• Psychedelic Drugs Welcome Guest
    View threads about
    Posting RulesBluelight Rules
    PD's Best Threads Index
    Social ThreadSupport Bluelight
    Psychedelic Beginner's FAQ

Health Deprenyl + phenethylamines alert!

Yep deprenyl and amphetamine. Temp went up rather alarmingly with not very large doses.

Thing is, harmala alkaloids are competetive inhibitors of MAO-A, but deprenyl is a non-competetive inhibitor of MAO-B. There not the same thing by a long chalk, so it's not surprising that things didn't go the same
 
I know a lot of people who love to mix MDMA with selegeline. To me this seems rather extreme, though... An irreversible (long-lasting) MAOI-B seems a dangerous thing to consume in general if you don't know what you are doing, and I imagine that there is potential danger when prohibiting the metabolism of PEAs.
 
Yes, I've experienced both 2c-c and 2c-d after having taken deprenyl in the past week, but never on the same day, as I knew it had the potential to do exactly what these trip reports describe.

There is no question that it strongly potentiates these substances. In my experiences they seemed at least twice as strong as normal. 2c-c was clearly active at an above-threshold level with an insufflated dose of less than 5mg, if I recall. I dosed very carefully because of the potential risk, and actually did not end up taking much more, because the body load was definitely worse than normal, as well.

From a standpoint of dose-efficiency, I suppose this could be viewed as a positive thing, but I see it as extremely dangerous. Deprenyl is generally marketed as a relatively innocuous supplement, and I don't think most people recognize its potential to interact with a wide variety of psychoactives.

On the other hand, I've used it in the past to intentionally get more out of amphetamines. It does not seem to potentiate amphetamine / dextroamphetamine as much as it does with other phenethylamines like 2c-c or 2c-d. I do recall feeling slightly overstimulated at times, but nothing major.
 
I used 2C-D while on 5mg/day selegiline. I had the impression that the effects lasted longer, but were not stronger of otherwise altered.
 
this post deserves an ongoing bump as the dangers of combining selegiline can not be overstated.

selegiline is an amazing agent with a broad therapeutic index, varied pharmacological profile and many subtle and not so subtle effects.

as we all know, selegiline is an irreversible MAOB inhibitor. irreversible means your enzyme levels will not be back to normal for at ~ 2 weeks after you stop taking it.

what’s more important to many of you balls-out readers, is it semipermanently hypersensitises you to psychedelics, which is not a good thing. you may go into overdose territory on a subthreshold Erowid dose.

i have extensive experience with combining selegiline, and have posted several times in the past as to the specific dangers of combining it with the 2C-X class. the combo is especially hazardous if you are in the middle of a course, which means your MAO-B is fairly fully suppressed.

MAO-A deaminates primarily serotonin, norepinephrine, dopamine and octopamine, while MAO-B takes care of phenylethylamine, dopamine, benzylamine and methyl-histamine. to paraphrase what Sasha wrote awhile back, many ring-substituted phens are readily deaminated by MAO and the invariably greater potencies of the corresponding phenylisopropylamines (amphetamines) is due to immunity from attack by these enzymes.

this is why selegiline does not pose much of a hazard when combined with amphetamines (and has been shown to be neuroprotective post acute MDMA intoxication), but has such radical and mostly negative effects when combined with 2C phens. when you are taking an irreversible MAOI is you are greatly reducing the metabolic clearance of your psychedelic substrate leading to who knows what, pharmacokinetics-wise.

again, in combining selegiline (l-deprenyl, Eldepryl, Jumex, Davur) and members of the 2C family, any potential benefits that you think might be gained are vastly overshadowed by the negatives.

THE NEGATIVES INCLUDE COMPLETELY UNPREDICTABLE POTENTIATION, SIGNIFICANT CNS AND CARDIOVASCULAR STIMULATION, CRAMPING OF THE EXTREMITIES, IRRATIONAL AND DELUSIONAL THINKING, AS WELL AS YOUR GENERAL PSYCHEDELIC DEATH TRIP FREAKOUTS.

so don’t do it. and if you are foolhardy enough to do so, CUT YOUR 2C DOSE AT LEAST BY 3.

/rant
 
mine and octopamine, while MAO-B takes care of phenylethylamine, dopamine, benzylamine and methyl-histamine. to paraphrase what Sasha wrote awhile back, many ring-substituted phens are readily deaminated by MAO and the invariably greater potencies of the corresponding phenylisopropylamines (amphetamines) is due to immunity from attack by these enzymes.
Click to expand...

I guess I'm confused then...what role does MAO-A and MOA-B play in the metabolism of MDMA? The friends I know who use selegeline together with MDMA say it extends the roll to about 8 hours and kills a lot of the negative comedown effects.
 
