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N-benzyl phens may not be as selective as we once believed.

P.S Some people report the NBOMes as being much worse for things like HPPD, visual artifacts, etc. Could at least that be blamed on the high affinities or should they just look more closely at their own drug usage?

I'll provide some anecdotal evidence of my own: I definitely noticed more visual artifacts after abuse of 25C, 25I, 2C-E, 2C-T-2, and 2C-I. The nbomes definitely did it to a greater extent than the 2C's. I still use 2C's somewhat often but I have limited my usage and my visual static is starting to become less noticeable. It got to a point before where when I was on certain drugs (like suboxone) it would bring it back and make rooms look so goddamn blurry with random color splotches and dots (not nearly as cool as it sounds, its like gray rainbow puke static). It's not as 'there' as I make it sound to be though, you can still see where everything is at it just kind of looked confusing for a few moments.

and it would make looking for small objects in a messy room a real pain in the ass.
 
@Psoood...I'm not sure how Br-Dfly got labeled as 5-HT2 selective. AFAIK, it hasn't been screened against any other receptors. Please enlighten me if you know otherwise.

With the NBOMe series, seizures seem to be the most common manifestation of toxicity...I could see this attributed to a 5-HT2A agonist with high intrinsic activity (though this is just a guess). This could also account for higher incidence of HPPD-like visual artifacts (now I'm just plain making stuff up).
 
Yeah bloodshed, I had the same effects as you I think but out of the blue they disappeared (when they disappeared I was using more psychs, including NBOMe, than before). I was asking for a friend of mine though, who now blames a whole bunch of shit on the NBOMes, but still abuses MDMA quite a bit. I believe the visual stuff he has has more relation to his MDMA usage than anything else. But yeah, you can't tell someone his god is doing bad things to him. (<-Heh, that came off way bitter but I was writing it in good spirits)
 
Yeah bloodshed, I had the same effects as you I think but out of the blue they disappeared (when they disappeared I was using more psychs, including NBOMe, than before). I was asking for a friend of mine though, who now blames a whole bunch of shit on the NBOMes, but still abuses MDMA quite a bit. I believe the visual stuff he has has more relation to his MDMA usage than anything else. But yeah, you can't tell someone his god is doing bad things to him. (<-Heh, that came off way bitter but I was writing it in good spirits)

In your friend's case I believe the nbomes may have contributed to the visuals, but I think not taking a break from MDMA is stopping them from clearing up. Of course that's all bullshit that I have a 'feeling' on. It doesn't really mean anything.
 
@Psoood...I'm not sure how Br-Dfly got labeled as 5-HT2 selective. AFAIK, it hasn't been screened against any other receptors. Please enlighten me if you know otherwise.

With the NBOMe series, seizures seem to be the most common manifestation of toxicity...I could see this attributed to a 5-HT2A agonist with high intrinsic activity (though this is just a guess). This could also account for higher incidence of HPPD-like visual artifacts (now I'm just plain making stuff up).
These are the two studies cited for the claim, but I have no full text access and there's no claim about 5-HT2 selectivity in the abstracts.
http://www.ncbi.nlm.nih.gov/pubmed/21592070?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/9857084

The quote from wiki (yeah, I know, but no full text) is:
Bromo-DragonFLY also has a high binding affinity for the 5-HT2B and 5-HT2C serotonin receptors, and is most accurately described as a non-subtype selective 5-HT2 agonist, as it is actually twice as potent an agonist for 5-HT2C receptors as for 5-HT2A, as well as being less than 5x selective for 5-HT2A over 5-HT2B.[4][5]
It seems like an odd thing to add in for the hell of it but who knows maybe some random editor had a pet theory.

Seizures were also reported in the DOB-Dragonfly overdose cases. It would be helpful to have access to medical reports of the NBOMe deaths to see if there were similar signs of severe vasoconstriction. I asked anybody who has journal access in ADD if they knew of such reports a few days ago to attempt to find any signs that both may be killing in similar ways but so far no response.

Edit: tried search for "non-subtype selective" along with quotes from each of those studies' abstracts in Google Scholar and didn't get any evidence they claim that in the results.

Edit 2: probably a wiki person talking shit then:
Bromo-Dragonfly is a non-selective 5-HT2 receptor agonist with particularly high affinity for the 5-HT2C receptor subtype, though its psychedelic properties are likely attributable to activity at the 5-HT2A receptor subtype. While studies have been performed in rodents, little to no analysis has been recorded in humans. Some evidence supports vasoconstrictive properties, caused by prolonged stimulation of peripheral alpha1 adrenergic receptors [5]. Likely contributing to vasoconstrictive properties is the compounds non-specific, and highly potent, affinity for serotonergic 5-HT2 receptors.
 
