Introduction to Ibogaine & Noribogaine
This section requires expansion
Preparing Ibogaine from Tabernanthe Iboga
Methods of administration
Method 1: Home-friendly Tek
Put the rootbark into a large clean jar and add approx half a 70cl bottle of vodka, two cups of red wine and the juice of a lemon. Some users like to also add a half-teaspoon of vinegar. Shake vigorously and then leave to stand for one week, shaking occasionally. After one week has passed, empty the contents into a bowl or pan and place gently over boiling water. DO NOT DO THIS CLOSE TO A NAKED FLAME AS ALCOHOL IS HIGHLY FLAMMABLE. ENSURE THE AREA IS WELL VENTILATED. Alcohol boils at around 80 degrees centigrade, (as opposed to water which boils at 100). When the alcohol has boiled gently away, remove the bowl and strain the contents through cloth. (The solid that remains should no longer have the bitter taste it did prior to beginning the extraction. If it does, mix everything back together and return it to the jar for another week. Then repeat the above.) Assuming that the solid is not now distinctly bitter, discard it and allow the liquid that remains after straining to stand for about 12 hours. Storage - It is recommended you consume the extract within a few days of making it. However, if necessary, it can be stored for about 2 - 3 weeks in a domestic refrigerator. After this period it will begin to brew, and the composition will be altered. Smelling the extract will tell you if it's started to deteriorate
In this case it was for the root/root bark of tabernanthe iboga used as the plant material, which may contain up to 2.5 % or 6 % alkaloids respectively. The plant material was extracted with methanol four times, filtered and the methanol reduced to a small volume. An equal amount of water and acetic acid solution is added and shaken with petroleum naphtha, which is then separated and backwashed with acetic acid solution. All the aqueous phases are combined. The aqueous phases are reduced in volume, then basified with ammonia hydroxide. This is then extracted four times with ethylene
dichloride (possibly chloroform too). The solvent is washed with water, dried and concentrated. An equal amount of ethanol is added and the whole reduced to the original volume, then about twice the amount of ethanol is added. After chilling in the fridge for two days or so, ibogaine crystallises out, and can be collected by filtration. The remaining liquid was again reduced in volume and re-chilled for a second crop of ibogaine. Evaporation to dryness of the liquid yielded other alkaloids and residual ibogaine, which can be separated by chromatography, though can be laborious. To purify the ibogaine 100 mg of the crude ibogaine, as obtained above, was dissolved in 1 l of acetone, then 53.1 ml of 1:1 HCl was added, with ibogaine HCl precipitating (108 mg in this case) out straight away, this compound being relatively insoluble in acetone, compared to the base. Isolated by filtration.
Extraction of T. iboga root (TA). One kg (2.5 L) of powdered T. iboga root and 5 L of 0.5% acetic acid were placed in a 6 L plastic bucket, stirred occasionally for one hour, and filtered through a cloth sack. The sack was wrung to expel all possible liquid from the root powder and the filtrate (pH = 3-4) was basified using 60 mL of 30% ammonia. The resulting flocculent, medium greenish-brown precipitate of TA was patiently gravity filtered through 30 cm filter paper and thoroughly rinsed with distilled water. This procedure was repeated twice more on the same root powder. The filter papers bearing the TA were placed on paper towels on a wire rack and left in a warm draft until successive weighings detected no more than 0.3% loss per day. The hard, dark brown solid weighed 30.037 g (3.0%) and was ground in a mortar and sifted to give a fine brown powder.
Conversion of alkaloids to the hydrochlorides (PTA HCl). 28.00 g of powdered TA was placed on a filter paper in a funnel and 450 mL of acetone was added in portions with gentle stirring. The funnel was removed and 2 mL of concentrated HCl was slowly added dropwise to the flask with swirling, occasionally adding a trace of PTA HCl from a previous batch to initiate precipitation. After waiting a few minutes to allow precipitation to begin, dropwise HCl (2.8 mL) was added with swirling until the liquid became acidic according to pH paper. A final 0.4 mL of HCl was added dropwise and the flask was placed in the refrigerator overnight. The yellow powder was scraped from the sides of the flask, filtered, rinsed with 84 mL of acetone, and dried at room temperature to give 9.493 g (33.9%) of PTA HCl. The black, spent TA weighed 14.521 g (51.9%) after drying.
