• N&PD Moderators: Skorpio | someguyontheinternet

Pro drugs - Is this even possible?

Renz Envy

Bluelighter
Joined
Sep 29, 2010
Messages
3,337
Foreword:
Lisdextroamphetamine aka vyvanse is the pro drug of dextroamphetamine. Many people think this is a bad thing as it is impossible to insufflate (or inject). The pros outweigh the cons in my personal opinion as vyvanse has a very smooth and almost inexistent comedown. Unlike an anti-social adderall shut-down. Many people hate stimulants solely because of the crash.

Would it be possible to create a pro-drug of other amphetamines? Like MDMA or Meth? What kinds of results would you expect?
 
possible perhaps, this has been discussed here before on at least 2 other occasions.
there are however serious legal issues surrounding it, and these are probably insurmountable.
 
Vyanase is jusr amphetamine made into an amide with an amino acid, so it would be possible with any primary or secondary amine, but not tertiary amines (so not possible with MDPV etc)

As vecktor points out, any will contain trace amounts of the amine, enough to make it effectivelly, a controlled substance
 
I want a sort of time release gabapentin.
I know you this is just running in circles, but I find pregabalin* to be akin in some respects to the graduated dosing of gabapentin in some ways to pain releif. I maybe just delusional.
*cannot get it with my health insurance.

I have enjoyed vyvanse but have done long binges, to getting more work done, only to be up WAY to long.
I've actually thrown them away in fit of drug madness, not once but twice, that makes in the #1 drug Ive thrown away, bwahha.
 
I want a sort of time release gabapentin.

Suggestion: 2-azaspiro[4.5]decan-3-one (gabapentin-lactam).

Pro: Neuroprotective effects were shown in animal experiments with Meriones unguiculatus (dissertation Natalie Eckhardt, University of Freiburg, Germany).
Contra: Convulsant activity in amygdala kindled rats (Naunyn-Schmiedeberg’s Arch Pharmacol (2000), 361: 200–205)


Edit: There are actually several referenes arguing pro resp. contra gabapentin-lactam...
 
Last edited:
man what the fuck, I swear I read this exact thread with this exact title and these exact responses in 2009.
 
Befuraline (a no-longer-made antidepressant) and other compounds metabolize into BZP. That's kind of cool.
 
An existing and actually quite effective solution is phendimetrazine, which metabolizes into phenmetrazine. Slowly, nicely, and lasts about 10-12 hours.

I was more centering the question around if a pro-drug of meth was possible. For some reason non-amphetamine stims just are not the same. However I'll definitely look into this phendimetrazine stuff.
 
Benzphetamine (N-benzylmethamphetamine, not to be confused with N-benzylamphetamine) could be considered a methamphetamine prodrug.

I would imagine you could make a lysine amide of M-AMP too. There's just no good medical reason to increase the half-life of a drug that's already amazingly fat-soluble. I think dosing the pure compound is more effective, cheaper, and safer.
 
Hypothetical situation: A child gets into a bottle of 5mg Desoxyn tablets. Compare this to a child getting into a bottle of extended-release methamphetamine prodrugs. One situation is going to be a lot easier to deal with.

There's also the issue that extended-release methamphetamine causing insomnia. Sleep deprivation is a key factor in amphetamine psychosis...
 
Oh right on! I figured in terms of over-dosing It'd be easier to cope with something that has to pass through your gastrointestinal tract as it doesn't all immediately hit your blood stream and can be partially reversed by flushing.

And yeah, in terms of general over-time safety it'd certainly be much worse. Just a hypothetical question.
 
I was more centering the question around if a pro-drug of meth was possible. For some reason non-amphetamine stims just are not the same. However I'll definitely look into this phendimetrazine stuff.

Apart from sekio's suggestion, I think that N,N-dimethylamphetamine is a meth-prodrug.
The compound itself has (presumably) only negligible activity on its own*, but gets metabolized first to meth, then to amphetamine in vivo. The metabolism step reduces the speed of onset and therefore considerably lowers overall toxicity.


* Edit: I need to correct one detail: N.N-dimethylamphetamine seems to be active on its own and doesn't require metabolic activation. Potency is ca. one tenth of meth. See: J Pharmacol Exp Therap 1990, 253(2): 466.
 
There may be something to that; I remember seeing N,N-dimethyl-cathinone as a "party pill" prodrug-ingredient. If memory serves there was also a pthaliminde or maleimide that I assume would function as a prodrug as well. I don't like the idea of generating a bunch of pthalic acid in vivo but... people buy it I guess.

You could also make trimethylamphetaminium chloride or something if you were desperate for prodrugs. Dunno how well that would fare, though.

Another interesting idea would be a fatty acid amide of methylphenidate.
 
Befuraline (a no-longer-made antidepressant) and other compounds metabolize into BZP. That's kind of cool.

In a similar vein, would it be possible for meclozine (OTC antihistamine/anti-emetic) to metabolize to 3-Methyl-BZP? If so, would it be active?
 
Neuropharmacological and neurochemical properties of N-(2-cyanoethyl)-2-phenylethylamine, a prodrug of 2-phenylethylamine.


1 N-(2-cyanoethyl)-2-phenylethylamine (CEPEA) was examined as a possible prodrug of 2-phenylethylamine (PEA). 2 Pharmacokinetics of PEA and CEPEA were investigated in rat brain, blood and liver by gas chromatography with electron-capture detection (GC-ECD). Interactions of PEA and CEPEA with putative neurotransmitter amines were investigated by use of high performance liquid chromatography with electrochemical detection (h.p.l.c.-e.c.). 3 Administration of PEA caused transient increases in PEA concentrations which decreased rapidly in brain and blood and at a slower rate in liver. Administration of CEPEA caused sustained elevations of PEA concentrations and elimination of PEA was markedly decreased in these tissues relative to the situation after administration of PEA itself. 4 Administration of CEPEA caused more prolonged decreases in brain noradrenaline, dopamine and 5-hydroxytryptamine concentrations than those observed after PEA administration, although values increased to control levels eventually.

so maybe prodrugs of PEA, are a way to get PEA active orally without messing with MAOIs? There's more on the side like "N,N-dipropargyl-2-phenylethylamine, a potential prodrug of 2-phenylethylamine: neurochemical and neuropharmacological studies in rat."

Wonder if these would work similarly on amphetamine or meth..
 
Top