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Cocaethylene

Pharcyde

Pharcyde

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A simple question!

Anyhow I decided to post this simple question in ADD because you all seem to be smart than the average drug user.

So if I consume cocaine and alcohol simultaniously, will the alcohol content of the drink make this dangerous substance even more dangerous.

Say I do blow and drink 80proof whiskey
compared to
Doing blow and drinking 151+ alcohol
 
The more alcohol you consume, the more of it will be converted into acetaldehyde which in turn creates more cocaethylene in your body. It doesn't make a different if you do three 50 proof shots or one 150 proof shot, the only difference is in the total amount of alcohol consumed. I'll note that there's probably a lot more acetaldehyde occuring later on 1-2 hours after you start drinking because the body needs time to start producing large amounts of it from the ethanol (the metabolic process is rate-limiting if I recall correctly).
 
You have to remember that cocaethylene will be more difficult for your liver to break down, leaving you amped up longer. The answer to the question of mixing alcohol with cocaine lies in whether you're more worried about a slight increase in liver toxicity or doing your coke too quickly.
 
nuke said:
I'll note that there's probably a lot more acetaldehyde occuring later on 1-2 hours after you start drinking because the body needs time to start producing large amounts of it from the ethanol (the metabolic process is rate-limiting if I recall correctly).
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I can vouch for this. I had been slamming a couple beers RIGHT before doing up the blow, and the difference wasn't noticeable until later. So, tonight, I downed more than a few beers at the bar for a couple hours, came home, and started blowing lines. Tonight's off to a great start.
 
Oh - please don't shoot coke or smoke crack if you've been drinking. There will be some pretty badass cardiotoxicity. Cocaethylene is more cardiotoxic because of it's greater anaesthetic effect.
 
MattPsy said:
Oh - please don't shoot coke or smoke crack if you've been drinking. There will be some pretty badass cardiotoxicity. Cocaethylene is more cardiotoxic because of it's greater anaesthetic effect.
Click to expand...

what is the ratio there? as well ratio of potency as a stim to C? if all is more or less equal as both are increased in accord than it is just ....more so to speak...

this was what i wanted to know regarding Dimethocaine as we know it is about 1/6 the potency of C, but what is its relative anaesthetic effect to C?

anyone?
 
Well, I'm sure it's not good for you, but plenty of people have drank with their coke and turned out OK so you'll probably be alright. Not saying I recommend it, in fact, I recommend against it, but people will do what they want to do and who am I to judge?
 
LuxEtVeritas: Well no it's just a correlation, not a causation. For example CFT works like cocaine does but it doesn't have the anaesthetic effect that cocaine does as I understand it.
So while cocaethylene might well be more potent than cocaine, and be a stronger anaesthetic too, I don't think the two are necessarily connected.
 
^^^The anesthetic effects of cocaine and its derivatives arise from sodium channel blockade, whereas the recreational effects are caused by antagonism of monoamine transporters. The pharmacophores involved in binding to the two different proteins are almost certainly not identical, so that in itself could explain differences in the relative strength of the effects between different drugs in that family.
 
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Yeah - the major difference between CFT (or CPT, if we want a even closer comparison) and cocaine is of course the loss of the ester link between the aromatic ring and the tropane nucleus.
So that ester link is almost certainly the part of the structure we need to be concerned with.
The DAT+NET+SERT inhibition that cause the recreational effects we want arises from the other structural features.

Anyway I reckon dimethocaine is not a safe drug to use recreationally because of it's significant Na-channel blockade effects. Cocaine does the same as you say but AFAIK the ratio of recreational:anaesthetic effects is much higher (so it's more of a recreational drug than an anaesthetic), whereas dimethocaine has a much lower ratio (so it's more of a anaesthetic than a recreational drug).

I do wonder whether it's possible to modify the structure of dimethocaine to intentionally ruin the Na-channel blockade, but I know nothing of the binding motifs needed to do that, and especially not when you have to avoid ruining the monoamine transporter activity too when you're modifying it!
 
dont do too much cocaine and alcohol together.
Save some good coke for the weekend and then do it but do more coke than alcohol... that is, just have 2 shots of vodka, or 2 to 5 beers... but not too often.
Excercise a lot and be health xD8(
 
Does dimethocaine transesterify similarly to cocaine in vivo to take that ethyl substitution? Is what one is sold as dimethocaine actually dimethocaine?

ebola
 
I would imagine that the ester in dimethocaine would be way more stable than the methyl ester in cocaine.
 
Given the fact it's a bulky PABA ester, I don't think that DMC is torn apart that easily. To my knoledge the methyl ester on cocaine is the one that is attacked easily.

If it did transesterify, you'd be getting benzocaine it looks like.
 
^ Yes and no. Given the extremely rapid metabolism of procaine, I believe that the ester linkage of dimethocaine is easily attacked by the relatively non-specific pseudocholinesterase enzymes which are abundant in plasma. I don't know if the pharmacokinetics of dimethocaine have been investigated yet, but I'd be very surprised if it's not extensively metabolised to PABA in a manner similar to procaine (but probably at a lower rate).

However, transesterification with ethanol, as seen with cocaine to cocaethylene and methylphenidate to ethylphenidate, is mediated in humans by the enzyme hCE-1, which is expressed primarily in the liver. hCE-1 is selective towards substrates having a large acyl moiety and a small alkyl moiety (Imai, Drug Metab Pharmacokinet 21(3), 2006). This would make dimethocaine a poor hCE-1 substrate, in contrast to cocaine and methylphenidate, and with (presumably) extensive metabolism in other tissues and blood, I wouldn't expect to see any significant transesterification of dimethocaine to benzocaine.

In individuals with a (hereditary) pseudocholinesterase deficiency, increased hepatic metabolism by hCE-1 and -2 might possibly lead to a higher rate of transesterification. Of course, those individuals should stay the fuck away from dimethocaine in the first place.
 
There is considerably more steric "bulk" around the ester group on DMC compared to procaine but I suspect you are right in that it is primarily metabolized to PABA without transesterification.
 
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