Ibogamine A better alternative to ibogaine for those who cannot tolerate or dislike

[Neuroprotection]

Ibogamine is an alkaloid profound in the same plant as that which Ibogaine comes from.
It shares the same anti addictive and tolerance reversing effects with Ibogaine but completely lacks the psychoactive or at least hallucinogenic effects.
However I have only found limited information on this substance and I would like to know more. Since it is a precursor to, and structuraly similar to Ibogaine, I believe more research should have gone into it.
Does anyone know about this compound?
Does anyone see this as being a possible legal replacement for Ibogaine?
Also would anybody consider extracting it from its plant sauce and trying it, I don't usually condone drug use, but I think I can safely say ibogamine is far safer than Ibogaine
What do you all think, I am fascinated by this substance so any contributions will be greatly appreciated
Thanks

 

[adder]

I don't think it's possible to extract ibogamine without extracting ibogaine and all the other alkaloids along with it. So without chromatography afterwards it's useless (perhaps some derivatization of some constituents and then playing with pH and ion-exchange resins might work as well) . If you consider the prices of tabernanthe iboga, it's not a task for an amateur enthusiast. But if you consider buying some iboga or the extract, you can send it to me and I'll gladly do the lab work.

 

[Raysu]

and I'd totally be your guinea pig ? Ibogaine minus hallucinations sounds worthy of clinical trials IMO.

 

[DotChem]

Ibogamine is an alkaloid profound in the same plant as that which Ibogaine comes from.
It shares the same anti addictive and tolerance reversing effects with Ibogaine but completely lacks the psychoactive or at least hallucinogenic effects.

Source?

Does anyone see this as being a possible legal replacement for Ibogaine?

Depending on which country you are located, ibogamine may fall under analog laws therefore illegal. As analog of a banned substance (ibogaine). But the roots of the tabernanthe iboga plant containing iboagaine/ibogamine and related alkaloids may be perfectly legal as supplement. The bark of the roots of the plant is where much of the pyschoactives are. So it may be perfectly legal to purchase and use (but always CHECK THE LAW in your country).

Also would anybody consider extracting it from its plant sauce and trying it, I don't usually condone drug use, but I think I can safely say ibogamine is far safer than Ibogaine..

IMHO it is waste of money and energy isolating ibogaine and/or ibogamine. You'll need a decent lab setup with "complicated" chromatography..etc. There's no extra benefits (like eating magic mushroom v psilocibin or smoking weed vs THC..etc) only way much more expensive. It won't make it any 'safer' lest you loose all the bioactivity (anti-addictive and such) you are after in the first place! The key is dosing!

 

[Solipsis]

Not that it's impossible but structurally speaking if this compound were not psychoactive that would be analogous to 5-MeO-DMT being psychedelic but not DMT.

Furthermore there is also a similar duo of iboga compounds called coronaridine and voacangine which are carboxylic acid methyl esters of ibogamine and ibogaine respectively... and before you object that iboga compounds are not simply psychedelic by virtue of 5-HT2a activity like those tryptamines... coronaridine, the ibogamine ester has micromolar affinities for opioid and NMDA receptors suggesting that the 5-methoxy group is not crucial for say NMDA antagonistic binding.

But I'm not disputing what is claimed in the TT: apparently ibogamine is more effective at anti addictive effects in animal models than the other tested iboga alkaloids so if a lower dose is required, it stands to reason that less or - who knows - even virtually no psychedelic effects would have to be 'endured' at doses effective for addiction. (I believe it was in one of the wiki reference articles for ibogamine but closed that tab).
I get the skepticism though, that regardless of kappa opioid effects and the like, a heavy trip would be more likely to psychologically consolidate a person's fight against addiction... so serious junkies might better take ibogaine after all even if they 'dislike' it.

 

[serotonin2A]

I think the argument for finding a less psychoactive version of ibogaine (hence the development of 18-MC) is that far too many people die during ibogaine treatment due to arrhythmia or because they use opioids while on ibogaine. It has also still never been worked out whether the tremorgenic effects of ibogaine (due to sigma-2 activation) reflect neurotoxicity. My understanding is that ibogamine is actually more potent than ibogaine at sigma-2 receptors.

