Drug info - Diphenyl-2-Pyrrolidinyl-Methanol (diphenyl prolinol)

[RIKECHE]

Please post info about Diphenyl-2-Pyrrolidinyl-Methanol here.
Can anyone add information about:

* names / synonyms
* molecule
* dose
* duration
* side effects
* have there been any reported incidents with this compound?
* legal status
* stability of the molecule / compound

Experiences with Diphenyl-2-Pyrrolidinyl-Methanol should be posted here: Diphenyl-2-Pyrrolidinyl-Methanol (diphenylprolinol) trip reports
These documents about diphenylprolinol are in the file archive
Also see this thread:
'Herbal' High Neuroblast turns out to contain diphenyl-2-pyrrolidinyl-methanol

Hospitalisations have been reported.

__________________________________________________ __________________

(R)(+)-Diphenyl-2-Pyrrolidinyl-Methanol

How do the effects of this compare to cocaine?

More info would be nice also THANKS!

[Alfa]

http://www.drugs-forum.com/chemistry...rolidinyl.html

And also:

Originally Posted by fastandbulbous

Yes, it's a moderately strong CNS stimulant at doses of about 10 mg (a bit like methylphenidate) - it's the 5-membered heterocyclic ring analogue of pipradrol.

It's quite pleasant, very little peripheral action and next to no appetite supression. It'd be nice for people who don't have much to do with stimulants, but is way short of the mark if you're looking for a replacement for one of the amphetamines

Names: Diphenyl-2-Pyrrolidinyl-Methanol, D2PM, diphenyl prolinol, Neuroblast

[RIKECHE]

Thank you so much for the quick reply!
This helps... "but is way short of the mark if you're looking for a replacement for one of the amphetamines"
Swim is used to much stronger amphetamines so this will prob let swim down.

[Nicaine]

Originally Posted by RIKECHE

Thank you so much for the quick reply!
This helps... "but is way short of the mark if you're looking for a replacement for one of the amphetamines"
Swim is used to much stronger amphetamines so this will prob let swim down.

IMO it's unlikely anything would ever really substitute for methamphetamine, effects-wise. SWIY might want to give it a try before drawing any conclusions based on one person's opinion.

In terms of effects profile, the stuff seems to resemble MDPV quite a bit (as far as recent RC's go). Anyone know if this stuff is a pure dopamine reuptake inhibitor, or what? The "next to no appetite suppression" would be surprising in a potent SDRI, and may be just one person's opinion.

Originally Posted by bob_arctor

SWIM will be planning bioassay for later today. Will report back.

Keep us informed (there's reason to be interested in this RC, but SWIM can't discuss details).

[bob_arctor]

SWIM will be planning bioassay for later today. Will report back.

[Iggypoop]

No you're right, i'll do a report on this and ask a mod to move it into the wider general forum.

I'm getting some of this very shortly, will report back my findings as soon as i have time to bioassay.

sweet

[Nagognog2]

I'll re-open this - FOR NOW. Steer far away from any semblance of a source. Good monkeys.

[radiometer]

According to Alfa's link, the R and S isomers, unsurprisingly, have different activity:

(R)(+)-Diphenyl-2-pyrrolidinyl-methanol - Ki binding: 0.04µM; Ki uptake: 0.17µM


(S)(-)-Diphenyl-2-pyrrolidinyl-methanol - Ki binding: 0.40µM Ki uptake: 1.65µM


What seems to be in people's hands is the R isomer. Can someone explain what would be the expected difference in effects from the two different isomers, based on that data?

[Rush]

Originally Posted by radiometer

According to Alfa's link, the R and S isomers, unsurprisingly, have different activity:

(R)(+)-Diphenyl-2-pyrrolidinyl-methanol - Ki binding: 0.04µM; Ki uptake: 0.17µM


(S)(-)-Diphenyl-2-pyrrolidinyl-methanol - Ki binding: 0.40µM Ki uptake: 1.65µM


What seems to be in people's hands is the R isomer. Can someone explain what would be the expected difference in effects from the two different isomers, based on that data?

R isomer is 10x more powerful than S isomer.
low ki=high potency

BTW this compound is not a piperazine.
this topic is in the wrong section me thinks

[lulz]

Originally Posted by radiometer

According to Alfa's link, the R and S isomers, unsurprisingly, have different activity:

(R)(+)-Diphenyl-2-pyrrolidinyl-methanol - Ki binding: 0.04µM; Ki uptake: 0.17µM


(S)(-)-Diphenyl-2-pyrrolidinyl-methanol - Ki binding: 0.40µM Ki uptake: 1.65µM


What seems to be in people's hands is the R isomer. Can someone explain what would be the expected difference in effects from the two different isomers, based on that data?

