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benzocaine - silly question

impulsive_state

Bluelighter
Joined
Feb 12, 2001
Messages
3,986
its it possible to get high on benzocaine? i came accross this in my throat lozenge and just wondered?
 
sure.. crush up those throat lozenes and snort a BIG BIG line of it. after the immense pain subsides, youll have a numb nose :)
 
Cocaine is the only local anestetic in its group to have recreational value.
 
You read "A Scanner Darkly", didn't you? :)
In the book some dude claims he can make cocaine from benzocaine, at least I think it was benzocaine. Can it be done?
Beats my ass.
 
what if you took the benzocaine containing substance (like abesol) and squirted it all over a plate and cooked it down to a powder and snorted it? the effects would be a numbing effect like cocaine!
oooooohh, it's like a whole new world of possibilities!!!
you could smoke a bud soaked in benzocaine and dried as well!
 
hahaha, next project = making LSD from morning glory seeds, lol :)
 
Well, okay... here's the chemical structures of the 2 chemicals:
Benzocaine
Cocaine
Now, with anything in chemistry, as long as you don't violate any laws (thermodynamic, quantum, etc.), you can in theory make something from anything. It could be that we don't know how yet, or that it's quite a contrived reaction that is all but impossible.
But, I guess, it you can cleave off the NH2 off of the benzene ring, then attach all of the crap on the other side, it probably COULD be done. But, it's probably not worth it.
 
[EDIT - you should NEVER HAVE POSTED IT IN THE FIRST PLACE.... if it was up to me you'd get a 5-day suspension for it but I will let it slide...]
[ 10 August 2002: Message edited by: PhreeX ]
 
There are no "caines" used pharmaceutically that are chemically related to cocaine.
I am not entirely sure, but it's my understanding that "caine" is just used to describe numbing agents.
If you try to abuse benzocaine, you will simply go numb. There are no pharmaceutical caines that will get you high.
 
De-mystifying the 'caines' ...
All the 'caines' are all local anaesthetic agents - or more specifically - fast sodium channel blockers.
They can be divided into amino-esters and amino-amides.
The amino-esters include:
(i) Benzoic Acid derivatives
eg. cocaine, amylocaine
(ii) Para-amino Benzoic Acid derivatives
eg. Procaine, amethocaine, oxybuprocaine, chloroprocaine, and benzocaine.
The amino-amides include the majority of the more clinically useful ones; eg lignocaine, bupivacaine, prilocaine, ropivacaine, mepivacaine and etidocaine.
So in fact they all have a chemical structure similar enough to each other to enable their action on the internal aspect of the fast sodium channel and prevent neural depolarisation.
Cocaine is unique in that it also inhibits noradrenaline and dopamine reuptake - and wa-la: the intense euphoria. (The euphoria afforded by the other agents does occur - but it differs from that of cocaine in that:
a) not reinforced pharmacologically by dopamine (and to a lesser extent, noradrenaline).
b) the dose of agent required for the euphoria is so close to the seizure and cardiovascular collapse threshold - that it has such an incredibly low margin of safety.
c) the euphoria is about 1000 times less than that associated with cocaine, and hence by the time there is any detectable - you are likely to be well over the LD50.
eg. Consider plasma concentrations required to produced the effects:
Bupivacaine: 2-3 ug/ml - lightheadedness, peri-oral anaesthesia; 4ug/ml cardiovascular collapse.
Lignocaine - similar with 6-8ug/ml but 26ug/ml for cardiovascular collapse (this might seem like a huge 3 fold difference - but in practice it makes it only slightly marginally safer than bupivacaine.
[ 10 August 2002: Message edited by: gasbo ]
 
Hmmm, looks like somebody violated Rule # something-or-other, giving false or misleading information.
Of course most of the "caine" drugs are chemically related to cocaine. Drugs are named according to their structure for the most part. If a drug has "codone" or "morphone" in its name, you can probably assume it has an opiod structure (same thing for "zolam" or "zepam" in the case of benzos). Cocaine was merely the first local anaesthetic drug to be discovered. It's structure was the starting point for discovering safer and less addictive local anaesthetic drugs such as procaine and tetracaine.
And like gasbo said, you can get a buzz from some of the other similar drugs. None of them have the potent CNS effects of cocaine, and the risks of trying to get buzzed are probably greater than with cocaine, so you just shouldn't do this.
Previous studies have shown that a variety of local anesthetics including procaine are self-administered at high rates by rhesus monkeys. In the present study two rhesus monkeys were given a mutually exclusive choice between various doses of intravenous cocaine and procaine. In almost all comparisons cocaine was preferred even when the procaine dose was 16 times that of cocaine. Other measures of performance such as rate of responding did not vary systematically with preference. These data provide further support for the idea that rate of responding under simple schedules of drug delivery is an unreliable measure of relative reinforcing efficacy. In addition, the consistent preference for cocaine over procaine in monkeys suggests that the infrequent abuse of procaine by humans may be related to its low reinforcing efficacy relative to drugs such as cocaine.
I can cough up some sources if you want, but gasbo's posts tend to qualify as sources themselves, given his profession and knowledge.
 
