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

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    The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread 
    #1
    Flask
    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.
     

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    acronyms! 
    #2
    what's a TRI? somekind of reuptake inhibitor?
     

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    #3
    A triple reuptake inhibitor or SNDRI.
     

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    #4
    ah, thanks.
     

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    #5
    What is the difference between bk(MDMA) and MDMA?

    What does the the Beta ketone do? Does it disassociate when the drug gets metabolized?
     

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    #6
    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.
     

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    #7
    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?
     

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    #8
    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?
     

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    #9
    Bluelight Crew negrogesic's Avatar
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    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...
     

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    #10
    ^^^

    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.
    Last edited by mad_scientist; 19-04-2009 at 03:42.
     

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    #11
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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?
     

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    #12
    Quote Originally Posted by mad_scientist View Post
    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.
    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.
     

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    #13
    Bluelight Crew Too many doses's Avatar
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    Why is tryptamine alone not a psychedelic?
     

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    #14
    Bluelight Crew negrogesic's Avatar
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    Quote Originally Posted by TheLastAxon View Post
    Do the cathinone series, such as bk-mdma and bk-mbdb assert their psychological effects primarily from uptake inhibition rather than monoamine release?
    Cathinones can also be release agents...
     

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    #15
    Quote Originally Posted by Too many doses View Post
    Why is tryptamine alone not a psychedelic?
    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.
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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)
     

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    #16
    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.
     

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    #17
    I'm pretty sure questions about how to better kill yourself aren't allowed by the BLUA.
     

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    #18
    Bluelight Crew Too many doses's Avatar
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    Thanks hammilton .
     

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    #19
    Tryptamine appears to be somewhat active,read the reference in TIHKAL!

    http://www.erowid.org/library/books_...tihkal53.shtml
     

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    #20
    Quote Originally Posted by nuke View Post
    I'm pretty sure questions about how to better kill yourself aren't allowed by the BLUA.
    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).
    Last edited by shibireru; 21-04-2009 at 12:17.
     

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    #21
    If the end result is death, I fail to see how helping someone do it 'better' is harm reduction.

    I mean, by the same logic, you could say that you're planning to murder a bunch of people and ask for the way that is the quickest and least painful and consider it harm reduction.
     

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    #22
    Of course it is! Death is, perhaps, the most harmful thing that can happen to somebody, but it is still possible to reduce the harm caused by it. And couldn't euthanasia be considered harm reduction?
     

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    #23
    Not according to the BLUA.
     

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    #24
    Going back to the tryptamine question, I noticed that Shulgin said this later on in the tryptamine entry about tryptophan:

    Tryptophan, a natural and nutritionally essential amino-acid, is a centrally active intoxicant and sleep-provider in man. It is converted metabolically to tryptamine which is a little bit psychedelic. When administered with methionine (another amino-acid known to methylate things) it produces methylated tryptamines, the two best studied being N-methyltryptamine (NMT) and N,N-dimethyltryptamine (DMT).
    Is he saying that tryptophan + methionine = methylated tryptamines in vivo? Does anyone know if there is any scientific articles about this, or if he's just guessing, or extrapolating from in vitro?

    This also seems to contradict what he says just before it:
    (with 15 g, orally, with 150 mg iproniazid) "This was a daily treatment given to schizophrenic patients, tryptophan along with an antidepressant which is a monoamine oxidase inhibitor. Most showed marked changes such as an elevation in mood, an increased involvement with other people in their ward, and an increased extrovertism. A separate study of this combination with the addition of the amino acid l-methionine produced in about half of these patients a toxic or delirioid state."
    Anyone have more information about this?
     

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    #25
    Quote Originally Posted by nuke View Post
    Not according to the BLUA.
    Sorry. It's just that... where else is one to go to obtain this information? The only forum on the internet that I can think of that allows this sort of discussion is alt.suicide.methods, but those people know next to nothing about pharmacology. Besides that, because they are all very depressed - notwithstanding the numerous trolls - they are phlegmatic and perfunctory participators; even if they actually had some valuable information to share, it'd be pretty hard to provoke the conative portion of their psyches into activity of such a degree that they'd feel any compulsion at all to toss their hands lackadaisically at the keyboard until some travesty of what they had intended to type appeared on the screen.

    tl;dr: I must turn to people with a good understanding of pharmacology who have enough energy to respond to my question. In my mind, that means bluelighters. I can think of no other more appropriate place for this question. Curse you, BLUA!
     

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