• N&PD Moderators: Skorpio | thegreenhand

  • Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread

Status
Not open for further replies.
I tried this earlier this year with suboxone and created a solution 2mg buprenorphine to 2ml sterile water and it worked fine after a couple of weeks, suggesting that there wasn't much decomposition. Naloxone is highly soluble in water but as bupe has a much higher affinity it's not worth thinking about.
 
Is N N dimethyllysergamide psychedelic when injected. Does this thing work like tryptamines. Are there any reports.
 
i are spectre said:
will it decompose in water? i've made a nasal spray, just wondering if it's stable or not.
Click to expand...

Yes, it is stable. I have made a buprenorphine solution and used it over the course of a month. This is why Buprenex is not a dry ampule like diamorphine ampules in the UK are.
 
the guy that started the now closed thread on putting 25i-NBOMe on blotter creeps me out
 
melange said:
from what I understand, all of the para halogenated amphetamines are neurotoxic
Click to expand...

No, they're certainly not all neurotoxic; it seems that only the bare para-halo-amp's are (excluding 4-FA, again) neurotoxic, and that the halogenated amphetamines DOI, DOC, DOB, and the like are not neurotoxic. It could be that because they are so potent they're never taken in doses that would have a substantial effect on monoamine transport and release, but I don't know for certain if that is the case.

While 4-FA and perhaps 4-fluoro-methcathinone are not neurotoxic, I wouldn't consider them safe. fluoro is not the same as trifluoromethyl, obviously, but I would worry about 5HT2b agonism.

Actually, all of those morons taking huge doses of mephedrone for days at a time should be incredibly concerned about potential 5HT2b agonism. There are bad things- panic attacks, depression- and then there are bad things like cardiac arrest.
 
Hammilton said:
No, they're certainly not all neurotoxic; it seems that only the bare para-halo-amp's are (excluding 4-FA, again) neurotoxic, and that the halogenated amphetamines DOI, DOC, DOB, and the like are not neurotoxic. It could be that because they are so potent they're never taken in doses that would have a substantial effect on monoamine transport and release, but I don't know for certain if that is the case.

While 4-FA and perhaps 4-fluoro-methcathinone are not neurotoxic, I wouldn't consider them safe. fluoro is not the same as trifluoromethyl, obviously, but I would worry about 5HT2b agonism.

Actually, all of those morons taking huge doses of mephedrone for days at a time should be incredibly concerned about potential 5HT2b agonism. There are bad things- panic attacks, depression- and then there are bad things like cardiac arrest.
Click to expand...


I see


and agreed with the 5HT2b agonism topic

scary stuff there

there is a reason I quit taking daily 5-htp a long time ago
 
would people assume Flephedrone has more side effects than mephedrone?
Click to expand...

Yes, but it's likely that they would be mistaken.
4-fluoro-amphetamine has been demonstrated non-neurotoxic, in the same way that bk-mdma was demonstrated non-neurotoxic, in contrast to mdma, the latter cast as mildly neurotoxic. White 4-methyl-amphetamine has not been as rigorously studied for such activity, anecdotes suggest that it leaves inordinately long-lasting mental effects.

As for cardiovascular side-effects, there is no clear evidence that 4-fluoro-ephedrine would be much better or worse than 4-methyl-ephedrine.

ebola
 
I have some sort of silly questions again:
Is it possible to produce benzodifuran analogs of DOM / DOI / DOC etc?
And is it possible to apply similar techniques to tryptamine?
Maybe NBOMe-tryptamines or benzodifuran-tryptamines?

PS I hear that syntesis of FLY analogs is the most expensive, is it true?
 
Lombergerh said:
Is it possible to produce benzodifuran analogs of DOM / DOI / DOC etc?
Click to expand...

Yes; I'm pretty sure Iodo-dragonFLY has been studied, or a similar relative.

Lombergerh said:
And is it possible to apply similar techniques to tryptamine?
Maybe NBOMe-tryptamines or benzodifuran-tryptamines?
Click to expand...

