• Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

  • N&PD Moderators: Skorpio | someguyontheinternet

Stimulants of the Future

Status
Not open for further replies.
Dear Jamshyd,
You can sell all this for cash. From a fake address (for security) and cash only (no banks).

S-)
 
Be careful, tetracaine is an MAOI too.

Differential effect of tetracaine and bupivacaine on catecholamine and 5-hydroxytryptamine turnover.
Rosenberg PH, Nissinen E, Mannisto PT, Tuomisto L, Heavner JE.

The effect of the local anesthetics, tetracaine and bupivacaine, on monoamine oxidase (MAO) activity of rat brain and on the major steps of catecholamine and 5-hydroxytryptamine (5-HT) turnover was examined. The IC50 of tetracaine for MAO-A and MAO-B inhibition was 1.2 microM and 19.5 microM, respectively. Up to 2.5 mM bupivacaine was without effect on either form of MAO. None of the following activities in rat brain or adrenal medulla were inhibited by 5-2500 microM of tetracaine or bupivacaine: catecholamine-O-methyltransferase, tyrosine hydroxylase, dopamine-beta-hydroxylase. Tetracaine caused only a moderately potent inhibition of synaptosomal uptake of norepinephrine (NE) (IC50 14 microM), dopamine (IC50 37 microM) and 5-HT (IC50 45 microM). The potent and specific MAO inhibition by tetracaine, in association with an impaired uptake of synaptosomal amines, may lead to an increase in the synaptosomal content of neurotransmitter amines, such as 5-HT and NE, with possible antinociceptive consequences.
Click to expand...

And rhesus monkeys don't like it:
On the relationship between the dopamine transporter and the reinforcing effects of local anesthetics in rhesus monkeys: practical and theoretical concerns.
Wilcox KM, Rowlett JK, Paul IA, Ordway GA, Woolverton WL.

Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, 2500 N. State Street, Jackson, MS 39216-4505, USA.

RATIONALE: Drugs that are self-administered appear to vary in their potency and effectiveness as positive reinforcers. Understanding mechanisms that determine relative effectiveness of drugs as reinforcers will enhance our understanding of drug abuse. OBJECTIVES: The hypothesis of the present study was that differences among dopamine transporter (DAT) ligands in potency and effectiveness as a positive reinforcers were related to potency and effectiveness as DA uptake inhibitors. Accordingly, self-administration of a group of local anesthetics that are DAT ligands was compared to their effects as DA uptake blockers in vitro in brain tissue. METHODS: Rhesus monkeys were allowed to self-administer cocaine and other local anesthetics i.v. under a progressive-ratio schedule. The same compounds were compared in standard in vitro DA uptake assays using monkey caudate tissue. RESULTS: The rank order of both potency and effectiveness as reinforcers was cocaine > dimethocaine > procaine > chloroprocaine. Tetracaine did not maintain self-administration. For inhibiting DA uptake, the potency order was cocaine > dimethocaine > tetracaine > procaine > chloro-procaine. At maximum, these compounds were equally effective in blocking DA uptake. Lidocaine did not inhibit DA uptake. CONCLUSIONS: The potency of local anesthetics as positive reinforcers is likely related to their potency as DA uptake inhibitors. Variation in their effectiveness as positive reinforcers was not a function of differences in effectiveness as DA uptake blockers, but may be related to relative potency over the concentrations that are achieved in vivo. Effects at sodium channels may limit the reinforcing effects of local anesthetics.
Click to expand...

Dimethocaine is probably the best bet..
 
Be careful, tetracaine is an MAOI too.
Click to expand...

Even more important & what everyone seemd to have missed is that local anaesthetics bugger the propagation of the synchronizing signal from the sino-arterial node across heart muscle tissue. They may be good dopamine reuptake inhibitors, but if there better at being local anaesthetics (bit rusty on this - they inhibit Na/K ATPase?) it's not going to take much above a theraputic dose for the user to be fucked in a way he never even considered. Add to that the propensity of the prototype stimulant for these drugs to, er, cause users to get a bit carried away with repeated/increased dosages and we have the most rabid anti-drugs campaigners vison come true. A cocaine analogue equivalent to 3-methylfentanyl in the 'drug serial killer' stakes. You can't even depend upon examples from clinical use of the drug, as then it's not IVed, it's IMed and with a vasoconstrictoe like adrenaline thrown in with it to massively slow the diffusion of the drug from the tissues into the main blood circulation

All potentially very nasty
 
what about the methamphetamine version of 4-fluoroamphetamine (4-fluoro-methamphetamine)?
can't find any info about it.
 
Last edited:
I believe the n-methyl analogue of 4 fluoro amphetamine was discussed in an earlier thread.

I don't see the logic of coding it as 4-FMP, when the standard coding for the chloro or methoxy analogue has always been PCA (Para Chloro Amphetamine)or PMA.

The 3 fluoro isomer appears much more intersting anyways.

there are some patents relating to the fluoroamphetamines and if I can dig up the reference I'll post it, I would be very suprised if the N-metyl cogener hadn't been investigated.
 
I found 4-FA to be as peripherally stimulating as ephedrine.

It is also definitely NOT what you'd look for in a stimulant - it is more like MDMA in its "stimulating" effects (ie. stupefying, scattered, lethargic).

I have no reason to think that 4-FMA would be better.

(And I prefer using the acronyms 4-FA or PFA over "4-FMP")
 
sorry 4-fmp is used as "slang" for 4-fluoro-amphetamine. can understand the confusion, i have already edited my original post for more clarity.

Bandil (from the bee site) tried to synth it, but it didn't want to form crystals iirc.
 
Last edited:
I bet 3,4-dichloro-methamphetamine is the best, but there's way too much in studies pointing to neurotoxicity for the two (unless you don't mind that, I guess, some people smoke meth all day!)
 
superpowers

You're right, I don't mind.
I am more than willing to try both 4-Cl-METH and 3,4-di-Cl-METH.
You could give me some if you wanted.

back on topic,
Stimulant of the Future:
2-Bz-2-(CO2CH3)-piperidine HCl.
 
So, dimethocaine has been shown to displace cocaine off it's receptors, in fact, in tests on monkeys, in fact, the self-administered monkeys got 0.1-0.3mg/Kg iv OR 0.030 to 0.17 dimethocaine. That makes it's DAT binding 2-3 times that of cocaine. Wonder if adding an alkyl group to that para amino (like tetracaine) would make it stronger again?
The thing to remember F&B is that your average dealer knows nothing of new chemicals. If they knew it worked, they would be cutting our coke with it right now! MDPV isn't shifting mountains because it's an acquired taste requiring that most had to come by in drug circles 'moderation'.

Quote: This data demonstrate the locomotor stimulant, reinforcing and anxiogenic actions of dimethocaine similar to those reported for cocaine in animals. In addition, these findings support a role for dopaminergic activity, rather than local anesthetic action, in the behavioral effects caused by dimethocaine.
 
Last edited:
^ I'd be surprised if this one isn't in PiHKAL. Wouldn't that be DMMA or something? Too lazy to look it up :p

In any case, shulgin does observe that alkylating the nitrogen in ring-substituted amphetamines renders the drug practically useless (or lowers potency at best).
 
Status
Not open for further replies.
Top