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Mitragynine — Compound Profile

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Mitragynine

2D structure of Mitragynine (C23H30N2O4) — source: PubChem CID 3034396
2D structure of Mitragynine (C23H30N2O4) — source: PubChem CID 3034396

Chemistry

  • CID: 3034396 · PubChem
  • Formula: C23H30N2O4
  • Molecular weight: 398.5 g/mol
  • IUPAC: methyl (E)-2-[(2S,3S,12bS)-3-ethyl-8-methoxy-1,2,3,4,6,7,12,12b-octahydroindolo[2,3-a]quinolizin-2-yl]-3-methoxyprop-2-enoate
  • CAS: 4098-40-2

Family & pharmacology

Family: Indole alkaloid (corynantheidine-type)

Pharmacological class: Partial agonist at mu-opioid receptors with additional activity at delta- and kappa-opioid receptors; also reported to interact with adrenergic and serotonergic systems in preclinical studies

Natural source: Mitragynine is the most abundant alkaloid in the leaves of Mitragyna speciosa (kratom), a tree in the coffee family (Rubiaceae) native to Southeast Asia, particularly Thailand, Malaysia, Indonesia, Myanmar, and Papua New Guinea

Historical context

Mitragynine was first isolated in 1907 by Dutch botanist E. M. Field from Mitragyna speciosa leaves, with its structure fully elucidated by Zacharias in 1964. The compound has been studied extensively as the primary alkaloid responsible for kratom's traditional effects, though 7-hydroxymitragynine (a minor alkaloid) has been shown in later research to be substantially more potent at mu-opioid receptors.

Traditional use

  • Chewed fresh or brewed as tea by laborers in southern Thailand and Malaysia to sustain work through heat and fatigue
  • Used in traditional Southeast Asian folk medicine for management of pain, cough, and diarrhea
  • Served in social and ceremonial contexts in rural Malay and Thai communities, sometimes as a substitute when other substances were scarce

Modern re-emergence

From the 2010s onward, kratom (and by extension mitragynine) became widely discussed in Western harm-reduction and self-management contexts, particularly in the United States. Regulatory status varies significantly by country: kratom is controlled in Thailand historically (now partially decriminalized since 2021), Australia, and several EU states, while remaining legal in others. Mitragynine as an isolated alkaloid is the subject of ongoing pharmacological research into analgesic mechanisms with reduced respiratory depression compared to classical opioids.

Safety

Documented adverse effects of kratom use include nausea, vomiting, constipation, tachycardia, and with chronic high-dose use, dependence and withdrawal syndromes. Case reports have described hepatotoxicity and seizures, often in the context of polysubstance use. Mitragynine is metabolized by CYP3A4 and CYP2D6; co-use with other serotonergic or opioid compounds, MAOIs, or strong CYP inhibitors has been associated with adverse interactions in case literature. Not recommended during pregnancy or with pre-existing liver conditions.

🏪 amama POV

Sourcing: amama sources kratom leaf powder directly from established partner farms in Indonesia (predominantly West Kalimantan and Sumatra), where the trees grow in their native habitat and leaves are harvested and dried using traditional methods. We do not sell isolated mitragynine — only whole-leaf kratom powder in which mitragynine occurs naturally alongside the full alkaloid spectrum.

Quality measures

  • Every batch is lab-tested for pesticides, heavy metals (lead, cadmium, arsenic, mercury) and microbiology (Salmonella, E. coli, yeast/mould)
  • Alkaloid profiling available on request — typical mitragynine content documented per batch
  • Certificate of Analysis (CoA) available on request
  • Sealed, opaque packaging to protect alkaloids from UV and oxidation; batch and lot codes on every package for traceability
  • No blends with synthetic enhancers or undisclosed additives — single-strain, single-origin powder only

Experience: amama has carried kratom since 2021 and it is one of the categories our team knows most intimately. Because we run two physical stores in Berlin-Neukölln in addition to the online shop, the team has in-person conversations about kratom every single day — strain differences, onset, tolerance dynamics, tapering — qualitative depth that purely online sellers simply don't see.

Customer feedback: Questions we hear in the store regularly are around strain differentiation (red vs. green vs. white), rotation to avoid tolerance, and comparisons between batches of the same strain. Customers tell us in person that batch-to-batch consistency and the ability to ask follow-up questions are the main reasons they return — feedback that rarely shows up in short online reviews.