Ibogaine HCl. 9.712 g of PTA HCl was patiently dissolved in 150 mL of boiling 95% ethanol, set overnight at room temperature, refrigerated for two hours, and the mother liquor was decanted from the yellow crystals (4.412 g). Recrystallizing again from 80 mL of 95% ethanol gave 3.666 g of mostly pure ibogaine HCl.
Recovery of residual alkaloids (RA). Most of the acetone was distilled from the filtrate from the preparation of PTA HCl and the remainder was evaporated using a stream of air. The dark residue was dissolved in 400 mL of distilled water, filtered, and basified to pH 9 using 3 mL of 30% ammonia. The medium yellow suspension was filtered through a fresh coffee filter paper and left on a warm surface to dry. The chunks of light, chalky, off-white alkaloid residue weighed 4.750 g (17.0%).
Extraction of V. africana trunk bark (VTA). One kg of powdered trunk bark was extracted in the same manner as the T. iboga root above, resulting in 59.723 g (6.0%) of crumbly brown voacanga total alkaloids (VTA).
Conversion of alkaloids to the hydrochlorides (VPTA HCl). 75.00 g of VTA was treated in a manner similar to the PTA HCl above, resulting in 35.929 g (43.6%) of medium brown VPTA HCl. The spent VTA weighed 31.534 g (42.0%).
Recovery of residual alkaloids. The filtrate from the preparation of VPTA HCl was treated in a manner similar to the PTA HCl filtrate above, resulting in 12.119 g (16.2%) of chalky, off-white solid.
Different Uses for IbogaineIbogaine has been used at high doses for addiction/dependence therapy for opiates, cocaine, alcohol, nicotine, and methamphetamine. Historically, it has been used as a mild stimulant and social enhancer at lower doses due to the fact that hallucinations are not experienced at such levels.
The dangers of IbogaineThese are the dangers common to all psychedelic drugs:
Accidental injury. When on a psychedelic drug, it is easier to accidentally injure yourself. Also because of the disorientating and potentially delusion inspiring nature of the experience, you could be lead to inflict harm on others or yourself. People have fallen off rooftops, run into traffic, attempted to throw people off rooftops as 'sacrifices', drowned, and so on. The best way of protecting against this is to have a friend with you who is sober to look after you and handle any negative situation that might arise.
Bad trips. A bad trip is a negative psychedelic experience. It can range from a mildly negative feeling of anxiety/discomfort, to full-blown psychosis. Bad trips usually ruin a psychedelic experience for the tripper and everyone else. Most bad trips are manageable, just very uncomfortable and difficult. Some are extreme and unmanageable though. It's not uncommon for a bad trip to result in lingering psychological issues. Usually just a few days of negative emotions and anxiety. Sometimes, however, a week or so of serious anxiety, destabilized mental state and impaired functioning is possible. On very rare occasions, a month or two of severely diminished functioning, traumatized mental state, depression & crippling anxiety can occur. More information on bad trips can be found here. The best way of avoiding a bad trip is having the correct set and setting.
Permanent psychosis. Psychedelics are believed by researchers not to cause permanent psychosis, however they could trigger a latent mental illness in someone who was already predisposed to it, or make existing mental illnesses worse. If there is a history of mental illness in your family, you are more likely to be predisposed. Everyone is at some risk, however.
PTSD, anxiety disorder, depression & depersonalization. There are anecdotal reports of the trauma inflicted by some bad trips leading to depression and anxiety which while usually temporary, could potentially develop into lasting disorders. While no different to the potential of any traumatic event to cause lasting disorders, nonetheless this is a danger of psychedelic drug use.