The Ki binding figures are a measure of how effective each isomer is at manipulating the dopamine transporter (DAT). The DAT is a protein that removes dopamine from between synapses, so the more a drug interferes with the DAT, the more dopamine will flow between your neurons.

The R isomer has a lower value for "binding", which means it would be more powerfully attracted to the DAT. And since the R isomer also has a very low figure for "uptake", when the chemical reaches the DAT it'll interfere with it's activity much more powerfully.

So on both measures, the R isomer would be much more powerful than the S isomer.

Originally Posted by radiometer

Keep in mind that this drug was developed to compete with cocaine for receptor binding in order to aid people trying to get off cocaine. If it had much abuse potential, then it probably wouldn't have gotten very far through trials.

I suspect that it didn't get very far through trials.

According to the link Alfa posted, they were trying to create a drug that was very good at attaching to the dopamine transporter, but was very bad at interfering with it's activity. This actually wouldn't have been any use with cocaine addicts, because cocaine works in very bizarre ways - it uses dopamine, serotonin, and noradrenaline, but it doesn't rely on any single one of them. If one of the transmitters is unavailable, cocaine somehow manages to create drug seeking behaviour anyway.

But the idea was that if dopamine plays a large role in cocaine seeking behaviour, then a chemical with a higher binding affinity than cocaine would be more powerfully drawn to the DAT, therefore preventing cocaine from attaching itself to the DAT and interfering with it. If you look at the binding values, they got this part right:

Kibinding

Cocaine 0.12µM
(R) isomer 0.04µM

The (R) isomer is an impressive 3 times more powerfully drawn to the DAT than cocaine is.

Unfortunately for them, they were trying to make a chemical that also has a high uptake value. A high uptake value would mean that when the chemical attaches itself to the DAT, it's very weak at interfering with it.

Fortunately for everyone else, they got the exact opposite, this drug has a very low Ki value for uptake, meaning it is very powerful at fucking up DAT activity.

In fact it's even better than cocaine at interfering with the DAT functioning. So in theory this drug should be very very good at raising dopamine transmission.

Maybe oral consumption is a bad way of consuming it? SWIM is going to order a gram to experiment with anyway, it's very cheap and has a great deal of potential.

Reputation Comments on this post:

excellent post, thank you

[Nicaine]

SWIM now has confirmed a gram of this stuff on order (the R isomer), and should be posting a report soon. He intends on starting with 10-25mg, most likely plugged in case the stuff has bioavailability issues causing variation with other test subjects...

P.S. it's good to know this stuff can take time to start working, although with plugging I'd expect the time to be dramatically reduced. It seems what usually causes 2+ hour delays is slow intestinal absorption, which could also indicate bioavailability issues under certain conditions (such as full stomach, digestive tract pH, etc).

There's also the possibility (of course) that the substance SWIM has on order is not what it's purported to be. SWIM can't go any further without getting back into the territory of sources, so he'll stop right here & post test results when he receives the product -- most likely in a completely separate thread.

[Psych0naut]

Asking for sources is against the rules, please read it and don't break them again. And SWIM means Someone Who Isn't me.
No one on this forum incrimates him/herself, only SWIM or their lab animals do this, read the part about self incriminations as well please, thanks!

[radiometer]

It is indeed in the wrong forum.

Early reports (with the exception of Mr. Arctor's) on this compound do not sound terribly exciting. Keep in mind that this drug was developed to compete with cocaine for receptor binding in order to aid people trying to get off cocaine. If it had much abuse potential, then it probably wouldn't have gotten very far through trials.

[allyourbase]

it has little or no reuptake ability...which means the initial "whoa" feeling would be the most one could probably get from it, unless one were to mix it with something with an almost wholly reuptake inhibitory method of intoxication. it might be interesting to know what mixing this with methylphenidate, buproprion, or even MDPV would be like. the push and staying power.....

