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Troparil and Dichloropane, chemist looking for serious answers...

Phazer1980

Bluelighter
Joined
Nov 27, 2004
Messages
7
I have access to these two in the sense that I CAN get them, if they are worth it.

Troparil is cocaine where the benzoate ester has been changed to simply a phenyl group attached where the -OH group in the hydrolized compound would be attached. The actually changes the molecule a lot. Simply removing the ester R-O-R and putting a C there in stead a leaving the carbonyl group, one would THINK would act more like the original molecule. Anyway, this is how they did that, and dichloropane is the same molecule as troparil just with two substituted chloride atoms on the phenyl ring.

Enough chemistry.

I have read all the data about DAT, NET and SERT affinity, and by that alone troparil look very promising.
But I CANNOT find any experience data on troparil, only some very sporadic stuff, like one guy said he liked troparil over cocaine.
Do any of you know anything about the actual effect of troparil un humans in practice? That would be very much valued.

On the other hand when it come to dichloropane there is a lot more, it sounds like a really enjoyable stimulant with some MDMA character, but always mild enough that you do no make a fool out of yourself. Like the best from coke, amphetamine, MDMA, and relatively mild. Can anyone tell me something?


I am not a huge coke fans, but there are things about it I like, I have the same issues with MDMA and stimulating amphetamine, plus that amphetamines works for far too long. Will I in one of there compounds MAYBE find something I like?


If so I will start finding a good supplier.


Thank for any info, basically any info would be greatly appreciated. Trip reports, any experience, dosage guides, even hearsay.


Thanks in advance
C.
 
Isn't Troparil the selective DRI? I think there is consensus that selective DRIs aren't enjoyable and that DA+NE is needed for euphoria, it may have been Nagelfar that said Troparil was disappointing. But my recollection could be wrong and there could also be differences from person to person.
 
I'm not too sure why, but it seems like the benzoate ester is hydrolysed much faster than the methyl ester (WIN 35428 lasts 7 times as long as cocaine, and it has no benzoate ester, but it does have the methyl ester). This is surprising to me as the methyl ester seems to be a lot less hindered.

Anyways, what this all means is troparil and dichloropane are going to have a duration comparable to amphetamine, and if you were looking for a coke analogue with duration in mind, these 2 won't be sensible choices.
 
They look more like amphetamine to me you can see the (benzene)/c\c/n/ch3.
 
They look more like amphetamine to me you can see the (benzene)/c\c/n/ch3.

These molecules still have a different mechanism to amphetamine (they are DRIs whereas amphetamine is a DA releaser). The 2 molecules do share structural similarity, but crucially, there is a longer C-N distance, the tropane skeleton and the carboxy methyl ester which turn cocaine et al from substrate to inhibitor.
 
I'm a bit thrown off by how close the tropane is to the benzene though normally every chemical I see has two two carbons attached to the benzene not one before they attach something
 
Here: http://www.bluelight.org/vb/threads/549618-CFT-(WIN-35-428)-7-mg-i-v is a thorough trip report for WIN-35,428 i.e. para-fluoro troparil which could interest you. In brief, it seems that OP deemed the experience worthwhile.

What a coincidence BTW: just yesterday or before I was reading on cocaine analogues and dichloropane (and tropoxane) stood out the most for its QUITE promising IC50 values. Personally I would be most interested in trying it and if you do then be sure to come back and tell us how it goes please. If it extrapolates to all three monoamines what cocaine does to the catecholamines then I'd expect it to be a rather cool drug. Plus such through so-called transporter inverse agonism as opposed to the usual amphetamine MoA could mean no neurotoxicity? (wild partial conjecture and uneducated speculation...) I'm not sure if you implied in your post that there were trip reports on dichloropane though if there were, can you share them?
 
Dichloropane aka RTI-111 actually did go around recently - much to my GCMS' surprise. Guess some lab got ballsy enough to make it.

I didn't have a lot to mess with, but it didn't seem all that unusual of a stimulant either. Methylphenidate-ish almost, but not so crashy.
 
Yeah, I found some reports on it, was surprised at first, hoping for it to live up to my expectations... :p
Your description although is more encouraging than the reports I've read elsewhere, which made me perceive it as a complete waste of time. I actually enjoy methylphenidate...

You recall your doses? People seemed to agree that this one was a real sting on the nose. You found this too?

Cool that it's the real stuff.