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These are the two studies cited for the claim, but I have no full text access and there's no claim about 5-HT2 selectivity in the abstracts.
http://www.ncbi.nlm.nih.gov/pubmed/21592070?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/9857084

Parker et al (1998), the second of those refs, gives the following affinities for Br-DFLY:


5HT2A - 0.04
5HT2B - 0.19
5HT2C - 0.02

(-)DOI in the same paper interestingly is given as:

5HT2A - 0.46
5HT2B - 42.7
5HT2C - 1.82

So Br-DFLY is less selective than (-)DOI.
 
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Nattering voice in my head: which cmpds are fullagonists at 5ht2a and which are only partial agonists?
 
^Good question...IIRC, the phenylalkylamines (e.g. DOI, DOB, DOM), Br-Dragonfly, and the 25x-NBOMe drugs are all close to full agonists. I think the phenethylamines, tryptamines, and LSD are generally weaker partial agonists, though I'd have to double check on that.
 
^Good question...IIRC, the phenylalkylamines (e.g. DOI, DOB, DOM), Br-Dragonfly, and the 25x-NBOMe drugs are all close to full agonists. I think the phenethylamines, tryptamines, and LSD are generally weaker partial agonists, though I'd have to double check on that.

Well, are we talking agonism to the PI or AA pathway?

PI hydrolysis NBOMEs are all roughly 85-90% intrinsic activity, DOI/DOB are 30-80% (depending whose results you read) mescaline either 85% or 30%, LSD 22%, psilocin 46%, 2C-x 10-30%.
 
^Generally PI, though some papers do both.

From wiki DOB entry: DOB is one of the most potent compounds in PiHKAL; while the active dose is similar to that of DOI, another psychedelic amphetamine, DOB has been shown to have a higher efficacy in triggering downstream effects mediated by 5-HT2 receptors,[2] making it likely to be slightly more dangerous than DOI in overdose, due to greater vasoconstrictive action. Omission of the amphetamine related α-methyl leads to 2C-B, a vastly safer compound that possesses a lower affinity for the 5-HT2A receptor and is a weaker receptor agonist.

Seems to be someone's pet theory...not a bad one, but vasoconstriction is not mentioned in the paper referenced. And, interestingly, some papers don't seem to find the same difference between DOB and DOI.[/B]

Intrinsic_activity.png


Jason C. Parrish, Michael R. Braden, Emily Gundy and David E. Nichols. Differential phospholipase C activation by phenylalkylamine serotonin 5-HT2A receptor agonists. Journal of Neurochemistry, 2005, 95, 1575–1584.

NBOMe_activity.png


Michael R. Braden, Jason C. Parrish, John C. Naylor, and David E. Nichols. Molecular Interaction of Serotonin 5-HT2A Receptor Residues Phe339(6.51) and Phe340(6.52) with Superpotent N-Benzyl Phenethylamine Agonists. Mol Pharmacol 70:1956–1964, 200.
 
I must be the only one that has no vasoconstrictive problems on any of the nbomes or DOC. 25i-nbome is one of the easiest on my body of any of the psychs. I just wonder if these medical problems and death are not just a simple case of over dose and people not knowing how much they are taking because of wrong measurements. Have any of these medical cases been from taking blotters or are they all from handling powders and/ or liquids?

Its very easy to accidentally take 6-7mg's of this nbome. Thats near 10X above a normal strong dose. Imagine taking 2,000mg of MDMA all at once instead of 200mg. Its harder to make that mistake with MDMA because of the higher dose range. Many normally (relatively) safe substances could be life threatening if you take 5-10x the normal recommended dose.
 
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I must be the only one that has no vasoconstrictive problems on any of the nbomes or DOC. 25i-nbome is one of the easiest on my body of any of the psychs. I just wonder if these medical problems and death are not just a simple case of over dose and people not knowing how much they are taking because of wrong measurements. Have any of these medical cases been from taking blotters or are they all from handling powders and/ or liquids?

Its very easy to accidentally take 6-7mg's of this nbome. Thats near 10X above a normal strong dose. Imagine taking 2,000mg of MDMA all at once instead of 200mg. Its harder to make that mistake with MDMA because of the higher dose range. Many normally (relatively) safe substances could be life threatening if you take 5-10x the normal recommended dose.

You are making the classic mistake of assuming that everyone has a body like yours, and that all factors can be externalized. They cannot, we have stories about people having severe difficulties at low doses - I do not believe that distrusting that these people knew that the doses were that low is a proper approach.
There are some drugs that are tolerated much more widely and predictably than other drugs, you need to understand that. The chemical is still the same and this goes beyond things like ROA. How could liquid be that much different than blotter or powder carrier? Basing ideas or approaches on the more predictable compounds is ignorant to the unpredictable ones.
 
You are making the classic mistake of assuming that everyone has a body like yours, and that all factors can be externalized. They cannot, we have stories about people having severe difficulties at low doses - I do not believe that distrusting that these people knew that the doses were that low is a proper approach.
There are some drugs that are tolerated much more widely and predictably than other drugs, you need to understand that. The chemical is still the same and this goes beyond things like ROA. How could liquid be that much different than blotter or powder carrier? Basing ideas or approaches on the more predictable compounds is ignorant to the unpredictable ones.


