pharmakos
Bluelighter
all this tryptamine talk is making me excited to try the 4-HO-MiPT that i just acquired
idk when i'll have a chance to, though... been super busy lately.

IV 4-AcO was innaresting. I'm not sure if I want to try that again.
http://www.iflscience.com/space/camelopardalid-meteor-shower-peaks-tonight
Meteor shower tonight--I hope to catch it while on the tail end of my trip later. I'm gonna skip the 2C-E & just take 4-AcO-DMT. Dosage tbd
:D
Is there any reason to believe that 4-AcO tryptamines would not cause the blood-brain barrier well? My understanding was that if anything they should cross it more readily. I know that this is at least known for a fact to be the case when going from 5-HO-DMT to 5-AcO-DMT. Kinetics may be a factor as well, but I would bet money that that's not the only thing happening.... I've taken a few different psychedelics by multiple routes of administration, including DMT, and for me no matter how different the experience is it's always been recognizable as the same psychedelic. But the beginning of 4-AcO-DMT and mushrooms for me are as different as night and day. There's no way in hell I could mistake one for the other. However, I could easily mistake 4-AcO-DMT for DMT, but I also seriously doubt that I could mix up DMT and mushrooms. This leads me to believe that there is much more than just a kinetic difference.
5-AcO-DMT is not really a thing, I think you mean 5-MeO-DMT. This difference is important / relevant because MeO, methoxy is an ether group which compared to a hydroxy is less polar, since it is a methyl put on the hydroxy covering / shielding it basically and methyl is non-polar. Still, it doesn't remove the fact that there is an ogygen there which has electron pairs bulking from it, and that is a polar thing.
With AcO, acetyl, its different. It is an ester, there is an extra oxygen on that which is not even protonated... And that is added on top of the oxygen present already. it is quite polar indeed I think, the fact that there is also a non-polar part to the acetoxy does not shield or compensate AFAIK.
I just seem to remember reading that 4-AcO-DMT probably does not pass the BBB all too well and I guess the extra polar stuff is the reason.
I must add though that despite the chemistry differences I just mentioned, they might not have the consequences I am talking about - I am not really sure about that is what I am saying.
Read some more though: polar molecules are prevented or delayed from passing the BBB, if you check some molecules you will see that they are 'economical' with their polarity and exposure (shielded or not) of it.
5AcO-DMT is of particular interest since its lipid solubility characteristics should permit it to cross the blood brain baarrier where by the action of tissue esterase it could give rise to 5HO-DMT (bufotenine) a compound which would otherwise not be expected to enter the nervous system too readily. Accordingly, an attempt was made to establish the dose-response curve for the behavioral effects of this compound. Thus, the effect of several doses of 5-acetoxy-N:N-dimethyltryptamine was investigated, using again a Latin-square experimental design (N = 6: 6 animals x 5 dose levels and saline). The conditioned avoidance response failure frequencies were converted first into percentage of total responses possible in the experimental period and then into probit units. The resulting regression line was calculated by the method of Finney and is shown in Fig. 1. Analysis of variance shows that there is significant regression. Interestingly, even 5 micromoles/kg, the lowest dose given, differed from saline in its behavioral effects at the 0.01 level of significance.
In the case of psilocybin to psilocin, this saponification is essential for activity, as the phosphate ester is far too polar to get across the blood-brain barrier. But this problem need not exist with the acetate ester. I have explored the 4-hydroxy-DET but I am more familiar with the 4-hydroxy-DIPT. It is of a rather rapid onset implying possible absorption directly from the stomach. However, in a group study with the corresponding ester 4-AcO-DIPT, we felt that it had an even faster onset and perhaps a increased potency. This would suggest that it might be considered an active drug in its own right rather than simply a precursor to the active drug 4-HO-DIPT."
https://www.erowid.org/chemicals/4_acetoxy_det/4_acetoxy_det_article1.shtml
Hmm
this, and the 5-AcO being mentioned as fat soluble (I had not heard about other AcO's, still by not a thing I meant that it is not used by people and very rarely mentioned probably), and Xorkoth plus this quote saying that a 4-AcO tryptamine acts fast goes pretty much against what I thought I knew about the compounds.
I guess sometimes things turn out to be way different than you thought.
And I guess I did misremember the thing about esters and the BBB. It would make sense, a lot of drugs are esterified to enhance pharmacological properties just like heroin is the double acetoxy ester of morphine. But I still thought that was pharmacokinetics stuff and the active wouldn't really mainly be heroin itself. Indeed apparently one of the mono acetoxy esters is the sweet stuff, but I guess it still does pass the BBB first.
There are apparently plenty of esterases in the body - blood, the hydrolyse of the tryptamine esters is assumed by many, but it is still interesting to see if the parent esters are centrally active.
Bufotenine (5-hydroxy-N,N-dimethyltryptamine) has been reported to be behaviorally inactive or only very weakly active in man and animals; this may be a consequence of its low partition coefficient and resultant inabbility to penetrate the blood-brain barrier. The acetyl, propionyl, butyryl, isobutyryl, and pivalyl esters of bufotenine were prepared for future pharmacological evaluation. Unexpectedly, it was found that all of these esters possess a relatively high affinity for the serotonin receptors of the isolated rat stomach fundus preparation. A semiquanititative chromatographic measurement of ester hydrolysis suggests that extensive hydrolysis of the esters to bufotenine does not occur under the conditions of the affinity assay.
Yeah, 4-AcO-DMT lasts 2, 2.5 hours maximum (orally ) for me, and feels like slowed down smoked DMT 100%, while pure 4-HO-DMT lasts for at least 4 hours total. I realize that for a lot of people 4-AcO-DMT lasts substantially longer and is quite mushroom-like, I wish it affected me that way actually, but it doesn't
Why do you maybe not wanna do that again? Was it overly intense, or is there something else 'off' about it?
This could have to do with different batches. A recent batch has tested positive for psilocin.Yeah, 4-AcO-DMT lasts 2, 2.5 hours maximum (orally ) for me, and feels like slowed down smoked DMT 100%, while pure 4-HO-DMT lasts for at least 4 hours total. I realize that for a lot of people 4-AcO-DMT lasts substantially longer and is quite mushroom-like, I wish it affected me that way actually, but it doesn't
That pipe looks fine-
I may be fucked in the head but I only ever smoke DMT from a bong and get fantastic results from it
YMMV.