"In June 1935, a 44 year-old woman died in France approximately 4 hours after receiving a dose of ibogaine of about 4.5 mg/kg p.o. The cause of death was concluded to have been acute heart failure in an autopsy carried out at the Forensic-Medical Institute in Zurich (176). Autopsy revealed evidence of a prior myocardial infarction of the left ventricle, severe atherosclerotic changes, and 70 to 80% stenosis of all three major coronary artery branches. This patient had a history of hypertension, and inverted T waves were noted on EKG three months prior to the patients death. The autopsy report concluded that the patients preexisting heart disease was likely to have caused the patients death, and it specifically excluded the possibility of a direct toxic effect of ibogaine. The report acknowledged the possibility that an interaction between ibogaine and the patients preexisting heart condition could have been a contributing factor in the fatal outcome."
176. W. Baer, Forensic Subsequent Autopsy/Report Case # N-138 1991. University of Zurich, Switzerland.” 
“The patient died 19 hours later of respiratory arrest. Some evidence suggested the possibility of surreptitious opioid use in this case, which was noted in the Dutch inquiry (178) and which is another source of uncertainty in this fatality. [n.b. Ibogaine has been shown to increase the effects and toxicity of opiates (Popick and Glick, 1996).]
178. G. van Ingen, Pro Justitia No. 93221/I057, Dept. Justice, The Netherlands, Lab. Forensic Pathol., 1994.”
“Prior complaint of recurrent intestinal malaise and diarrhea. "On April 21, though, she flew back down to Miami for a medical exam at the U. of Miami--part of the followup to her Panamanian re-treatment. No ill-effects of Ibogaine--but still no explanation of her diarrhea and recurrent vomiting. She was released from the hospital. Much later that evening she was found dead at the apartment where she was staying, collapsed in her vomit. Estimated time of death, 9:40 PM." ”
"The coroner, Dr Paul Knapman, found that JW died approximately 40 hours after ingesting 6g of a Tabernanthe iboga preparation, (T. iboga is the source of numerous active alkaloids including ibogaine), in an attempt to break a lengthy heroin addiction, having had no success with other detoxification strategies."
“The death occurred about one and a half hours after taking the dose. "The woman, aged 35 years and weighing 63 kg, had used the drug previously on one occasion without problem." There appears to be no information about whether she had taken advised medical tests.”
“Private Correspondence to Ibogaine List from a Close Relative involved in treatment:
Died 3 days after an ibogaine detox in Las Vegas, Nevada. According to a relative on the Ibogaine List an autopsy stated that cause of death was due to vascular heart disease. Apparently this is something which would not show up on a standard EKG but could be detected using a stress test.”
“UNION-TRIBUNE STAFF WRITERS,
By Anna Cearley and Penni Crabtree.
February 2, 2006.
"TIJUANA - A 38-year-old Santa Barbara man died Tuesday while receiving treatment at an alternative detox clinic that primarily serves U.S. citizens struggling with drug addictions. The cause of death was pulmonary thrombosis, according to an autopsy report."
Definition of Pulmonary Embolism:
The obstruction of the pulmonary artery or a branch of it leading to the lungs by a blood clot, usually from the leg, or foreign material causing sudden closure of the vessel. (Embolus is from the Greek "embolos" meaning plug.)
The risk factors for pulmonary embolism include advanced age, cancer, genetic predisposition, immobilization (especially in the hospital), pelvic or leg trauma, pregnancy, and surgery.”
Journal of Analytical Toxicology, Vol. 30, Issue 7, pp.434-440. Pub. Sept. 2006, Received Mar. 2006.
"Distribution of Ibogaine & Noribogaine in a Man Following a Poisoning Involving Root Bark of the Tabernanthe iboga Shrub".
"In the present paper, we report for the first time the tissue distribution of ibogaine and noribogaine, the main metabolite of ibogaine, in a 48-year-old Caucasian male, with a history of drug abuse, found dead at his home after a poisoning involving the ingestion of root bark from the shrub Tabernanthe iboga."