 

[Solipsis]

What alludes to tremors being a sign of neurotoxicity? Aren't tremors possible from various tryptamines, in which case I don't think I ever heard a link to neurotoxicity? (Oh wait it does seems like you are saying the tremorogenic effects being from sigma-2 activity is definite, nice to know if true - I thought sigma was mostly linked to psychiatric syndromes, not extrapyramidal or peripheral effects?)

Also I'm confused how it seems you are calling arrythmia psychoactivity? If it's possible to isolate kappa agonism from whatever contraindicates concurrent opioid use that would be very interesting.

 

[serotonin2A]

What alludes to tremors being a sign of neurotoxicity?

Because ibogaine and harmaline have been shown to cause neuronal degeneration. They cause rhythmic (4-10 Hz) activation of neurons in inferior olive, which increases glutamate release from climbing fibers onto cerebellar Purkinje cells. The rhythmic activation of Glu receptors on Purkinje cells causes tremor and can also cause those cells to degenerate.

http://www.ncbi.nlm.nih.gov/pubmed/10966515
http://www.ncbi.nlm.nih.gov/pubmed/9348351
http://www.ncbi.nlm.nih.gov/pubmed/21640732
http://www.ncbi.nlm.nih.gov/pubmed/20498062

Aren't tremors possible from various tryptamines, in which case I don't think I ever heard a link to neurotoxicity? (Oh wait it does seems like you are saying the tremorogenic effects being from sigma-2 activity is definite, nice to know if true -

Tryptamines do not cause this type of tremor.

I thought sigma was mostly linked to psychiatric syndromes, not extrapyramidal or peripheral effects?)

Sigma-1 and sigma-2 are completely unrelated, with very different structures and functions. It just so happens that some ligands bind to both of those receptors.

Also I'm confused how it seems you are calling arrythmia psychoactivity? If it's possible to isolate kappa agonism from whatever contraindicates concurrent opioid use that would be very interesting.

I'm not calling arrhythmia psychoactivity. My point is that people sometimes die after taking ibogaine and that is one reason why it would be useful to develop ibogaine derivatives that are more selective. The point Neuroprotection brought up (lack of hallucinogenic effects) is another reason why there is interest in compounds that have better selectivity.

 

[DotChem]

IMHO, Iboga indoles alkaloids "hallucinations may be required for anti-addiction activity. At least with psychostimulants and opiates but not alcohol or nicotine!. Here is why imho:

For one, Ibogaine is a kappa opioiod receptor agonist and kappa activation is pretty well known to induce hallucinations. Example: the selective kappa agonist Salvia (Salvinorum A) is hallucinogenic . So Ibogaine might be inducing similar type of "hallucinations" as Salvia divinorum via kappa agonism but not via 2A like DMT/LSD... One should note that it is not really "psychedelic hallucination" via 2A activation. So technically Ibogaine, Salvia or other kappa shouldn't be classified psychedelic. Anybody who've tried acid and Salvia should know the difference. Iboga hallucination is very much close to lucid dreaming ie waking up in a dream with all the dream characters, plots, interactions..etc That's for one.

Second, Kappa agonists (this one compound in particular) was shown to give some of the effect of Ibogaine. Plus, Kappa antagonists block (some of)the "hallucinogenic" action of ibogaine. (https://www.ncbi.nlm.nih.gov/pubmed/9668680) The anti-addictive effect (both short-term and long term) of Kappa agonists is pretty much very well established now (see kappa wp entry and refs there). Especially beneficial is the long-term kappa agonists treatment since kappa activation induces up-regulation of D2 receptors in the nucleus accumbens and striatum that opiates or psychostimulants long-term use down-regulate. Back to baseline with the added bonus of resenzitation to opiates and stims. Like for example sexual drive back to pre-stims use!

So I think Ibogaine may be inducing the anti-addiction effect via kappa activation. And since Kappa activation induces BOTH hallucinations AND detox (it virtually reverses effect of opiates/stims on NAcc/striatum), it is going be hard to separate the two effects with Ibogaine by using non-hallucinogenic analogs...but that's assuming detox mechanism via kappa ?

imho if one is seriously considering Ibogaine detox (stim/opiates but not alcohol or benzos) and worry about cardiac toxicity, then he should try a Kappa agonist+NMDA antagonist to get same result as Ibogaine without worrying about cardiac problems. The so-called "hallucinations" will still be there though only this time via a kappa agonist other than Iboga indoles alkaloid. The reason for adding NMDA antagonist is that it counters the dysphoric effect of kappa agonism so it makes it make it easier to redose without beeing pissed off by the dysphoria of kappa agonists. Remember, kappa seems to do the exact opposite of stim/opiates in NAcc and striatum including the opposite of euphoric effect of stims ie dysphoria and aversion... Which may help explains why Ibogaine as well as other kappa agonists developed by pharma don't work on alcohol or nicotine addiction. I guess they won't work on GABAergic benzos either!!?