Well, those were just IC50 values really, no promise of monoamine flooding. Someone ought to feed each and every one of Singh's compounds to rats and check for monoamine levels!! I mean dichloropane could be not even binding to the cocaine site for all we know!?
 
Well, those were just IC50 values really, no promise of monoamine flooding. Someone ought to feed each and every one of Singh's compounds to rats and check for monoamine levels!! I mean dichloropane could be not even binding to the cocaine site for all we know!?
It is extremely time consuming, not to mention expensive, to run microdialysis studies in rats. For most if the compounds, they used locomotor activity as an indirect measure of DA release. It's not perfect, but it does yield useful info.
 
I took it orally, at or below 20mg. I tend not to put strange compounds in my nose.
 
Isn't Troparil the selective DRI? I think there is consensus that selective DRIs aren't enjoyable and that DA+NE is needed for euphoria, it may have been Nagelfar that said Troparil was disappointing. But my recollection could be wrong and there could also be differences from person to person.

I have repeated what another has said of it, though have not myself partaken of it; but who knows whether the individual (though my intuitional cyber-sense gave me the feeling that this individual was an informed one, also with regard to their opinion: knowing whether or not what they were testing was troparil and experienced enough to gauge it with cocaine; but the subjectivity of circumstance cannot be tested in suchwise)

Also, yes, the affinities are lacking SERT in relation to cocaine which is a much more even spread, in terms of phenyltropanes Troparil is DAT selective, and therefore may be lacking the same feature which makes so many connoisseurs prefer cocaine to run-of-the-pharm-mill methylphenidate.

I'm a bit thrown off by how close the tropane is to the benzene though normally every chemical I see has two two carbons attached to the benzene not one before they attach something

Maybe scrolling over this page will get you used to how that appears. (However I do not think what you say is really so rare, many more classes and categories above and beyond over than those alluded to in this topic bear such a feature.)
 
Does the sodium channel blockade have any effect on the euphoria ? I would think it could at least definitely do something because of how important sodium channels are in the brain
 
Not really - trying to get a selective therapeutic effect from modulating sodium channels is difficult because of their abundance within the brain.
 
Not really - trying to get a selective therapeutic effect from modulating sodium channels is difficult because of their abundance within the brain.

From "sodium channels" blocking alone, but there has been some speculation that MAT specific sodium channels might be effected in proximity enough to the ligand site with cocaine to have any number of effects with cocaine (or any Na+ blocking DARI).
 
Does the sodium channel blockade have any effect on the euphoria ? I would think it could at least definitely do something because of how important sodium channels are in the brain

The fact that the transporters MAT(DAT/SERT/NET) are Na+ mediated in function/nature and firstly described thus in all current academic contexts:

ZUfat3.jpg


Makes me wish more study (*any* real study) would be done with this in correlation to potentiating inhibited reuptake, bridged etc.
 
The fact that the transporters MAT(DAT/SERT/NET) are Na+ mediated in function/nature and firstly described thus in all current academic contexts:

ZUfat3.jpg


Makes me wish more study (*any* real study) would be done with this in correlation to potentiating inhibited reuptake, bridged etc.
Monoamine transporters are driven by Na/Cl concentration gradients, and cocaine is a Na channel blocker, but it is extremely unlikely that the latter effect of cocaine influences the function of DAT. The reason is that the neurons with the highest sensitivity to local anesthetics are GABAergic cells, hence why local anesthetic overdoses cause seizures. So cocaine brain levels would likely have to exceed the threshold concentration for seizures in order to block sodium channels on dopaminergic neurons.
 
And even if dopamine neurons were more sensitive to sodium blockers, that would just result in the neuron not actually firing, because there would be no Na+ gradient for DAT to dissipate.
 
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And even if dopamine neurons were more sensitive to sodium blockers, that would just result in the neuron not actually firing...

The fact that it influences only non-dopaminergic neurons was the basis for my thinking that it added to efficacy of it's influence as a reuptake inhibitor; i.e. electron energy resonance via electron clouds on the *quantum* level. Na+ channel blockers block the channel, a static/tribo-electric exchange of resonant energy once docked as a ligand at the reuptake pump at DAT where DA itself is influenced by the electron cloud from it's Na+ blocking ability at *non*-DAT sodium channels "on the way to" DAT reuptake ligand site and having garnered electron resonance energy from channels elsewhere on the way there.
 
I like diphenhydramine with amphetamine because I feel like it increases the euphoria. And it is a sodium channel blocker. Idk if sodium channel blockade has anything to do with it though.
 
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