Sources

  • PubChem CID 3034396
  • Wikipedia: Mitragynine; Mitragyna speciosa
  • Kruegel & Grundmann 2018, Neuropharmacology — 'The medicinal chemistry and neuropharmacology of kratom'
  • Hassan et al. 2013, Neuroscience & Biobehavioral Reviews
  • Warner et al. 2016, International Journal of Legal Medicine
  • EMCDDA kratom drug profile
  • Prozialeck et al. 2012, Journal of the American Osteopathic Association
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Nicotine — Compound Profile: Chemistry, Pharmacology, and Sources

Nicotine is a naturally occurring pyridine alkaloid from plants of the genus Nicotiana that acts as a full agonist at nicotinic acetylcholine receptors (nAChR) and ranks among the most intensively studied psychoactive substances in modern pharmacology. Pyridine alkaloid with a chiral structure; the pharmacologically active enantiomer is (S)-nicotine Full nAChR agonist with particular affinity for α4β2 and α7 subtypes in the central and peripheral nervous system Primary source is plants of the genus Nicotiana (Solanaceae), with N. rustica being especially potent at up to 18% nicotine content by dry weight Rapid pharmacokinetics with pulmonary absorption: onset in the CNS within 7–10 seconds, half-life 1–2 hours High addictive potential: neurobiologically, nicotine ranks among the most potent addictive substances known, comparable in the intensity of its reward-system hijacking to heroin or cocaine What Is Nicotine? Nicotine (IUPAC: (S)-3-(1-methylpyrrolidin-2-yl)pyridine) is a tertiary amine and bicyclic alkaloid first isolated and characterised from tobacco leaves in 1828 by German chemists Wilhelm Heinrich Posselt and Karl Ludwig Reimann. It belongs to the group of pyridine alkaloids and is biosynthetically assembled from L-ornithine and nicotinic acid via the putrescine–nicotinic acid pathway. As a secondary plant metabolite, nicotine presumably serves a defensive function in the plant against herbivores and insects — a mechanism explained by its acute neurotoxicity towards invertebrates. In humans, however, the same substance produces a complex pharmacological effect on the central and peripheral nervous system. Property Value IUPAC Name (S)-3-(1-methylpyrrolidin-2-yl)pyridine Molecular Formula C₁₀H₁₄N₂ Molecular Weight 162.23 g/mol CAS 54-11-5 PubChem CID 89594 Primary Sources Nicotiana tabacum, Nicotiana rustica Pharmacology: Mechanism of Action Nicotine acts as a full agonist at nicotinic acetylcholine receptors (nAChR), a family of ligand-gated ion channels (Na⁺/K⁺ and Ca²⁺) expressed in both the central nervous system and at neuromuscular junctions and autonomic ganglia. Two subtypes are of particular pharmacological relevance: α4β2-nAChR: Predominantly expressed in the mesolimbic dopamine system. Activation of this subtype by nicotine leads to dopamine release in the nucleus accumbens — this is considered the central mechanism of addiction development. PET imaging studies have shown that nicotine produces pronounced α4β2 occupancy even at very low concentrations (Brody et al., 2006, Arch Gen Psychiatry). α7-nAChR: Widely distributed in the cortex and hippocampus, modulates glutamate release and cognitive processes. This subtype is the subject of active research in the context of neurodegenerative diseases. Beyond this primary receptor binding, nicotine induces a cascade of neurotransmitter releases: dopamine (reward), noradrenaline (alertness, heart rate), acetylcholine (cognition), serotonin, and β-endorphin. This broad profile explains the subjectively experienced effects of relaxation, enhanced concentration, and mood elevation. With chronic exposure, a paradoxical receptor up-regulation occurs: although nicotine activates the receptors and causes short-term desensitisation, the total number of nAChR in the tissue increases. This mechanism is substantially involved in the development of tolerance and dependence (Benowitz et al., 2009). Pharmacokinetics The pharmacological effects of nicotine depend strongly on the route of administration, which determines the speed and extent of bioavailability: Route of Administration Bioavailability Onset Pulmonary (smoking) ~80% 7–10 seconds Nasal (rapé / snuff) ~50–70% 10–60 seconds Oral (snus, chewing gum) ~20–40% Minutes Transdermal (patch) ~10–30% Hours The plasma half-life of nicotine is approximately 1–2 hours, which is why the subjective effects are relatively short-lived — a factor that contributes to frequent repeated administration. The primary metabolite cotinine, by contrast, has a half-life of 16–20 hours and therefore serves in medicine as a biomarker for nicotine exposure. Metabolism occurs primarily via the hepatic enzyme CYP2A6. Genetic polymorphisms of this enzyme explain inter-individual differences in processing speed and may influence addiction risk (Malaiyandi et al., 2005, Clin Pharmacol Ther). Nicotine crosses both the blood–brain barrier and the placental barrier. Plant Sources Nicotiana tabacum The commercially cultivated standard tobacco. Nicotine content in the leaves typically ranges between 1 and 3% of dry weight, with considerable variation depending on preparation method and variety. N. tabacum is the basis of virtually all industrial tobacco products. Nicotiana rustica Known by indigenous names such as "Mapacho" (Amazonia) or "rustica tobacco," N. rustica is considered the most pharmacologically potent known Nicotiana