So bottom line: the anti-addiction effect of ibogaine and the hallucinations are one and the same thing. Just my opinion.

(someone on this forum or reddit has mention a3b5 nicotinic channels blockade by Ibogaine as basis of its anti-addiction properties. does anubdy have a ref on that? thanks)

 

[Limpet_Chicken]

Well coronaridine/18MC are antiaddictive are they not? never tried them however.

I'd suggest a lot of the tremorogenic properties of ibogaine could be adrenergic in nature. A full dose of ibogaine requires the user to endure intense peripheral sympathomimetic effects doesn't it? its certainly a physical stimulant because its used in gabon by the natives not only in Bwiti cult ceremonies, but in much much smaller doses as an endurance booster and stimulant to go hunting on. Never taken it myself but can only compare it to Iporuru, which is meant to be similar in effects and is reportedly dug up and eaten by gorillas as well as people for psychotropic and stimulant effects, its meant to be used in a manner similar to iboga, but I'm not sure of the action of the constituents. And I only explored Iporuru at
doses up to a gram or two of dried rootbark, powdered, which was stimulatory but not hallucinogenic. Didn't want to push it because I HATE adrenergic effects like that, and usually keep my adrenergic output as suppressed as practical before orthosteric hypotension makes it too difficult to move, using clonidine and tizanidine.

 

[Solipsis]

Ah I see ser2a, and yes I read about harmaline (acting as a sort of pacemaker for those synchronous neuronal firing creating the tremor but also a tolerance effect). Thanks for the insight. This thread turned out to be very informative in general.

Dotchem: I agree, and kinda wanted to say something along those lines in post 5

 

[adder]

The anti-addictive effect (both short-term and long term) of Kappa agonists is pretty much very well established now (see kappa wp entry and refs there). Especially beneficial is the long-term kappa agonists treatment since kappa activation induces up-regulation of D2 receptors in the nucleus accumbens and striatum that opiates or psychostimulants long-term use down-regulate.

Both kappa agonists and kappa antagonists are said to be "anti-addictives" though I never really understood how either can work in the long run. Kappa agonism is much responsible for depression in long-term opioid users, the beneficial effects in addiction are short-term but I can't remember the exact mechanism by which it happens to be so. Similarly with kappa antagonists - how can buprenorphine be a remedy for cocaine addiction for instance if it actually should increase its effects? I caught myself that just after buprenorphine kicks in, I tend to use much more tobacco as if there was a synergistic dopamine kick, I imagine the same is true for cocaine, so it's a bit like treating a strong stimulant addiction with a weaker stimulant that partially substitutes for the stronger one but on top of that potentiates it if they're taken together. How is that anti-addictive?

 

[Limpet_Chicken]

The tobacco enhancing effect is generic to opioids acting as MOR agonists, after doing a shot of say 700-1g morphine sulfate, I find I smoke like a chimney. I smoke very little before I've taken my morphine/oxy for the days first dose, a couple of smokes a day usually, and too, I find opioids make me no longer satisfied with my e-fag, I but I want real tobacco, and LOTS of it, for some reason.

 

[Dracarys]

I suppose that the NMDA-antagonism and the fact that noribogaine is an SSRI, also contributes to the anti-addictive effect. Addiction is often rooted in depression, and these two mechanisms are both antidepressant. Noribogaine can stay within the bloodstream for long enough to have this effect. And i believe that both ibogaïne as well as noribogaine have some dopaminergic effect as well.

 

[DotChem]

Both kappa agonists and kappa antagonists are said to be "anti-addictives" though I never really understood how either can work in the long run.

Kappa agonists actually up-regulate dopamine D2/D3 receptors in the Nucleus Accumbens[] and the striatum which basically are down-regulated in long term stims uses. They also up-regulate MOR receptors in NAcc that have been down-regulated by heavy OP use. That's is why kappa agonists re-sensitize to stims or OPs . How that is related to the hallucinations induced by kappa agonists such as Ibogaine and salvia, I have no idea! Probably it's the brain rewiring and reprogramming mechanism, kind of like a way a crashed computer can be rebooted to a previous State!(but with all the memory intact including more recent memory!!)