"In the blood, concentrations of ibogaine and noribogaine were 5-20 fold greater than those reported by Mash et al. (16) after a single oral dose of 800 mg of ibogaine in humans. The highest concentrations were found in the blood sample drawn at the death scene."
"The differences in the concentrations of ibogaine and noribogaine in blood drawn at the scene and blood taken at the autopsy may indicate that degradation (oxidation) of these two drugs occured after death."
Additional resource: http://myeboga.com/fatalities.html
Available online at: www.jatox.com/abstracts/2006/september/434-bressolle.html
D.C. Mash et al., Ibogaine: complex pharmacokinetics, concerns for safety, and preliminary efficacy measures. Ann. N.Y. Acad. Sci. 914: 394-401 (2000).”
Effects of Ibogaine/Noribogaine
The effect of ibogaine lasts between 15 and 36 hours, depending on the dose and individual metabolism. A longtime addict should allow her-/himself a convalescent period of one to three days after the 2 days dedicated to ibogaine. Methadone users should allow themselves at least a week. 
"Duration lasted anything from 12hrs to 6 days although the latter was extremely unusual. Generally people would hallucinate for up to 12 hours and then enter stage 2, which was characterized by introspective reflection. Not much communication would take place but restlessness would begin to be apparent after the 12th hour (except for those who were hit really hard). Stage 2 could last up to 24 hours plus and then would move into a desire for
sleep and discomfort in the body. At this point [the author] would offer valiums to help the subject sleep if they were distressed by the discomfort and inability to sleep. After waking from the sleep (however short that may have been) they usually moved into stage 3 characterised by optimism and an experience of reset. They were aware they were clean and were happy about it at this point. With some people physical discomfort lasted some
days in which case they would stay longer at the farm. [Author] would say 5 out of the 18 people treated suffered extremely physically. Getting sick at the 12 hour point and then retching for the next 12 hours or so. Followed by a weakness and nausea that could continue for another 12 hours (24 in total). Any longer than that and [author] would assume that withdrawal was taking place. This happened more frequently with women than men (see discussion
on women). This is something [the author] have never been entirely clear on and may warrant discussion in the manual. If someone is very sick 12 hours into the experience what can one do and does it indicate withdrawal symptoms (the nausea was usually accompanied by sweats and cramps and leg twitching). Can we administer anti nauseates at this stage and will they help? This is not something [author] experimented with. The problem with the vomiting was that it was often dry retching as there was obviously nothing to bring up. This can tear the oesophageal lining, which [author] believe can be dangerous. [Author] would definitely want some information on how to alleviate this or prevent it from happening. [Author] treated
one woman who had an experience for about 8 hours, 4 of which included hallucinating. She then however went into severe withdrawal for the next five days (during which [author] stayed with her). [Author] concluded from this and from my other experiences with women that women needed as much if not more ibogaine than men, something contrary to what I had read. I had always been led to believe that women should have a slightly lower dose (DR Mash advised this) but as a result I found that ibogaine didn't work as efficiently for women as for men." 
This depends, to some extent, on the purpose for which the ibogaine is being ingested. A long-term heroin addict will not necessarily have the same experience as a patient wanting a resolution to chronic depression, post-traumatic-stress-syndrome or anxiety
* 40 minutes after ingestion a buzzing in the ears heralds dreamlike visions, dancing lights, flashes of images, symbolic or actual representations of current subconscious themes.
* Some 2 to 4 hours later "the waken dreams" will slowly fade away giving room to what is often described as resetting the biochemistry of the brain, i.e. an integration of the first phase.
* 20 to 36 hours after ingestion the last signs of dizziness, ataxia, inability to sleep will disappear and the patient is fully functional again.
Ibogaine is demethylated to 12-hydroxyibogamine (noribogaine), which has been characterized to linger in the blood for over 24 hours, and to exhibit a higher affinity for the SERT protein than ibogaine . Apparently, there is ongoing research at the University of Miami to more specifically identify the mechanisms involved in the metabolism of ibogaine and noribogaine, funded generously by the Multidisciplinary Association for Psychedelic Studies (MAPS) . Interestingly, significant inter-individual differences have been evident in the current analysis of the metabolism of ibogaine; such studies have categorized individuals as either extensive or poor ‘metabolizers’ . There have been studies conducted on the metabolites of 18-MC as well; the major metabolite identified was 18-hydroxycoronaridine (18-HC). However, two other metabolites were characterized as hydroxylated metabolites.