[Rush]

yeah, i think this chemical may have some useful effect in combination, and alone but in high dosages.

i think it is still a drug, perhaps in the right forum.
it just needs some research to find its place

[snapper]

What doses have provided euphoric effects for SWINicane ?
SWIM has just started with this product and has found it unimpressive, though doses so far are lower than those reported to be active (ie-tesd doses to rule out any sensitivity to the drug). SWIM plans to start with 25 mg soon as a hopefully active dose and work up from there. SWIM is currently rough around the edges from 4 weekends of MDPV use, so will likely not be running a marathon with this product. SWIM is nonetheless interested in more assays, esp. considering SWIM ended up with more than expected..

[Nicaine]

SWIM is thinking this may be the elusive stim that's attractive to both recreational and utilitarian users.

ISO at low to moderate doses it is a nice, mild and smooth "pick up" and motivational aid, with little compulsivity and almost no effects on appetite. It also appears to be pro-social (e.g. stimulating conversation). At high to extreme doses it becomes much more intense, recreational, and an end in itself as far as use, but then it's about as compulsive as MDPV or cocaine.

The main problem: Proper dosing (i.e. getting it into the body) can be tricky. The only method SWIM has used is plugging, which unfortunately is at minimum inconvenient for people with "real lives" who can't keep hitting the bathroom... and some refuse to do it at all. I'm sure the stuff works well taken orally, but we definitely need some input on this stuff from those who fed it by mouth to their lab rats. If SWIY has acquired any and dosed orally, please mention the dose required for a recreational effect.

[fastandbulbous]

it has little or no reuptake ability...

Thats not what the binding and reuptake Ki figures indicate and as the piperidine version, pipradrol, works be reuptake inhibition I'd be very surprised if this wasn't very similar in action.

The other pipradrol derived stimulant currently of interest (desoxypipradrol) acts in the same way but has much more overt CNS stimulation and is active at a much smaller dose 2-5mg for awake up, 10mg for gibbering territory and anything over 15-20mg in one go will have you strutting around in an arrogant manner!

[Nicaine]

Originally Posted by fastandbulbous

The other pipradrol derived stimulant currently of interest (desoxypipradrol) acts in the same way but has much more overt CNS stimulation and is active at a much smaller dose 2-5mg for awake up, 10mg for gibbering territory and anything over 15-20mg in one go will have you strutting around in an arrogant manner!

Not to mention the (purported) duration of action for some, 24-48 hours! That is actually about the amount of time SWIM prefers, from a recreational standpoint... it would mean (if he enjoys it) a sweet, uninterrupted stretch of deeply immersed focus, with no need for redosing at all.

He's looking forward to seeing how his rats react, but first they have to recover from going overboard with the thread title substance. He's still not quite sure what happened, but to him the compulsiveness was outrageously out of proportion to its other properties. Possibly just a quirk of biochemistry, or maybe it was the stupidly high doses required to get the desired effect. SWIM's general stimulant tolerance may be a bit too high for comfort.

Originally Posted by Cuberun

swim's just back from a long vacation and is glad to see something "new".
Could SWIY shed some more light on the sexual effects;

They'll probably vary from lab rat to lab rat, but for SWIM's it isn't half as potent in a general sense as MDPV. However, it seems to result in earth-shatteringly powerful orgasms... he's not sure why, as the overall length of the sexual experiences involved weren't unusual.

anything similar to the way methylone brings up the sex drive and inhibits ejaculation/orgasm?

Nope... unlike MDPV (which for SWIM shortened the experiences but made them possible 10x more often than usual) it doesn't seem to affect male orgasm latency at all, and certainly doesn't inhibit anything.

Also, sorry if this was mentioned but which amount of mg's (dpm & water) do SWIY find most successful for rectal administration?

At first he was doing 5-10mg or so in a shot, then the shots became machine-gun fire and SWIM both lost count + stopped caring. Beware...

[bob_arctor]

SWIM found insufflation not impossible, oral (capped) also OK. Plugging removes hours of coming up (preferred)

[radiometer]

LOL. Repeat:

So, barring exotic options, you've pretty much left only rectal admin and injection. Any theory as to how this stuff might be worth bothering taking? Could you elaborate on why insufflation and smoking are not viable? Thanks!

[fastandbulbous]

The (R) isomer is an impressive 3 times more powerfully drawn to the DAT than cocaine is.

Unfortunately for them, they were trying to make a chemical that also has a high uptake value. A high uptake value would mean that when the chemical attaches itself to the DAT, it's very weak at interfering with it.

Fortunately for everyone else, they got the exact opposite, this drug has a very low Ki value for uptake, meaning it is very powerful at fucking up DAT activity.

In fact it's even better than cocaine at interfering with the DAT functioning. So in theory this drug should be very very good at raising dopamine transmission.