As for antagonists, I am not sure, but I think it is the opposite: a single dose of a kappa antagonist will dramatically increase cocaine seeking behavior of rats [check pub med "kappa cocaine antagonists"] compared to control rats. But they are antidepressants though just like you mention OP depression mostly due to Kappa agonism.(the mechanism of which:the depression) I don't know)

Similarly with kappa antagonists - how can buprenorphine be a remedy for cocaine addiction for instance if it actually should increase its effects? I caught myself that just after buprenorphine kicks in, I tend to use much more tobacco as if there was a synergistic dopamine kick, I imagine the same is true for cocaine, so it's a bit like treating a strong stimulant addiction with a weaker stimulant that partially substitutes for the stronger one but on top of that potentiates it if they're taken together. How is that anti-addictive?

Buprenorphine is a partial MOR agonist in addition to KOR antagonism so it is probably not the best candidate with respect to the thread topic ie anti-addiction effect of ibogaine and KOR agonists. It will indeed potentiate the effect of cocaine So yeah, it is more like methadone, not really antiaddictives in the true sense just more convenient OP!

Selective Kappa agonists will be things like SalvinorinA or Menthol found in mint plants like peppermint, spearmint..etc (a weak agonist but nethertheless kappa selective). Salvia is actually from the same mint family) or synthetics like U-50488 (notice the 1 carbon difference with the popular opiate RC U-47700 (a MOR agonist w/7-10x morphine!!!!

 

[DotChem]

@ solipsis: that's what I thought too. The question is: can the hallucinogenic effect of Ibogaine be dissociated from its anti-addictive effect say by eliminating the 18-methoxy of ibogaine? Ibogamine. voacangamine, 18MC and related alkaloids have all kappa OP activity. So the hallucinogenic 2A type that people are trying to avoid may not work, lest the anti-addiction effect is also suppressed along with the underisable 2a agonism....but who knows?

 

[Limpet_Chicken]

I Imagine that the psychic processes are as important as the physical and pharmacological. After all an addict must want to quit. The psychedelic properties could well prove to act as a teacher, other psychedelics can., and for me, have.
I used AMT and MXE to help deprogram myself of PTSD, by going off for long solo meditative hiking sessions and whilse successful IMO most of the effect was already in me, I just needed help to get it out again, and to be able to look at highly
emotionally charged themes and yet be dissociated enough to view therm dispassionately.

 

[Dracarys]

I have experimented with both ibogaïne as well as salvia, and i found them to have very different subjective effects. The NMDA-antagonist effect is much more present, at least in the felt effects, than the kappa effect. Ibogaïne does have some simmilarity with salvia, but much more with N2O. It even has effects that are somewhat simmilar to hallucinogenic tryptamines, though differently. In the dark you can get some of those fluorescent type colourfull Visuals that classic hallucinogens tend to produce, but they're not as elegant and caleidoscopic, but more a jackson pollock type of chaotic randomness. All of these effects are clearly present. When you take so much iboga that you get strong distinguishable salvia-like effects, you automatically also get very powefull tryptamine-like effects and the NMDA-antagonist effect will still be dominant.

 

[Limpet_Chicken]

How was the ibogaine, physially? was it a rough stimulatory experience on the body. Would love to explore moderate doses but I really do not get on well with adrenergic crap. Not harmful I just fucking loathe it.

I didn't experiment much with the iporuru for that reason. Was it ibogaine or iboga?

 

[Dracarys]

I ate around 15 grams of iboga rootbark. The first time i ate it all at once, the second time i ate slightly more, but spread over a period of two days. The first time was physically demanding, and the second time was actually not that hard, physically. The puking is probably the hardest part, because you realy puke like hell. If you trie to eat something, it will come straight out again. So there was some dehydration and not eating for three days the first time. The second time, i didn't have to vomit, because the dose was spread over multiple days. The experience was not that rough then, and it was shorter. I believe that this realy is the way to go with iboga. The Bwiti also do it this way. You just eat iboga until you blood is sort of saturated with the stuff, but because you have spread it out over several days, your stomach and guts aren't burdened with large amounts at once.