it over again, which is what the majority of physicians say. You have lateral mobility but almost every specialty is highly regulated.


Idiopathic HCM in athletes = undocumented growth hormone and steroid abuse/dysfunction. Our local gym is full of unfortunate fellas destined for a similar fate. The world is strange; everyone pays for their hangups whether they know it or are totally oblivious.

 

[tweex]

Found a few more relevant journal articles:
http://www.ncbi.nlm.nih.gov/pubmed/22374819
http://www.ncbi.nlm.nih.gov/pubmed/21543168
http://www.ncbi.nlm.nih.gov/pubmed/19900772

Overall seems to lend a lot of credence to 2-FMA and other fluoroamphetamines being fairly stable from a metabolic point of view. Also interesting about difluorophenylethylamine tending to be attracted to fat cells, resulting in reduced stimulant potency per dose. I wonder if 2-FMA has some of the same issue?

 

[bennyZA]

Tweex, I don't have your background in science. Do you think you could break down what you said for laymen? What does being fairly stable from a metabolic POV mean?

This is a substance that I'm very curious about, so I'm trying to get as much info as possible.

 

[21p]

Also interesting about difluorophenylethylamine tending to be attracted to fat cells, resulting in reduced stimulant potency per dose. I wonder if 2-FMA has some of the same issue?

"Fluorine in psychedelic phenethylamines" was the name of the paper. I'll try to make it user friendly for ya, Benny ZA and explain it without getting too cray with the words.

Purpose of experiment:
-They injected rats with a chemical to slow their body's processing of a psychedelic drug chemically attached to flourine to figure out:

1. What does this drug do when it's just hanging out in the body? You'll notice the research is from 1973, which means the writers were probably the first to do these types of experiments.

2. How does this fluorinated drug affect the body when there is an excess? This may be where the answer is, Tweex.
-They found that the drug was taken up by fat cells in the rats at a faster rate,but it didn't stick around for very long at all. it was more of a footnote in the research to show the differences between the drug and others.

-Most pertinent point of article from a medical perspective: fluorinated compounds acidify the blood, although most recreational doses probably don't have as serious of an affect. This absolutely does not mean fluorine was detaching from the main molecule as the rats started to get high.<--That would be bad, bad.

What is 'acidic blood'? -It's a roundabout way of saying that if you overdose on some fluorinated compounds, you may run a higher risk of fever, rapid breathing and pulse, and weight loss than their 'cousin' drugs (meth, amp, etc). All of these likely apply to binge use as well as a mega-dose, althought the weight loss is definitely gonna occur with binge use.


"4-FA in drug testing" Didn't check the full article, but I'm guessing that fluorine would stick out on a mass spec. The main question is: is it now part of a regular panel? Don't know, don't care to speculate for obvious reasons... again, give it a little time and they'll be screening for all of em. Guarantee a Quest dx would pick up MDPV after the face-chewing incident down in Miami last year.

 

[HighestWhenLow]

Haven't checked in on this thread in some months, so glad discussion on this largely unknown but useful chem has picked up! Big thanks to the people keeping the knowledge flowing, especially regarding biological & scientific aspects that have probably never been researched before! Imagine that, doing actual research on a research chem

In particular, thanks to tweex for answering the often-asked but rarely answered question of whether or not fluorinated amps show up on drug tests, and thanks to those who posted results of marquis reagent tests!

Much love

 

[Diapsiquir]

Can now someone surely say if the BA of 2-FMA is higher when plugged compared to oral/nasal? Did it a few times but I still cannot tell if it´s worth it plugging 2-FMA and the reports on the net are contradictory.

 

[tweex]

"4-FA in drug testing" Didn't check the full article, but I'm guessing that fluorine would stick out on a mass spec. The main question is: is it now part of a regular panel? Don't know, don't care to speculate for obvious reasons... again, give it a little time and they'll be screening for all of em. Guarantee a Quest dx would pick up MDPV after the face-chewing incident down in Miami last year.

Oh, the tl;dr on that: even though they aren't specifically tested for, the FA/FMAs will cross-react to most immunoassays (eg. the typical 10 panel piss in a cup and stick a stick in it type). For GC/MS they won't show as amp/mamp, and have to specifically to be sought out to show up. They are apparently hard to distinguish between with GC/MS testing, it is more a question of testing for "fluoroamphetamines" and "fluoromethamphetamines".

And of course as I posted before, they won't react much to a Marquis reagent for "field narcotics identification."