It should also be noted that both ibogaine and noribogaine are stored in adipose tissue, which likely contributes to the comparatively long duration of effects that characterize both compounds. Studies on the roles of the various cytochrome P450 enzymes with selective inhibitors and antibodies failed to reveal any role for this family of enzymes in the metabolism of the alkaloids in iboga. However, observed results indicate that the polymorphic enzyme, CYP2C19, plays a critical role in the metabolism of 18-MC, and therefore likely plays a role in the metabolism of other Ibogaine-related compounds .
Multiple actions of ibogaine have been described in scientific literature; monoamine oxidase inhibition, agonism of 5-HT2A receptors as well as κ-opioid, sigma-1 and sigma-2. It has also been characterized as modulatory for ligand binding to µ-opioid receptors, antagonism of dopaminergic (DAT) and seratonergic (SERT) transporters, antagonistic at both N-methyl-D-aspartate (NMDA) and nicotinic receptors [5, 9]. Interestingly, studies with laboratory animals have shown attenuation of withdrawal symptoms in opiate dependent animals, attenuation of morphine, cocaine, and ethanol self-administration - as well as synergism with morphine on antinociception, modulation of anxiety, and an amplification of learning and memory capabilities. One of the most intriguing facets of the pharmacodynamics of ibogaine is that some of the subjective and observed effects last much longer than any pharmacokinetic model could support. The primary mood elevating effects generally persists for a day or two subsequent to ingestion, while tissue concentrations of ibogaine have already reduced to minimal levels. The mood elevating effects lasts for days to weeks, when both ibogaine and its active metabolite noribogaine is no longer present in measurable quantities. These prolonged effects are taken to represent more complex biochemical, neuroendocrine, and possible structural and functional changes in terms of plasticity, signal transduction, and modulation of gene expression
Ibogaine Effects Brain Energy Metabolism
The foundations of such modification of multiple functional domains that comprise neural activity are expected to be associated with some profound metabolic changes in the expression of proteins. In a study observing the effect of ibogaine, administered via intraperitoneal injection to12 male Wister rats (two groups treated with 20 mg/kg, while two control groups received water), changes in protein expression were observed to be most significant 72 hours subsequent to ibogaine administration . The glycolytic enzymes glyceraldehydes-3-phosphate dehydrogenase (G3P), aldolase A, and pyruvate kinase were increased about 3.2-, 2.5-, and 2.9-fold, respectively, at 72 hours. When compared to levels at 24 hours, the levels of enzymes were only slightly heightened above control values – averaging between 1.1- and 1.4-fold increases. Each of these enzymes participates in central metabolic pathways dealing with the production of energy-rich compounds, therefore suggesting that ibogaine interferes with aggregate metabolic turnover. The influence of these effects is best observed in phases of high energetic demands, during which they can support constant production of metabolic products – in the case of this study, maintaining neurotypical ratios of ATP to ADP instead of a decrease of ATP to ADP. However, the authors of this study are careful to caution that it is unclear whether the elevated energy availability 72 hours subsequent to administration is a secondary, compensatory effect resulting from elevated demand on energy during the acute phase in the first few hours. Regardless, they posit that the dissipation of capabilities characterizing functional elements in cells to produce high-energy metabolic products underlies the functional and structural changes in drug dependence. Therefore, modulation towards a higher metabolic turnover would be favorable, and they suggest that it is reasonable to assume that the induction of energy metabolism directly influences mental agility and acuity, learning, and retrieval of memory.