Benzodifuran wouldn't work on tryptamines, unless you change it from a indole to a benzodifuran body by replacing the nitrogen with an oxygen. However this replacement of nitrogen with oxygen leads to less effective activity at the 5-HT2A site. You could add a furan ring to a tryptamine psychedelic however tryptamines and phenethylamines do not dock the same way thus there is no promise of it playing out as effectively. N-benzyl series could be applied to tryptamines though again considering they do not dock the same way there is no certainty of it being an improvement. I can't recall if this has been done before.
 
IIRC it has but produces only minor improvements, unlike the 200x improvement seen with 2C-C
 
modafinil

i read alot of article about modafinil and i found if we replace amine group with n-aryl, the activity of drug change to sedative(like piperidine), do you know why, and have you ever seen a compound to ignore this comment?
 
synthesis of modafinil

do you know what is the difference between the activity of modafinil and the same compound without the oxidizing sulfor? i want to found how much this functional group are important in cns activity of drug, because the oxidizing sulfor need a difficult sittuation like the degree under 20 to prevent make sulfon.
 
arez00 said:
i read alot of article about modafinil and i found if we replace amine group with n-aryl, the activity of drug change to sedative(like piperidine), do you know why, and have you ever seen a compound to ignore this comment?
Click to expand...
There is no amine in modafinil, but only an amide.
And the reason why replacement of the amide moiety -C(O)NH2 with -C(O)N(CH2)5 (i.e. piperidine) leads to sedative derivatives (as reported in EP 0097071 A1 or Bioorg Med Chem 2008, 16, p.9904) is not known to my best knowledge, at least not in the peer-review literature.
And by the way, the mechanism by which modafinil reaches its biological effects is currently not known with certainty at all. Much speculation here, but hardly any viable SAR to play with.

arez00 said:
do you know what is the difference between the activity of modafinil and the same compound without the oxidizing sulfor? i want to found how much this functional group are important in cns activity of drug, because the oxidizing sulfor need a difficult sittuation like the degree under 20 to prevent make sulfon.
Click to expand...
The last part I didn't understand completely...

The sulfone-analog of modafinil was shown to have almost the same activity like modafinil itself, shown with mice in a maximum electroshock assay (Bioorg Med Chem 2004, 29, p.1481). Don't know how this one translates into stimulating activity in humans though, but I'd be really careful with preliminary conclusions. Toxicity was in the very same range, too, like modafinil.


Peace! - Murphy
 
Last edited:
As in low toxicity right? Or I'd better do my modafinil homework again. I do like the stuff, for its non-addictive properties (at least found by me) and that it doesn't really stimulate but achieves unparalleled wakefulness nonetheless. And still, it's not a disaster when you try to sleep.

About the similarity with sedative compounds, might this have something to do with the possibility of paradoxical effects that modafinil can have i.e. some people have to run for their beds after taking it! And one time I got mega drowsy from it as well.
 
Alpha-hydroxymethylphenethanamine and N-methyl-alpha-hydroxymethylphenethanamine are commercially available, but are they psychoactive?

My guess is that they are both stimulants with a shorter duration of action than their amphetamine analogues, as the hydroxymethyl group would be metabollized to the carboxylic acid rather quickly. And since each has only one -OH group per molecule, they should both pass the blood brain barrier rather easily.
 
About that last question: it depends on the absorption but anything that gets absorbed subligually or buccally or whatever follows a parenteral route and should therefore potentiate your dose compared to oral administration, but that completely depends on the bioavailability though these different RoAs.

AFAIK alpha-(de)methylation is not done very easily?
 
Last edited:
The PiHKAL synthesis for DOI and 2C-I start with 2,5-DMA (2,5-Dimethoxyamphetamine)and 2C-H (2,5-Dimethoxyphenethylamine).

So I would assume that it would be pretty hard to do.
 
Status
Not open for further replies.
Top