Maybe oral consumption is a bad way of consuming it? SWIM is going to order a gram to experiment with anyway, it's very cheap and has a great deal of potential.

It's the ratio of binding to reuptake Ki's that are most important in giving a gauge of what it'll be like:

Cocaine has a Ki binding value of 0.12uM and a Ki reuptake value of 0.20uM. Now just because something binds to the protein receptor doesn't mean it's going to do anything, so the ratio of binding to reuptake is important. If most of what binds also inhibits reuptake, you end up with a drug like cocaine with a sizable abuse potential (ratio of binding:reuptake of 1.67). Although the Ki binding value of the compound in question is 0.04uM, it takes 0.17uM to inhibit reuptake. The higher ratio of 4.25 means that it's much less effective at inhibiting reuptake as a percentage of the DAT that it binds to leading to a less abuse prone stimulant. If you got one with a ratio of say 1.2, you'd have a problem drug on your hands, even if the Ki reuptake was say 2uM (would just require a higher dose, but once achieved would be frightenly efficient ).

Subsequently, it wouldn't be a bad choice as a drug to treat coke addicts as it still provides some stimulation, but can't be made like coke by increasing the dose; it'd also partially block any coke consumed on top of it. All in all an improvement for the coke user as the compounds of this type (pipradrol derivatives - diphenylmethanol/diphenylmethyl substituted onto a nitrogen heterocycle such as piperidine, pyrrolidine or morpholine) are of very low toxicity, esp regarding the cardiovascular system; in which respect cocaine is a rather cardiotoxic drug

Reputation Comments on this post:

Informative as always. Making the abstracts and so on understandable for non-academics

[lulz]

Originally Posted by fastandbulbous

If most of what binds also inhibits reuptake, you end up with a drug like cocaine with a sizable abuse potential (ratio of binding:reuptake of 1.67). Although the Ki binding value of the compound in question is 0.04uM, it takes 0.17uM to inhibit reuptake. The higher ratio of 4.25 means that it's much less effective at inhibiting reuptake as a percentage of the DAT that it binds to leading to a less abuse prone stimulant. If you got one with a ratio of say 1.2, you'd have a problem drug on your hands, even if the Ki reuptake was say 2uM (would just require a higher dose, but once achieved would be frightenly efficient ).

I don't quite understand the logic to this. From the article:

The lower the Ki, the higher the potency.

Kiuptake is how well the compound is at inhibiting the functioning of the DAT

Therefore a lower Ki for uptake should mean the better that the drug in question inhibits DAT activity.

So if Diphenyl-2-pyrrolidinemethanol has a higher affinity to the same site on the DAT receptor that cocaine binds to, and it interferes with the DAT better than cocaine does when it gets there, by simple logic Diphenyl-2-pyrrolidinemethanol must increase dopamine levels better than cocaine does.

The ratio on it's own can't mean anything without reference to one of the variables in each substance.

Also I've heard accounts from more than one person that if rectally adminstered, Diphenyl-2-pyrrolidinemethanol is in the same league of addictiveness as cocaine.

[snapper]

As it binds, it uses up open receptor sites, so if more binds, more receptor sites are used. In spite of more binding, less dopamine reuptake is occuring which means that 4x more receptor sites need to be occupied to equal the reuptake inhibition of cocaine, but binding there blocks those sites from endogenous dopamine, cocaine or other dopamine receptor ligands. In this sense, D2PM functions in part as an antagonist, or maybe a better term is a mixed agonist. It would theoretically also block the effects MDPV, etc.
The reason rectal dosage works better is that it bypasses the liver, and consequently gets more of the D2PM into the bloodstream faster. This causes a rush as the receptors are occupied quickly, unlike oral dosing which from the onset of effects means receptors are being bound more slowly and diluting the effects. Does that help ?

Reputation Comments on this post:

thanks

[lulz]

Aha, I didn't understand the significance of the ratio before, thanks for explaining it.

So cocaine's ratio means that 60% of the time when it binds to the DAT, it switches it off, which is much better than D2PM's "success rate" of about 24%.

But since D2PM has a higher affinity for DAT, wouldn't the lower "success rate" be compensated for at least partially if large enough doses were taken? I'm assuming that all DAT proteins aren't typically saturated by either cocaine or D2PM.

Also I am slightly confused about how D2PM blocks postsynaptic receptors on the neuron, I thought it binds directly to the DAT protein.