I have had the experience that subthreshold doses of 2-cb where active while on deprenyl. And where there for at least the next day (especially after drinking a cup of green thee). I would not willingly take an pea psychedlic with deprenyl. Mdma seems ok. And i am wondering about mushrooms and lsd. Somehow i feel mushrooms with some deprenyl would actually be a nice combination, but have never tried.
 
I have experience with selegiline and (d)-amphetamine. I have taken a 5-10mg dose of selegiline along with my regular 30mg dose of (d)-amphetamine. There was a potentiation, but it did not seem to be "too much" to handle in either a central or peripheral 'over-tweaked' sense or in terms of negative phenomenological effects. Interestingly, I felt a tad hyperthermic/ferbile, but the highest oral temp I recorded was 36.8 (+/- 0.11 deg). Since the amphetamine molecule largely escapes metabolism by MAO-B and the dose I took was not enough to overcome MAO-B selectivity, it would seem that the amphetamine was not affected. Perhaps the slight potentiation was due to brain-specific metabolism of selegiline to (l)-amphetamine. While weaker than its lovely (d) brother, if (l)-amphetamine is already in the brain, it too can act as a monoamine releaser.

Perhaps most interestingly, I find that 5-10mg of selegiline (do not take daily) combined with around 1.5-2.0g of (dl)-phenylalanine (which should be readily decarboxylated to phenethylamine, the preferred substrate for MAO-B in vivo) produces a phenomenological effect nearly identical to that of (dl)-amphetamine itself.

While I have no experience with the selegiline / 2C-X combination, it is important to note that the pharmacodynamics of the 2C-X series of chemicals is unknown--some believe that they solely directly agonize 5-HT2a receptors, while others believe they also act as monoamine releasers. Still others believe that they have a diverse pharmacology, such as LSD. Many trip reports fail to state the selegiline dose taken and the duration of selegiline use (it builds up over time and starts to more intensely ethinylate MAO-A). However, this little anecdotal data suggest that the 2C-X compounds are metabolized similarly to non-aryl substituted phenethylamines; that is, by oxidative deamination via MAO-B.
 
Last edited:
^and that effect, referred to as "antidepressant" is much stronger when you just take the levo phenylalanine isomer...
 
yeah why is that? I have found that 1 gram of d-phenylalanine does not do too (but still something) much in combination with deprenyl. Maybe the depressant effect of the enkephalin degradation inhibition masks some of the other effects. But it is strange in the light of the information on the we stating d-phenylalanine is a better precursor to PEA. L-phenylalanine seems uncomfortable (maybe because of cck effect?). Chocolate extracts feel nice with deprenyl (equivalent of 1 mg PEA). Haven't tried dl, i think.
 
Sorry this is a bit off topic. Tried some PEA (unknown low dose maybe a few mg's) with deprenyl and this did not feel like low dose amphetamine (more relaxing than stimulant). Maybe the dl-phenylananine except for being an PEA precusor also changes the effect by being precursor to Ne and Da. The PEA with depren. did not feel speedy. The dose was too low for a real estimate of the character of the effects, but i am wondering what a high dose (100mg?) of PEA with deprenyl would do. ...Questions. ... Anyone?
 
Last edited:
SWIM is currently taking a very small dose 1mg selegiline once a week. Would it be inadvisible to add a small threshold dose of 4-fmp or methylone(10mg or less) occasionally while taking selegiline? SWIM notices subtle, but pleasant effects from small dose methylone/4-fmp normally.
 
I doubt it would present too much of a problem, just be sure to monitor your body temperature very closely and be careful to avoid overheating.
 
Harmine and 2CI made me nearly go crazy, man it was nuts stronger than when I did it with mushrooms, oh man that was crazy intense.
 
Experience w/ 5-10mg selegiline + 500-1000mg L-phenylalanine daily showed a noticable positive antidepressant effect after only a couple days. Phenylalanine & tyrosine are both phenethylamines carrying a carboxyl group (COOH) in the alpha position. I believe tyrosine & selegiline have been said to produce a comparable antidepressant effect.

There is a lot of information out there about the pros & cons of combining selegiline w/ amphetamine. I have nothing to add to that.

I've only read bad things about combining selegiline w/ 2C's (especially 2C-B for some reason). I wouldn't try it.

Selegiline seems to interact in markably different ways with different classes of phenethylamines. Best to be careful w/ this combination.
 
yes, lots, but i find these days the information i offer as often as not get misinterpreted, perhaps causing harm instead of reducing it as per my original intent, so i will waylay my comments till proper time comes.

suffice to say, caution is urged, if you are fucking with critical enzymatic systems, put in there for a specific, xenotoxin eliminating purpose.
 
You must log in or register to reply here.
Top