Ibogaine Stabilizes the Desensitized Conformation of Nicotinic Receptors in a Reward Pathway
In a study published in 2008, Glick et. al. demonstrated that, due to the high densities of α-3-β-4 nicotinic receptors in the medial habenula and interpeduncular nucleus (IPN), as well as moderate densities in the basolateral amygdala, with local administrations of 18-Methoxycoronaridine (18-MC), the introduction of an iboga alkaloid congener changed the behavior of rats dramatically. The researchers observed that local intracerebral injections, most potently in the IPN, were able to elicit decreased self-administration of several common drugs of abuse , including morphine, cocaine, methamphetamine, nicotine, and ethanol – as well as reduced sucrose self-administration . They identified the primary mechanism of action to be a selective blockage of α-3-β-4 nicotinic receptors, though not as a traditional open-channel blocker. Their support was a comparison of activity to mecamylamine and α-conotoxin, two nicotinic acetylcholine receptor antagonists. They suggest that it acts as a non-competitive, negative allosteric modulator acting by stabilizing the ligand-bound, desensitized state of the nicotinic receptor. This renders 18-MC to have a pretty unique antagonist profile, in that it shouldn’t have significant effects on fast cholinergic transmission and therefore shouldn’t induce peripheral side effects associated with other nicotinic antagonists like mecamylamine. The IPN receives its main input from the medial habenula, forming the habenula-interpeduncular pathway in the fasiculus retroflexus. It has been known since the 1980s that the habenula-interpeduncular pathway can function as a reward system distinct from the more commonly known mesolimbic pathway – a study preformed by Sutherland and Nakajima in 1981 found that the two pathways likely exhibit a mutually modulatory relationship. Therefore, 18-MC might be characterized to act in the habenula-interpeduncular pathway to selectively dampen the activity of particular functioning components of the mesolimbic dopaminergic pathway – namely, the signals underlying addictive tendencies. The researchers further suggest that 18-MC appears to act in three circuits: the medial habenular-interpeduncular, basolateral amygdala, and dorsolateral tegmental pathways, and this proposition has been confirmed by additional research performed by Taraschenko, Shulan, & Maisonneuve . The relative significance of the activity of 18-MC at each one of these pathways appears to vary with the particular reward in question; the basolateral amygdala is significantly less important for opiate than stimulant reward, and some preliminary data from this study suggest that intracerebral infusion of 18-MC into the basolateral amygdala actually has no effect on morphine self-administration. Regardless of which pathway experiences the greatest impact from exposure to the compound, 18-MC (and therefore, ibogain and related compounds) should promote a desensitization of receptors and reduce inhibitory GABAergic influence, ultimately altering dopamine levels in the mesolimbic reward pathway.
Ibogaine & Noribogaine Stabilize the Desensitized Conformation of the Serotonin Transporter
However, a study performed in 2007 adds some additional nuance to the activity of iboga alkaloids – nicotinic antagonism isn’t the only activity of the compounds. Jacobs, Zhang, Campbell & Rudnick found that ibogaine inhibited the serotonin transporter (SERT), which is responsible for the reuptake of the neurotransmitter out of synaptic clefts. The researchers propose that the compound binds to, and stabilizes the state of SERT, from which serotonin dissociates to the cytoplasm – in contrast with cocaine, which stabilizes the state of the transporter protein that binds extracellular serotonin. It is important to note that SERT undergoes a conformational transition between two distinct states: an extracellular state, stabilized by cocaine, and a cytoplasmic state, favored in the presence of serotonin. While the majority of SERT inhibitors are indeed competitive, an inhibitor that binds the cytoplasmic state likely wouldn’t act as a competitive inhibitor due to the fact that it would stabilize a conformation of SERT to which extracellular serotonin would be unable to bind. Interestingly, the researchers found that the inhibition of serotonin wasn’t reversed by higher concentrations of serotonin, and when administered concurrently with β-CIT, a cocaine analog, ibogaine acted as a competitive inhibitor of the effects, ostensibly due to decreased accessibility of extracellular positions characterizing SERT. The compound’s noncompetitive inhibition of transport suggests that ibogaine and serotonin don’t bind to the same site, yet the competition between serotonin and cocaine analogues suggests that those two do indeed bind at overlapping sites – thus the researchers speculate that serotonin and ibogaine bind to mutually exclusive sites. It makes sense that ibogaine and serotonin would have related effects at a common protein; they both contain an indole nucleus with an amino group separated by two carbons from the 3-position on the indole ring, as well as a substituted 5-position. The first figure below presents an excellent comparison of the two structures, while the second provides a comparison of the binding affinities of Ibogaine vs. Noribogaine.
