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Stimulants of the Future

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bk = benzyl ketone; C6H5-(C=O)-R

benzyl = C6H5-CH2-R

I bet 2-amino-5,6-dichloroindan is a winner but is probably more of an entactogen than a stimulant.
 
Holy_cow said:
^A compound with similar properties to your pill has been created:N-methylindatraline: Slow-Onset, Long-Duration 3-(3',4'-Dichlorophenyl)-1-indanamine Monoamine Reuptake Blockers as Potential Medications To Treat Cocaine Abuse. J. Med. Chem. 2000, 43, 4981-4992. A high dose will last several days. The lasting stimulantion and lack of sleep might not be too good for your mental health.
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Except he wanted a releaser, not a reuptake blocker. For DA, there isn't a major difference of course, the end is both stimulation and euphoria (with some minor differences in subjective feel), but for SE the difference is major.

prozac v. MDMA
 
>>I would love to see new stimulant come out that relases serotonin and dopamine like the way meth does
in Depot form tablets that start from 100% relase decreasing each day in 7 days and you'd get no come down at all.
>>

I don't think that the time-release would defeat the crash entirely. You'd still be in want of sleep, food, dopamine, have too much nor-epi, etc. As an additional piece of evidence, long-acting stimulants, like meth-amp, can still have nasty crashes.

>>Wouldnt hurt if it relased all serotonin the way mdma does, but kept the high going on for as long as you wanted..>>

This isn't physiologically possible. The endogenous synth for 5ht is rather slow, so 5ht releasers can deplete (but not entirely) your brain of 5ht within a matter of hours. This is why meth users can do multi-day binges but ecstacy-users can't really (or when they try, it turns into an expensive stimulant).

ebola
 
I would love to see new stimulant come out that relases serotonin and dopamine like the way meth does
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It's because methamphetamine acts on both dopamine & serotonin release/reuptake that it exhibits it's neurotoxicity (amphetamine has very little effect on serotonin and shows only a tiny amount of the neurotoxicity that methamphetamine does) as serotonogic neurones start hoovering up dopamine molecules, whivh because of free radicle oxidation, completely bugger the neurone. On top of that, some drugs that are stimulants with serotonogic activity can cause a really nasty, pretty much untreatable problem for the cardiovascular system, namely pulmonary hypertension; it is related to the 5HT2B receptor. The world can do without a bigger, stronger, faster meth.

A better avenue might be that seen in fencamfamine, which has some activity at the mu receptor (although not enough to cause an opiate sependance). It leads to a smoother stimulant that facilitates concentration (for learning tasks etc) far more than stimulants like amphetamine, meth etc. which quickly lead to repetitive, compulsive behaviour & thought patterns, which do nothing for concentration
 
With stimulants like Dimethocaine, is the tertiary amine necessary? Perhaps replacing one of the 2-methylpropyl groups with a phenyl would result in opioid affinity.
 
Ham-milton said:
With stimulants like Dimethocaine, is the tertiary amine necessary? Perhaps replacing one of the 2-methylpropyl groups with a phenyl would result in opioid affinity.
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How - I can't see how that would get it to fit into the model pharmacophore proposed for mu agonists (where are the 2-methylpropyl groups in it's structure?)

structure given here - http://en.wikipedia.org/wiki/Image:Dimethocaine.png
 
I'm sorry, I don't mean one of the two dimethylpropyl groups. I mean one of the two methyls attached to the propyl. It made more sense in my head than on paper. Hope this clarifies.
 
visualising the likely metabolic breakdown products of desoxypipradrol, got me wondering whether anyone has ever heard anything as such of beta phenyl derivatives of amphetamines. my logic goes, the most likely spot on the molecule it can be attacked is the adjacent carbon to the nitrogen on the piperidine ring, which would produce a lactam, which could then be further oxidised. several people have talked about a secondary effect that occurs somewhere around 4-8 hours after absorption and i was thinking maybe active metabolite?

oh also, i got one hit in this thread on adamantane, a little known stimulant called bromantan which got banned as either a stimulant or a steroid masking agent or both, which is a stimulant with little other than CNS activity, and imunostimulating effects.

o for a bluelighter living in russia at a university involved in pharmacology research. there's a lot of stuff coming out of russia that you never hear about in the west. http://www.nextbio.com/b/home/home.nb is a site that appears to host summaries of studies of some of these novel russian drugs. http://www.nextbio.com/b/home/home.nb?q=bromantan
 
i found a place willing to synth it but like i said, it's expensive. i also examined the idea of synthesis using adamantane with a keto group and bromophenylamine and still the quote i got came up pretty decent.
 
Substituted anilines don't sound all that appetizing. para-Bromo aniline is extremely toxic.
 
I'm still thinking the favorable route would be a short acting stimulant, that is a blast of euphoria that is extremely intense/orgasmic and can last as long as you want to redose, to be able to come down whenever you choose, a la freebase coke but needn't be smoked and can be attained by hcl absorption across a membrane, that can be cheaply & easily made for potential of achieving quantity to control length of stimulation more readily.
 
I hate short durations and having to redose, probably because I prefer to dose orally. 4-6 hours is the perfect duration (a la caffeine).
 
^I also hate having to redose frequently. With methylphenidate for ADD, I had to redose 3-4x times per day...sometimes I would completely forget, until the rapid come-down phase started to kick in. I like a nice 12hr duration, something that works over the course of a day. I have yet to find anything better than dextroamphetamine XR (especially with respect to the lack of a 'come-down' effect), but I have yet to encounter any desoxypipradrol. I would love to try that one, but am not expecting miracles, as I tend to respond far better to DAT/NET substrates than DAT/NET inhibitors.
 
I suppose making anything short acting an extended release formulation may be able to help depending on the nature of the absorption? I'd like to think of the 'dream stimulant' as versatile in that it can last a short time if need be. Troparil always sounded good to me, basically coke with no local anesthetic cardiotoxic properties which didn't cause internalization of DAT on the magnitude of the amphetamine & phenethylamine class stimulants and was maybe three times the duration of coke. Anyway, I would think short acting would always equal safer for the most part. I like being able to eat when I want and etc too, that seems to be a large part of the "come down", forgetting when you ate last and neglecting basic bodily functions such as that.
 
Nagelfar said:
I'm still thinking the favorable route would be a short acting stimulant, that is a blast of euphoria that is extremely intense/orgasmic and can last as long as you want to redose, to be able to come down whenever you choose, a la freebase coke but needn't be smoked and can be attained by hcl absorption across a membrane, that can be cheaply & easily made for potential of achieving quantity to control length of stimulation more readily.
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That is a recipie for disaster as the potential for psychological dependance is so large it would be a nightmare. The last thing you want is a short acvting stimulant. Also the euphoria doesn't last, just like repeatedly administering stimulants - it just leads to compulsive behavior & psychosis
 
anything that favors dopamine reuptake and less norepheniphrine stimulation is gonna be a big hit duh! to0much adrenal stiimulation makes u jittery example! caffeine! and levo amp in adderrall, and benzedrine ect...
 
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