Chemically I imagine it would be possible to convert the shit in those cough drops to PURE COCAINE - but it's something that would have to be carried out in a well-stocked lab by an experienced chemist - to put it gently, 'if you have to ask how, you couldnt do it' ..
 
I am a little confused. Gasbo you claim these other drugs can offer euphoria but you seem to suggest they don't stop the reuptake of dopamine/noradreniline. Are you implying that the sodium channel blocking properties of cocaine are significant in providing the euphoria (I have heard hints of this but wasn't sure).
Secondly there are some seemingly plausible recipes for synthing cocaine on the net. However they seem quite complicated difficult and overall useless. I mean the small amount of cocaine still used for eye and nose surgery still comes from actual coca plants (I think..tho am not sure). This tells you something about the efficency of directly synthing the agent.
 
Hi quale,
Are you implying that the sodium channel blocking properties of cocaine are significant in providing the euphoria (I have heard hints of this but wasn't sure).
The sodium channel block certainly does afford some CNS changes in 'perception'. This is reported well even in the older texts (and new ones). The texts say: lightheadedness, mild confusion, progressing to decreased level of consciousness, fitting, and coma.
From a practical point - occasionally there are some conditions (in the treatment of chronic pain states) where I have had reason to give IV lignocaine to subtoxic doses (a treatment largely gone by the way-side). I was always taught to push the syringe rather than let a syringe driver do it for me - the reason being - is that in order to get the most out of this therapy - you needed to take the patient to the brink of toxicity - and you gauge this by continuous verbal contact and observation. The moment I know the patient is 'on the edge' - is the peri-oral anaesthesia/paraesthesias (pins and needles), an odd look on their face (hard to explain that one), and they become overly chatty, and uninhibited. When they start telling me that I look good - then I know I have given them too much !! Thank god we don't do this as much now days.
So yeah - There is a component of sodium channel block with the CNS effects. I have also done this with patients who were familiar with the effects of cocaine - they reported it felt nothing like the headspin from it however.
Again - according to the literature, the euphoria is apparently dopamine driven centrally (and to a lesser extent noradrenaline). However - it is a little difficult to separate the effects of the sodium block from those of the dopamine .... My honest opinion (and it is only that) - is that the CNS effects are more likely to be 'synergistic'.
Secondly there are some seemingly plausible recipes for synthing cocaine on the net. However they seem quite complicated difficult and overall useless. I mean the small amount of cocaine still used for eye and nose surgery still comes from actual coca plants (I think..tho am not sure). This tells you something about the efficency of directly synthing the agent.
What can I add to that - hit the nail on the head. It is so much easier to purify the raw product than it is to purify the synthetic derivatives. And yes - cocaine is the naturally occuring alkaloid from the leaves of Erythoxylon coca (someone may have to correct my spelling of that ... )
Hope that helps.
 
For practical purposes, cocaine could not be made from benzocaine. I think proparacaine has a higher incidence of CNS effects than benzocaine.
"Although exceedingly rare with ophthalmic application of local anesthetics, it should be borne in mind that systemic toxicity (manifested by central nervous system stimulation followed by depression) may occur".
Atropine which occurs naturally datura, is amazingly similar in structure to cocaine, and is also an local anesthetic:Cocaine and Atropine
Maybe it could be used in a bio-synthesis?
 
My understanding of the 'local anaesthetic' action of atropine lies in that it is a quaternary nitrogen compound - not any other features of the structure, despite how similar it otherwise looks. I agree - by looking at its structure you would predict it - but in fact - it is the quaternary ammonium which leads to the local effect with atropine !
Similar can be found with pethidine, quinidine, anti-histamines, propranolol, and other tera-ethyl ammonium derivatives. The specificity for the sodium channel however is many times less than the 'caines'. In Atropines case it is classified as a direct acting Muscarinic Antagonist.
Of particular concern with LA ophthalmic drops is not the systemic absorption - but the corneal damage that can occur. Cocaine provides excellent topical anaesthesia of the cornea - however - people corneas started to ulcerate and scar - and hence it has been abandoned (like many of the concentrated local eye drops). The current ones on the market appear 'corneal'-safe.
 
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