I have experimented with IV 4-AcO-dmt a few times. The first time hit me instantly. Was pretty awesome. The second time I over did it. Not so awesome. Thought I was dying. Was doing everything I could not to die. I think if I stopped fighting so hard, the experience would have been better. But I felt the minute I stopped fighting I would die, and I didn't want my family to find me like that...
Did you just dissolve it and inject (the #yolo way) or did you use a micron filter first? What solvent did you use since anything left over would go bad very fast in water? Or did you make just enough? Or freeze the left overs (I assume this would give you at least a few months)? Or just accept the loss? Or what?
I wanted to make a multi use injectable psychedelic/disso mix in a 10 ml vial but never figured out how to use 4-ho/aco trypts so these were out, I don't like 5-meo trypts so these are out too, stability wise the 2c-x make the most sense + I imagine it would do wonders for 2c-cs potency.... another problem is that buying sterile vials with rubber stoppers, bacteriostatic water or sterile water + benzyl alcohol would make for a very expensive experiment unless you made a lot of it..... so this is something that remains in the would be an interesting experiment but wont happen any time soon. I was also thinking more of im/subq injections than iv and that's even more sensitive to sterility.
Dissociatives are the best pain killer, even better than opiates. Believe me that drive my MXE/3-MeO-PCP use/abuse!
Oh yes. And you (or at least I don't) don't need to use high doses to achieve it, so the side effects are minimal. Now it's hard to notice small cognitive impairment on yourself, but for what it's worth I never had any problems with that. I'd do get the weird gait (even from one low dose.... obviously with one low dose it doesn't last long after the psychoactive effects are gone and isn't very obvious but it's noticeable enough that people who know me enough can tell easily..... while I can pass for sober on high doses of psys and or entheogens (as long as it's dark so that my pupils don't look out of place or very sunny so that they don't get huge)/benzos (even if I don't remember anything the next day people only know if I start asking what we were doing)/stims (I'm always sweaty anyway and my pupils stay the same size)).
And I might be a bit biased here since I don't like opis (basically what I get is some relatively weak painkilling, a headache, that shitty opi nausea and some make me very itchy..... but that famed euphoria/bliss? Nope, tbh strong hypnotic benzos or dissos + stims are pure euphoria, psys can be very euphoric too but it's never a sure thing, entheogens are more loved up and relaxed than euphoric, stims alone are euphoric too but dissos + stims have more euphoria/mania and the negative effects of stims get covered up.... and yes, dissos + stims can quickly go from mania to psychosis so be careful if you try, start very low, have some benzos on hand just in case and vaped (at least the stim (a-pvp is a winner) if the disso you have doesn't vape well) is probably the best way to dose since the effects are almost instant... ).
He didn't claim it without proving @ 4-AcO, he just suggested that as esterases are abundant in the body the AcO is expected to be cleaved just like psilocybin is. For psilocybin itself though, it is a zwitterion and too polar to cross the blood-brain barrier. 4-AcO-DMT is not zwitterionic and it seems 'even less' polar than psilocin so it should be able to cross the BBB better.
There are other possible reasons why 4-AcO-DMT may feel different - perhaps it is active itself (but I have a feeling a little less than psilocin because of the missing proton donor of 4-HO) but the different kinetics could also play a role - it's what I always suspected. [so imo that is my opinion yes kidklmx but not proven, hard to prove anyway - you would have to do a study with varying kinetics of same compounds]
Seems like a mistake to involve psilocybin in this since mushrooms also contain other alkaloids that may serve as competitive MAOIs and it is very rare for people to try pure psilocybin, plus the zwitterion thing.
I think 4-AcO-DMT feels different - it does feel like a more dilated slow smoked DMT trip like Xorkoth said, but I actually think synthetic 4-HO-DMT does too only less slow and smooth. Mushrooms feel more messy and complex to me. Anyhow, it is best to be skeptical and just consider the possibilities rather than jumping to conclusions based on subjective effects either way. Countless mistakes have been made that way such as that some dissociatives must have opioidergic effects. Hardly any have been shown to bind directly to opioid receptors, yet it must not be forgotten that the NMDAR system is very closely latched onto the opioid system.
It would be interesting to see if there are other orally taken DMT analogues that do not cause tolerance the same way DMT doesn't - even as ayahuasca. Which is remarkable and thought to be due to different conformational changes in 5HT2A that are pretty unique compared to LSD but probably also compared to psilocin etc since those clearly produce tolerance.
[even psilocin is not expected to be able to cross the BBB normally, and would need help in administration like 5-HO-DMT, but it's thought that psilocin is able to coordinate with itself 4-HO to amine to reduce polarity - it would be interesting to see 5-AcO-DMT... i have the means to make it I think, but unfortunately my experimenting is retired for the time being and no interest in taking bufo or bufacetin. Also I think you can calculate things like log P for these compounds to have a fair idea of whether they have a chance crossing the BBB so I don't think it's all guesswork at all.]