Chemistry of Ibogaine
Column 1 Column 2 Systematic (IUPAC) name: 12-methoxyibogamine Synonyms: 12-methoxyibogamine Molecular Formula: C20H26N2O, C20H26N2O.HCl Molar mass: 310.44 g/mol, 346.89 g/mol (hydrochloride) CAS Registry Number: 83-74-9 Melting Point: 152-153°C Boiling Point: no data Flash Point: no data Solubility: Freebase soluble in ethanol, ether, chloroform, acetone, benzene; practically insoluble in water. Hydrochloride soluble in water, methanol, ethanol; slightly soluble in acetone, chloroform; practically insoluble in ether. Additionnal data: Freebase sublimes at 150°C (0.01 mmHg); pKa 8.1 (in 80% methylcellosolve). Hydrochloride decomposes at 299-300°C Notes: Freebase aspect : prismatic needles; crystallized from ethanol. Hydrochloride aspect : crystals
Ibogaine content of Tabernanthe Iboga :
- Root : 1.27 %
- Rootbark : 2-6 %
- Stems : 1.95 %
- Leaves : 0.35 %
Forms/Sources of Ibogaine1. Tabernanthe iboga - 6 to 10 g/kg of ibogaine from Iboga, depending on samples
2. Voacanga Africana – 5-10% in root, 4-5% in trunk, .3-.45% in leaves, 1.5% in seeds
3. Tabernaemontana -
4. Tabernanthe orientalis
5. Tabernanthe pubescens
6. Apocynaceae family – Contains ibogaine-like compounds
7. Callichilia barteri
8. Peschiera echinata – 2% alkaloid in leaves
9. Voacanga schweinfurthii var. puberula – 3.5% in root bark
Legal status of Ibogaine
Ibogaine is a controlled substance 21 CFR 1308.11
USABoth Ibogaine and its source plant Tabernanthe iboga are Schedule I in the United States. This means they are illegal to manufacture, buy, possess, or distribute (sell, trade or give) without a DEA license 
As of late 1998, the Home Office Drug Unit reported that Ibogaine is not specifically listed in the Controlled Substances List in the UK. The Medicines Control Agency (MCA) does not recognize Ibogaine as a drug, but does note that it is credited with having hallucinogenic properties. This apparently means that it is legal to buy or import for personal use, but to sell it, administer it to others, or make it available as a treatment would likely be illegal without a prescription.
We have been told that ibogaine and its parts are uncontrolled in Finland.
Tabernanthe iboga, Tabernanthe manii, and ibogaine were all added to the list of controlled substances in France on March 12, 2007. See rb.juris-classeur.com: "Tabernanthe iboga, Tabernanthe manii, ibogaine, ses isomères, esters, éthers et leurs sels qu'ils soient d'origine naturelle ou synthétique ainsi que toutes préparations qui en contiennent." (thanks CHG) (last updated Mar 31, 2007)
Ibogaine is not scheduled in Poland. (unconfirmed)
We have been told that T. Iboga as a plant (including it's dried and/or powdered parts, extracts and pure ibogaine) are not listed in any group of the PAS list, so it should be legal to possess. It is probably not legal to sell it as a food supplement.
We have heard that purified ibogaine is the equivalent of a Schedule I drug in Sweden. It is unclear whether the plant T. iboga is also restricted. (unconfirmed)
Purified ibogaine is restricted. It is unclear whether the T. iboga root powder is also restricted, but may be
CanadaIbogaine appears to be uncontrolled in Canada. We have been told that it is available in headshops in Vancouver.
JapanWe have been told that powdered iboga root is available in headshops in Japan.