Agreed. Clearly NBOMe are kinda hard on the system and are not meant to be treated as casually as LSD and mushrooms. Personal Health, diet ect ect could all play a large role with these pheny deriviative.


As I have always said the 500 ug dose I took as a alergy test had more noticable vasco constriction then my 1mg experience, but it was not so much about my personal sweet spot as it was about the amount of magnesium and potassium I had in my diet, along with Icarin, which I take as a daily supplement. Icarin and Magnesium probably have the most to do with easing vascoconstricition. Still though, Since discovering this in November I have only done this a grand total of 3mg spread out over 3 trips. ANd currently I don't have any real plans to be able to do this again soon. Summer would be ideal, but it also a very busy time for me.


I am really interested in exploring the 4-HO substituted tritamines as an option. From what I have read they seem to be just as interesting with the same erotic/euphoric potential as NBOMe's. Plus it doesn't hurt that they don't last quite as long.


I think NBOMe's have a place in the world of psychadelics, but in an advanced adult tripper sense. When I was yonger I would be more tempted to push this drug further then I am willing to as a 37 year old.
 
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I am really interested in exploring the 4-substituted tryptamines as an option. From what I have read, they seem to be just as interesting, with the same erotic/euphoric potential as NBOMe's.

The 4-sub tryptamines are *much* nicer than the NBOMe's. Some are more erotic, some are more euphoric, and in my experience, all of them are more "magical" and rewarding. They are far safer as well.
 
You are making the classic mistake of assuming that everyone has a body like yours, and that all factors can be externalized. They cannot, we have stories about people having severe difficulties at low doses - I do not believe that distrusting that these people knew that the doses were that low is a proper approach.
There are some drugs that are tolerated much more widely and predictably than other drugs, you need to understand that. The chemical is still the same and this goes beyond things like ROA. How could liquid be that much different than blotter or powder carrier? Basing ideas or approaches on the more predictable compounds is ignorant to the unpredictable ones.

I understand what you are saying. I personally have less faith that people are dosing themselves properly and also the point about liquid and powder is I have a feeling that someone might be making their own liquid dose and not calculate the ratio correctly or not measuring correctly with powder and dosing by drops is known not to be the most accurate. Its not about the ROA its about the likelyness of making an error using different ROA.

My opinions are mostly anecdotal but using reasoning and logic I am curious why none of these medical emergencies have come from someone using blotters.
 
^Generally PI, though some papers do both.

From wiki DOB entry: DOB is one of the most potent compounds in PiHKAL; while the active dose is similar to that of DOI, another psychedelic amphetamine, DOB has been shown to have a higher efficacy in triggering downstream effects mediated by 5-HT2 receptors,[2] making it likely to be slightly more dangerous than DOI in overdose, due to greater vasoconstrictive action. Omission of the amphetamine related α-methyl leads to 2C-B, a vastly safer compound that possesses a lower affinity for the 5-HT2A receptor and is a weaker receptor agonist.

Seems to be someone's pet theory...not a bad one, but vasoconstriction is not mentioned in the paper referenced. And, interestingly, some papers don't seem to find the same difference between DOB and DOI.[/B]

Intrinsic_activity.png


Jason C. Parrish, Michael R. Braden, Emily Gundy and David E. Nichols. Differential phospholipase C activation by phenylalkylamine serotonin 5-HT2A receptor agonists. Journal of Neurochemistry, 2005, 95, 1575–1584.

NBOMe_activity.png


Michael R. Braden, Jason C. Parrish, John C. Naylor, and David E. Nichols. Molecular Interaction of Serotonin 5-HT2A Receptor Residues Phe339(6.51) and Phe340(6.52) with Superpotent N-Benzyl Phenethylamine Agonists. Mol Pharmacol 70:1956–1964, 200.

It looks like DOI-nBOMe might be a winner: its binding affinity is a great deal weaker than 25i-nBOMe's, but maybe that means that it'll be active at levels people can actually measure. Its partial agonism should improve safety.

ebola
 
rushdafunk said:
I must be the only one that has no vasoconstrictive problems on any of the nbomes or DOC. 25i-nbome is one of the easiest on my body of any of the psychs.

No, I fare fine on them too. I think that it's more that people tend not to report non-complaints as often as they do adverse effects.

weedazoid said:
As I have always said the 500 ug dose I took as a alergy test

Why did you take a known active dose as an allergy test?


laman said:
The 4-sub tryptamines are *much* nicer than the NBOMe's.

They have rather distinct effects, and responses vary a lot.

ebola
 
The first post in this thread shows a table of affinities and interestingly 25I NBOH and 25B NBOME have very high 5-HT2c affinities, which should result in anti-euphoria and general ill feelings. Haven't tried either of them myself. Regarding 5-HT2b causing heart valve problems, Shulgin had to have an operation for a heart valve problem and he's known for taking lots of X and other psychs. No way to know if there's any connection but it does seem a little curious.
 
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