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The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

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Cook: In a 1ug/ml solution of 25I, for example, there are 2.571821e+19 molecules per ml. It's not an issue on any scale that we will ever be using.
 
Transform said:
Cook: In a 1ug/ml solution of 25I, for example, there are 2.571821e+19 molecules per ml. It's not an issue on any scale that we will ever be using.
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Ok thanks for that, so it seems that any known psychoactive substance can be reliable dosed this way if the calculations and measurements are correct.
 
Can some one explain to me, in very few words, what a ligand is? And yes, I did read the wikipedia page, but it's too advanced.
 
In this context it is a molecule which binds to a receptor and in doing so causes a pharmacological response.
 
A ligand in pharmacology terms is a molecule that binds to a protein. The 3 types of ligands are:

Agonists: activate the proteins function.

Antagonists: blocks the protein function.

Allosteric modulators: Alter the function of the protein by binding somewhere other than the active site.

There are multiple subtypes of each of these but thats the basics of what a ligand is.
 
I have a question or two about exceeding max solubility of a drug in a syringe.

For example, if one were to make a super saturated solution of aqueous morphine sulfate by mixing 200mg morphine so4 into .9ml of water and sucked it up into a 1cc syringe, would all or most of the precipitated out morphine make it into the bloodstream upon pushing down the plunger, or would the crystalline precipitant simply stay in the syringe? I know upon registering, this would introduce blood into the syringe and allow more of the morphine to dissolve, but I'm not sure of the solubility of morphine in blood, and surely the 140+mg of undissolved morphine wouldn't dissolve into the new water/blood solution.

Another question I have regarding this is, would the precipitant morphine still "work" upon entering the bloodstream, and also, would giving the super-saturated mixture a good shake before registering and plunging help to allow more of the precipitant to enter the blood or would it still pool near the bottom of the syringe/in the needle and possibly clog it?

If anyone could shed some light on this for me it would be greatly appreciated.
 
would all or most of the precipitated out morphine make it into the bloodstream upon pushing down the plunger
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yes, it will be a suspension of solid in water. the excess blood volume will dissole the morphine solid (in theory). of course the crystalline matter may clog the needle or do otherwise untoward things, which is why suspensions are not injected...

just get a bigger syringe
 
would the crystalline matter still work if it made it into the bloodstream?

also, if the needle is large enough (27g) is it possible that it wouldn't get clogged?

one other question, if the crystalline matter did make it into the bloodstream, would it do any damage as it's not in an aqueous solution?
 
the majority of it would be active yes (think of the most crude-approach: rubbing crushed pills into a gaping wound. blood is a liquid and more than capable of getting water-soluble compounds from a solid)
(edit: unsure if 'majority', or 'same as if it were fully dissolved'; i'm not seeing the "point of loss", once in the blood there shouldn't be any reason it all dissolves)

re the needle it's possible, it's just a function of particle size, needle gauge, etc etc.

i can imagine there's some potential concerns if it's undissolved (ie, if it needs to become aqueous in the blood(from solid-susp. in your rig), how would you know it was fully-dissolved in blood b4 it was being pumped through your heart? blood is very thick, and you use filters because you certainly don't want solids getting into your bloodstream and being pumped around. If you're depending upon the blood to dissolve a suspended solid, that's obviously very very risky ansd foolish)

mainlining is fun, in large part, because it allows efficiency achieved by removing your body's natural filters. you're talking about approaches where you're removing the accepted standards/safeties of safe-IV'ing. i hope these q's are more theoretical for you, surely you see how dumb it is to play around w/ compounds directly into blood/body w/ liver and other organs processing 1st; removing safeties like filtration or suitable fluid volume (and leaving product undissolved) is foolish at best.
 
Does anyone know anything about 4-acetoxy-tryptamine? has this ever even been made? what about 5-methoxy-tryptamine? Does the book version of tihkal differ a lot from the erowid online resource one? I'd really like to read more about the effects of tryptamines that aren't dialkylated, and tryptamines with an acetoxy group.
 
^ you obviously have very little faith in me if you think I didn't first at least check wikipedia. I was wondering more about the subjective effects of tryptamines that are inactive orally and already are produced by the body, and if 4-aco-tryptamine (acetoxamine?) is something that can actually exist.
 
if 4-aco-tryptamine (acetoxamine?) is something that can actually exist.
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yes. naturally produced? probably not

I think shulgin pretty much established that anything less than a N,N dialkylated tryptamine is basically no fun, maybe N-mono-alkyl substituents would work if they are real bulky - like tert butyl maybe.
 
General Chemistry Discussion

Hey there, I'm looking for some information on predicting receptor binding based on the chemical structure of the molecule.

First of all, is this discussion allowed on Bluelight?
Second, where is the appropriate forum for it?

I've seen a lot of posts talking about the binding affinities of certain chemicals and they said that particular moieties would facilitate binding at certain receptors.
What theory is this based on? Is there a general guideline or is it basically instinct, acquired by working in or studying organic chemistry?
 
I've seen a lot of posts talking about the binding affinities of certain chemicals and they said that particular moieties would facilitate binding at certain receptors.
What theory is this based on?
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Best guesses and logical inferences, usually.
 
This is called a structure activity relationship (SAR) analysis. Unless this is your profession, the best way to go about this is to find all (or a good proportion) of the compounds that bind at a certain receptor, "line them up" in some logical way so that common elements overlap, then compare the differences in structure and look for things like, an acetyl group at the 4 position always made the compound more potent than similar structure with a methyl at that position.

There are whole books filled with theories on how to do this more accurately, but in practice it's never perfect and there will always be surprises.
 
The more I learn about SAR, the more I realise its complete luck. N-Ethyl-Norketamine should have been more potent and longer than Ketamine but otherwise identical. Instead it was shorter, weaker and caused significantly greater nasal damage.
 
Of course, product quality of vendor wares can vary wildly. Was this a verified, and cleaned up sample of N-ethyl-norketamine?
 
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