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

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nuke

nuke

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This is a thread for topics which are not substantial enough to require their own threads due to their nature.

Please ask questions and ADD regulars will try to answer.
 
What is the difference between bk(MDMA) and MDMA?

What does the the Beta ketone do? Does it disassociate when the drug gets metabolized?
 
The beta-keto refers to the ketone carbonyl group on the beta carbon (alpha carbon is the one connected to the nitrogen).

The ketone allows the drug around some laws and also makes the drug a little less lipophilic and gives it a different receptor binding profile compared to MBDB.

The oxygen ketone group (oxygen with a double bond to a carbon that is bonded to two other carbons) does not dissociate but is likely metabolized to an alcohol in the body.
 
What exactly does the "nor" prefix mean? Is it simply a dealkylated version of the original? Does it mean that it always comes off of the amine group?
 
Is it possible to synthetize ω-conotoxin in such a way that it is effective IV, IM or PO? If so, how? If not, why not?
 
Without residue; NOR is short for "nitrogen one rest", German for "no residue at the nitrogen" (or something to that effect, spelling may be off).

Often times its an alkyl functional group...
 
^^^

True but the term is used more loosely now and doesn't always refer to nitrogen (e.g. noribogaine is the O-demethylated derivative). Usually for when a methyl group has been removed, but may be used more generally.

As for ω-conotoxin, it won't be orally active as its a polypeptide and will be broken down by stomach acid, peptidase enzymes etc. It probably is active IM or IV but I imagine administering it peripherally will produce really nasty side effects, and only by selective central administration through intrathecal route can these be minimised and the central analgesic effects maximised. Or it just has really poor blood-brain barrier penetration and so won't get into the brain at all unless injected spinally.
 
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Do the cathinone series, such as bk-mdma and bk-mbdb assert their psychological effects primarily from uptake inhibition rather than monoamine release?
 
mad_scientist said:
As for ω-conotoxin, it won't be orally active as its a polypeptide and will be broken down by stomach acid, peptidase enzymes etc. It probably is active IM or IV but I imagine administering it peripherally will produce really nasty side effects, and only by selective central administration through intrathecal route can these be minimised and the central analgesic effects maximised. Or it just has really poor blood-brain barrier penetration and so won't get into the brain at all unless injected spinally.
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It won't cross the BBB as mere ziconotide, but would it glide right through the BBB if enclosed in a liposome? Then there's still the challenge of getting it to not affect the PNS.
 
Too many doses said:
Why is tryptamine alone not a psychedelic?
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It's metabolised by MAO very rapidly, for one. For two, I don't believe it has enough (any?) 5HT2a affinity. I'm having trouble finding a paper that would even address this.

Interestingly, though, is evidence for tryptamine receptors (not serotonin receptors) in the brain.

J Pharmacol Exp Ther. 1985 Apr;233(1):75-9.
Related Articles, Links
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Relationship between serotonin and tryptamine receptors in the rat stomach fundus.

Cohen ML, Wittenauer LA.

Tryptamine and serotonin (5-HT) are relatively potent contractile agonists in the rat fundus, a tissue in which contraction to 5-HT is not mediated by interaction with 5-HT1 or 5-HT2 receptors. The identification of [3H]tryptamine binding sites in the brain and fundus that show high affinity for certain beta-carbolines raised the possibility that 5-HT and tryptamine may be interacting with a similar receptor that is best described as a tryptaminergic receptor in the fundus. The affinity of five 5-HT receptor antagonists, ketanserin, metergoline, 1-(1-naphthyl)piperazine, LY154930 and LY175041 was similar when 5-HT or tryptamine was the agonist, indicating that 5-HT and tryptamine are interacting with the same receptor in the fundus. Furthermore, maximum contractile response to both 5-HT and tryptamine was reduced to the same extent by the calcium channel blocker, diltiazem, and by the calmodulin inhibitor, trifluoperazine. Inasmuch as diltiazem and trifluoperazine did not similarly inhibit contraction to agents interacting with other receptors (i.e., carbamylcholine), these data are consistent with the contention that 5-HT and tryptamine are interacting with the same receptor in the fundus. Consistent with this conclusion is the observation that affinity of the beta-carbolines, harmaline and harmine was also similar when tryptamine or 5-HT was used as the agonist. However, affinity of the beta-carbolines for the tryptamine/5-HT receptor in the fundus was dramatically lower than reported for [3H]tryptamine binding sites in brain membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
 
What are some readily obtainable substances which can produce death quickly, painlessly, and reliably?

Difficulty: No helium, carbon monoxide, nitrogen, nitrous oxide, or other inert gas.

P.S. I recently discovered that the handgun that I was planning to use if ever my hope should be exhausted was locked up. The cathartic feeling of safety and control that it produced to know that I could use that gun to kill myself is now gone and I'm feeling claustrophobic. I don't plan on killing myself right now, I just want these feelings of fear and worry over what travails the future has in store for me to abate; there's nothing worse than being trapped / cornered / helpless / stuck between a rock and a hard place.
 
I'm pretty sure questions about how to better kill yourself aren't allowed by the BLUA.
 
nuke said:
I'm pretty sure questions about how to better kill yourself aren't allowed by the BLUA.
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Isn't such advice subsumed under "harm reduction"? Because a person intent on killing himself will try, regardless of how good or bad his methods are. If a person goes about it in the wrong way, he may simply end up paralyzed or brain-damaged or something. By providing this information, you'd be reducing the likelihood of such eventualities, and I needn't tell you that that is a good thing.

Moreover, from a moral perspective, to force a person to live (either actively or passively by omitting to provide information that could be used to end one's life) who wished to die is to do no better than to force someone to die who wished to live (i.e. murder).

If this is about warranting the site owners and members against legal trouble, then fine, but if this policy's purpose is to uphold morality, then I see no issue here.

And, as I say, this is more about creating a feeling of comfort and control for me than it is about actually killing myself. I still have a number of options I am considering and only when/if those options are exhausted fruitlessly will I begin to more seriously contemplate suicide. When the time comes for me to kill myself, I'll do it at all costs, so you may as well grant my request: better that I make use of a lower-risk method of suicide than higher-risk.

/I'm truly very sorry to steer the topic of conversation to my personal problems yet again, but this site is really one of the very few places I have to turn to. I can't afford professional help anymore, and even if I could it would be pointless; I have tried 8 or more psychiatrists and psychopharmacologists in the past, each of whom has made things worse for me either by prescribing something that made me feel worse or by refusing to prescribe what I wanted whilst failing to refuse to take payment (which in my mind is fair if you're, you know, not actually providing a service).
 
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