Selegiline vs Methylphenidate ? (deprenyl vs ritalin)

[arcimboldo]

Could anyone who have experimented with both differentiate the main differences in effects between these two?

(i think the endphysiological effect of both is dopamine increase, by two different mechanisms)...

...so Is it only a potency difference?



--
Thanks in advance.

 

[Keif' Richards]

I'm going to move this to advanced drug discussion, as I feel they will probably have some better answers for you.

 

[doxylamine]

The physiological response is definitely different and I have reason to believe the subjective experience would be too, so they are definitely unique from one another in aspects beyond potency. Selegiline produces L-Methamphetamine as a metabolite which adds to the peripheral effects with very little additional psychoactivity.That aside, MAO-B inhibition and dopamine reuptake are 2 very different actions. I don't think they're very comparable drugs in terms of therapeutic use, and much less recreationally.

 

[AlphaMethylPhenyl]

Selegiline mainly acts as MAOI-B inhibitor, with higher doses additionally inhibiting MAO-A.

Methylyphenidate is a NDRI.

EMSAM, the transdermal selegiline patch marketed for depression, produces much less l-methamphetamine and l-amphetamine than Deprenyl, marketed for Alzheimer's. Selegiline has some other effects too, possibly a NRA, and some mechanisms that seem to make the brain age slower. Even at 6mg, the lowest EMSAM dose, it does inhibit MAO-A, but to a small extent. MAO-A inhibition is generally thought to be necessary for a MAOI to have an antidepressant effect. Selegiline failed late-stage trials for ADHD.

Ritalin/Concerta is marketed for ADHD and narcolepsy. As far as I know, this is its only action. I have heard that it's a bit more safe a treatment than amphetamine, and may actually have some positive effects on the brain. But it isn't recognized as an antidepressant.

 

[bindingaffinity]

I haven't heard anything about selegiline used in Alzheimer's disease (cholinesterase inhibitors are more common for dementia) but it is used in Parkinson's disease, since slowing down dopamine metabolism can help with that.

Very high doses (10 to 20 times higher than used for MAO-B inhibition) of selegiline substitute for dextromethamphetamine and cocaine in rats. This seems to mostly be mediated by metabolism into levomethamphetamine. This may also be mediated by reduced breakdown of phenethylamine. A selective MAO-B inhibitor, N-(2-Aminoethyl)-4-chlorobenzamide hydrochloride, did not substitute for psychostimulants. Another study claims that selegiline only partially substitutes for cocaine at high doses, and it depends on what test you use, but D-deprenyl (which metabolizes to dextromethamphetamine) fully substitutes at a wide range of doses. There don't seem to be any studies on selegiline or D-deprenyl against methylphenidate directly, but dopaminergic stimulants typically behave pretty similarly in these discriminative stimulus tests from what I have read.

 

[AlphaMethylPhenyl]

Righto, I meant Parkinson's.

You cited a study with r-selegiline, not l-selegiline, only the latter of which is in mainstream use. R-selegiline breaks down into d-meth and d-amp, not l-meth. l-selegiline breaks down into l-meth and l-amp, which again are quite small in quantity via patch.

It's commonly known that facilitated exchange diffusion mediated by the stimulants amp and many of its structural analogues works against other psychostimulants: those which exert their action primarily through norepinephrine-dopamine reuptake inhibition...Fairly basic neuroscience/pharmacology.

 

[bindingaffinity]

I thought that the common name selegiline was, per this list of synonyms from PubChem, identical to L-deprenyl. The naming seems very confusing, since the first paper I cited, as well as PubChem, seem to claim that L- and (R)- are the same thing, and the other isomer would be D-deprenyl/(S)-deprenyl/(S)-(+)-deprenyl. On rereading the first paper I linked, I really have no idea which isomer they're talking about.

EDIT: I found a paper that is actually talking about L-deprenyl, the clinically used isomer, and they say that it takes doses that are much, much higher than clinical use to substitute for D-amphetamine. Specifically, L-deprenyl engenders full substitution at 17 mg/kg in rats, and 5.6 mg/kg in monkeys. Maximum therapeutic dose in humans seems to be 12 mg per day, total.

 

[asecin]

ive tried them both and selegiline is something else. you dose that crap for a week with nothing really noticiable, and one day i try to sleep and im having some type of hallucinations it feels like fireworks or seizures but mostly euphoric, not downgrading and painful. ive never had that before not sure if it probably counteracted with something or what as MAOIs tend to do that.
anyway, i would recommend moclobemide if you ever wanna try MAOIs, much safer , same effect.

on the other hand i did ritalin and all the other crappy stimulants US produces, they are all the same basically, crappy stimulants few levels readjusted from meth so people can dose them in safer form but cause same problems and health issues.
imagine this, US government allowing companies taking out and adjusting the addiction potential of cocaine and meth and turning it into profitable safer duller forms of the former so people can "get the idea" so to say and still be safe and not immediately die, thats how it is basically with these shitty RX stimulants.

personal recommendation, get selegiline and be smart or just get moclobemide which is prescribed to anyone with no knowledge of drugs and still no lawsuits out there