N&PD Moderators: Skorpio | someguyontheinternet
<pyridinyl_30> said:I would love to taste
3,4-di-trifluoromethylamphetamine. Sadly, fenfluramine (N-ethyl-3-TFM-amp) was shown to cause heart valve defects.
cool. i always had a suspicion that fenfluramine would be interesting in higher doses.MokumChemist said:Slightly OT, but I did try dexfenfluramine before it was withdrawn. Initially, and at lower doses it felt similar to 4-fluoroamphetamine, a bit less stimulating though. Quite pleasant and calmly euphoric, but nothing incredible. Later on, and at higher doses, it became somewhat psychedelic. It even produced some simple OEVs - patterning and colouring over every surface.
Unfortunately I can't remember the dosage because it was years ago. I used it only 3 times, no sign of heart valve damage yet...
MurphyClox said:Well, the most probable sites of metabolic degradation are supposed to be the amino-function (...MAO), the methoxys (maybe COMT or other methyl transferases) and the CF3. Then again does our body not posess the ability (i.e. the necessary enzymes) to degradade any organic fluorine compound (IIRC). Therefore, metabolism is "reduced" from 3 possibilities (like with 2C-B or alike) vs. just 2 possibilites with 2C-TFM.
So, your "theory" and FnB's statement are not mutually exclusive IMO.
Peace! Murphy
http://www.sciencedirect.com/scienc...serid=10&md5=7b5fd81af0f9ea1ef4475b216b234e7bStudies on the metabolism and toxicological detection of the designer drug 4-ethyl-2,5-dimethoxy-β-phenethylamine (2C-E) in rat urine using gas chromatographic–mass spectrometric techniques
The phenethylamine-derived designer drug 4-ethyl-2,5-dimethoxy-β-phenethylamine (2C-E) was found to be mainly metabolized in rats by O-demethylation, N-acetylation, hydroxylation of the ethyl side chain at C2′ or at C1′ followed by oxidation at C1′ to the corresponding ketone, by deamination followed by reduction to the corresponding alcohols or by oxidation to the corresponding acids, and finally combinations of these steps. Most of the metabolites were excreted in conjugated form. The authors’ systematic toxicological analysis (STA) procedure using full-scan GC–MS allowed the detection of an intake of a dose of 2C-E in rat urine that corresponds to a common drug users’ dose. Assuming similar metabolism, the described STA procedure should be suitable for proof of an intake of 2C-E in human urine.
King Kong said:In a larger subject. Branched alkanes is lipophilic, maybe good size... It must be a good "4-" substituents! Someone try to put a isopropyl or tertbutyl? I have find no data...
Ok, one thing after another.nuke said:That doesn't explain the duration and potency of 2c-e though, which has quite a few more different routes.
...
You would expect that the iodine in 2c-i would prevent clearance and have a longer duration than 2c-e, but 2c-e seems to run most people longer.
Ok, one thing after another.
First, my comment was mainly referring to the duration and not so much to the potency of 2C-TFM.
Second, I admit that I oversimplified the situation a bit. Of course (and here you are absolutely right) there are more than just 2 metabolic pathways available to degradate 2C-E and most probably for 2C-TFM as well.
But: The trifluoromethyl-moiety is a highly unnatural substituent and does everything but facilitate degradation of the compound. Even if the CF3 isn't touched, lets say in a MAO-catalyzed reaction, it does interfere with the substrate's binding to the enzyme. And IMO does that count for probably most (if not all) of the involved metabolising enzymes. This counts in particular for the directly neighboured hydroxy-function (pos. 5) and the meta-postitioned hydroxyl (pos. 2).
In other words: The CF3 makes 2C-TFM an overall bad substrate.
Fig. 2 in the article that you linked (J Chromatograph B 2006, 842, p.76) proposes that the metabolism of 2C-E starts with 4 main reactions (followed by numerous others), one of them involving the pos. 4-ethyl (not working with 2C-TFM!), one with the ortho-hydroxy (hindered metabolism by the CF3), and two involving the amino-function. One of the two latter pathways starts even with acetylation of the amine, a reaction that should
So, I conclude that the CF3-group indeed has (presumably) a major impact on the overall metabolism of 2C-TFM, and thus, slowing down degradation.
About the potency-issue, I can only comment that fluorine has a very special position in nature (...organo-fluorine compounds being the least abundant natural organohalides).
Some examples: There are practically no enzymes known that can handly any F-containing moiety. Fluorine possesses an outstanding electronegativity, paired with it's small size. This implies special properties that are hardly shared by any other element or functional group. I don't want to go too much into detail with fluorine's specialities, but can recommend Science 2007, 317, p.1881 (article avaible upon PM-request) as a good reading for this topic.
With iodine (2C-I) it is different. To my knowledge is the human metabolism able to handle it. Therefore, I would rather expect the iodine-congener getting metabolized faster. And indeed, as you said, most people report about a shorter duration compared to 2C-TFM.
Peace! Murphy
I'd say this is very well thought out and aligns with my reserach. I recently received a batch of 2C-TFM (I received an H-NMR with it and a COA, conducted a melting point test also - its the real deal). I found it to be worthwhile if you want to compare and contrast to other 2Cs. Akin to 2C-T-21, based on Shulgin's reports, not personal research (interestingly and obviously another fluorinated compound). 2C-TFM doesn't quite have the magic I had anticipated. A remarkably clear-headed, egoless material. Not exceptionally potent compared to other 2Cs, DOx, NBOMes. I enjoy it of course. High affinity to the 5HT2A receptor doesn't directly translate into "yeehaw." I anticipate that this alone was where the doses on wikipedia got pulled from (comparing affinities to DOx.)
It is active at 3mg, but rats would feel comfortable with 10-15mg for sure, at least IMO. I wouldn't hesitate to push the envelope, other than the fact that there are things working behind the scenes that I might not be aware of. It'll be a slow slow titration to see if there is a breaking point into the rodeo.