Evidence that psilocybin indeed dephosphorylates:
http://197.14.51.10:81/pmb/AGROALIMENTAIRE/Bioactive Compounds in Foods.pdf page 120
In 1962 Horita and Weber demonstrated that if you inhibit alkaline phosphatase in mice, you see much less behavioral changes from psilocybin supporting the claim that psilocybin must be dephosphorylated. 4-AcO's would require different esterases... I don't know if you can test the same in mice by inhibiting all those esterases, your mice may explode..
The active by itself, rapidly metabolised to 4-ho-dmt (or 4-ho-whatever tryptamine) and the possibility of the ester having an effect on blood brain barrier penetration theory feels the best, but I have nothing that backs it up other than anecdotal evidence and my gut feeling. But it's not like this is a widely researched topic or anything. There is some indirect in the form of evidence from the effects of esters changing the effects of other drugs via the same mechanism (GBL, heroin, ....).
To be fair looking back the disso mistake was not hard to make both cause at least some of their positive effects not by direct binding to receptors/transporters/and so on but by downstream effects. So it is plausible that both would cause similar downstream effects via different pathways. And since these speculations were based subjective effects they were easy to make especially since many people did find quite large similarities in subjective effects. Just like dissos don't bind to the same receptors as benzos but can reduce withdrawal symptoms by antagonising glutamate at nmda receptors (and increased glutamate + decreased gaba/gaba receptor sensitivity is probably the biggest cause of benzo wds).
But again, this is all speculation based on feeling and anecdotes (not even personal ones since I don't really get benzo wds which is weird on it's own and if anyone has some speculative explanation I would love to read it... and no, I'm no, just taking other drugs that act on gaba to compensate... I truly can go cold turkey (basically when it becomes pointless since 10 mg of flam is just a light buzz) from extreme benzo abuse (grams grams of the best (aka strong hypnotics like flam, nifoxipam nasal spray (completely different than pellets... as in once upon a time 4 mg flam = light buzz and 2 mg flam + 2 mg of the spray = woke up on my keyboard a few h later wondering wtf happened) ones + grams of good ones (either just strong ones or weak but longer acting hypnotics... clam/fpam/norflurazepam) taken for months which should by all accounts end with a trip to the ear or the morgue and to make matters even stranger a few weeks later 2 mg diazepam is a light buzz... yes I know it's hard to believe but why would I lie? I'm not suggesting this to anyone nor selling benzos nor disos so......I never got addicted to ghb either, but I wasn't taking more than one dose per day which is supposed to be safe, haven't tried with anything else since I never had almost unlimited access to any other good drugs that act on gaba (methaqualone, barbs, z-drugs, .... only alcohol which just makes you feel bad if you drink enough to get drunk daily, rc methaqualone analogs which suck, phenibut, and one prescription of zolpidem this summer for insomnia (sadly ac isn't covered by insurance... I also have a prescription for a baby dose (3x25 mg) of lyrica for anxiety/nerve pain which works great (some shrink insisted that that's not true and wanted to increase it to 300 mg daily + ssris + low dose antipsychotics (which feel/act like poison on me and I was like wtf, thought to myself 'this is why psychiatrists are one of the more disliked doctors' (couldn't actually say (the words just couldn't come out) it thanks to a few doses (got one first which just want me to go hulk Smash puny doctors and orderlies and then more plus a lot of benzos so my memory is a bit fuzzy except the whole Hulk smash wish which the benzos luckily made me to lazy to act on) of the supposedly much safer than benzos anti psychotic risperidone.... also walked even weirder than from dissos (had to use my arms to hold my head straight while walking otherwise I would look straight up) and felt like a retard for a week and this was an oral immediate release form not some extended release stuff). I think this should be enough for one post
Sorry I just had to...
>They should definitely do a study using radioactively labeled 4-AcO-DMT (the isotope being on the Ac), and measuring if that Ac makes it into the brain and at what rate... wouldn't be that complicated.Getting funding and approval would be the hard part
>Who knows what they might find. I must say though I found the results of 25B-NBOMe metabolism VERY surprising and clarifying regarding the bad oral activity... they used a similar technique for that.
Do you happen to have a pdf (or just the doi, I'll find the full text on my own)
>still kinda dealing with some stuff, but coming out of pregabalin taper better and going to some art lab on a weekly basis starting next week. I should keep an eye on my K use in the meanwhile...
If it's not too personal, how much were you on and for how long? Did it help with whatever it was given for? How hard was it to come off/how long did it take? Feel free not to answer if it's too personal.