ArticlesPlease visit the document archive and perform a search including 'Ibogaine' for pages of documents related to Ibogaine. Here are a few:
Ibogaine File Archive
Ibogaine File Archive
History of Ibogaine File Archive
History of Ibogaine File Archive
Attenuation of Alcohol Consumption with Ibogaine File Archive
References1. History Including Research from 1995 & 1996. (1999). Ibogaine: A Brief History [Review Article]. Retrieved May 2, 2009, from The Ibogaine Dossier Web site: http://www.ibogaine.desk.nl/ibo-hist.html
2. Maçiulaitis, R., Kontrimaviçiute, V., Bressolle, F., & Briedis, V. (2008). Ibogaine, an anti-addictive drug: pharmacology and time to go further in development. A narrative review. Human & Experimental Toxicology, 27, 181-194.
3. Traditional Use/History. (2008, November). In Iboga/Ibogaine (pp. 10-23). N/A. (Original work published 2008) Retrieved from https://drugs-forum.com/forum/att...4&d=1226687991
4. Alper, K. R., Lotsof, H. S., & Kaplan, C. D. (25, 2007, August). The Ibogaine Medical Subculture. Elsevier, 115, 9-24.
5. Paskulin, R., Jamnik, P., Zivin, M., Raspor, P., & Strukelj, B. (16, 2006, September). Ibogaine affects brain energy metabolism. Elsevier, 552, 11-14.
6. Strubelt, S. (2008, February). The Near-Death Experience: A Cerebellar Method to Protect Body and Soul - Lessons from the Iboga Healing Ceremony in Gabon. Alternative Therapies, 14(1), lessons from the iboga healing ceremony in Gabon.
7. Glick, S. D., Sell, E. M., & Maisonneuve, I. M. (2008). Brain Regions Mediating α3β4 Nicotinic Antagonist Effects of 18-MC on Methamphetamine and Sucrose Self-Administration. Behavioral Pharmacology, 599, 91-95.
8. Taraschenko, O. D., Shulan, J. M., Maisonneuve, I. M., & Glick, S. D. (2006, December). 18-MC Acts in the Medial Habenula and Interpeduncular Nucleus to Attenuate Dopamine Sensitization to Morphine in the Nucleus Accumbens. Synapse, 61, 547-560.
9. Jacobs, M. T., Zhang, Y.-W., Campbell, S. D., & Rudnick, G. (5, 2007, October). Ibogaine, a Noncompetitive Inhibitor of Serotonin Transport, Acts by Stabilizing the Cytoplasm-facing State of the Transporter. The American Society for Biochemistry and Molecular Biology, 282(40).
10. Ibogaine Related Fatalities [Ibogaine & Iboga Related Fatalities]. (2008). Retrieved May 2, 2009, from Myeboga Web site: http://myeboga.com/fatalities.html
11. How Aspirin Turned Hero [Sunday Times]. (1998, September 13). Retrieved May 2, 2009, from http://www.opioids.com/heroin/heroinhistory.html
12. Mash, D. C., Ph.D., Staley, J. K., Ph.D., Pablo, J., M.S., Raymon, L., Pharm.D.,Ph.D., Levin, B., Ph.D., Doepel, F. M., D.V.M., et al. (1999, November). Development of Ibogaine as an Anti-Addictive Drug. University of Miami School of Medicine, progress report. Abstract obtained from The Ibogaine Dossier.
13. Drugs.com. (n.d.). Drug Addiction. In Iboga [Clinical Overview]. Retrieved May 3, 2009, from Walmart Web site: https://drugs.com/npp/iboga.html
14. Zhang, W., Ramamoorthy, Y., Tyndale, R., Glick, S., Maisonneuve, I., Kuehne, M., et al. (2002, June). Metabolism of 18-Methoxycoronaridine, an Ibogaine Analog, to 18-Hydroxycoronaridine by Genetically Variable CYP2C19. Drug Metabolism & Disposition, 30(6), 663-669. Abstract obtained from The Ibogaine Dossier.