species. Its nicotine content amounts to 6–18% of dry weight — depending on the analytical method and growing conditions, in some cases 5–10 times higher than N. tabacum. N. rustica is an integral component of ceremonially used tobacco preparations in indigenous cultures of South America. It forms the basis of many rapé formulations (ceremonial snuffs), in which it is combined with plant ash additives and other medicinal plants. Due to the high alkaloid content, even small quantities may trigger intense physiological responses; informed handling is absolutely essential. Other Sources Several species within the Solanaceae (nightshade family) contain nicotine in measurable but pharmacologically negligible traces: tomatoes (Solanum lycopersicum): ~100 ng/g fresh weight; aubergines (Solanum melongena): ~100 ng/g; peppers (Capsicum annuum): ~7–9 ng/g. These amounts are well below any physiologically relevant threshold. Clinical Significance Neurobiologically, nicotine is considered one of the most addictive substances known. The rapid onset, short half-life, and intense dopamine activation in the mesolimbic system create the classic conditioning loop characteristic of substance use disorders. The WHO classifies tobacco dependence as "Tobacco Use Disorder" (ICD-10: F17) and emphasises in its Global Tobacco Epidemic Report 2023 that tobacco continues to rank among the leading preventable causes of death worldwide. Therapeutic applications of nicotine are currently limited primarily to smoking cessation (nicotine replacement therapy: patches, chewing gum, nasal spray, inhaler). The efficacy of these approaches is well-established, although long-term abstinence rates remain moderate. In addition, active research is ongoing into α7-nAChR agonists in Alzheimer's dementia (cognitive neuroprotection) and in ADHD (attention modulation). To date, however, these approaches have not achieved clear breakthroughs in clinical development; the body of evidence remains exploratory. Safety Profile Acute toxicity: The oral LD₅₀ in humans is cited in the literature at approximately 0.5–1 mg/kg body weight. In an adult (70 kg), this corresponds to a potentially lethal dose of approximately 35–70 mg — a figure that may become relevant with improper handling of highly concentrated extracts or N. rustica products. Cardiovascular: Nicotine increases heart rate and blood pressure, causes vasoconstriction, and is contraindicated in pre-existing cardiovascular conditions. Pregnancy: Nicotine crosses the placental barrier and is associated with foetal developmental impairments, increased risk of premature birth, and possible long-term neurobiological consequences for the child. Interactions: Particular caution is warranted with concurrent use of MAO inhibitors (potentially dangerous sympathomimetic potentiation), certain SSRIs, and insulin therapy (nicotine may affect insulin sensitivity). Nicotine in the amama Context Within the amama.space range, nicotine is relevant exclusively in the context of rapé — a ceremonial snuff from indigenous Amazonian traditions that contains Nicotiana rustica as a core ingredient. Given the high alkaloid content of this species, an informed and respectful approach is essential. Further information on effects, application, and context can be found in our Rapé Guide and in the article Rapé Experience. amama does not sell pure nicotine products, conventional tobacco products, or vape products. Rapé is the only context in which nicotine plays a role within our range. Common Myths About Nicotine Myth 1: "Nicotine causes cancer." This statement is not scientifically accurate. Nicotine itself is not carcinogenic according to current research. The carcinogenic properties of tobacco smoke are attributable to combustion products — in particular polycyclic aromatic hydrocarbons (PAHs), nitrosamines, and other toxic pyrolysis products. Nicotine contributes to addictive potential, not to carcinogenesis. Myth 2: "Nicotine only occurs in tobacco." Incorrect. As outlined in the section on plant sources, nicotine is detectable in trace amounts in numerous Solanaceae species — including tomatoes, peppers, and aubergines. The quantities are pharmacologically insignificant, but demonstrate the widespread distribution of this alkaloid within the plant family. Myth 3: "Nicotine without smoking is harmless." This simplification is misleading. While forgoing combustion does eliminate the inhalation toxicity of smoke, addictive potential and cardiovascular effects are retained with every form of administration. Nicotine replacement products are considerably less harmful than smoking, but by no means risk-free — particularly in heart disease, during pregnancy, or with long-term use. References Benowitz NL, Hukkanen J, Jacob P III. Nicotine chemistry, metabolism, kinetics and biomarkers. Handb Exp Pharmacol. 2009;(192):29–60. doi:10.1007/978-3-540-69248-5_2 Brody AL et al. Cigarette smoking saturates brain α4β2 nicotinic acetylcholine receptors. Arch Gen Psychiatry. 2006;63(8):907–915. Malaiyandi V, Sellers EM, Tyndale RF. Implications of CYP2A6 genetic variation for smoking behaviors and nicotine dependence. Clin Pharmacol Ther. 2005;77(3):145–158. WHO. Report on the Global Tobacco Epidemic 2023. World Health Organization, Geneva. PubChem. Nicotine. CID 89594. https://pubchem.ncbi.nlm.nih.gov/compound/89594 Related Compound Profiles Mitragynine Nuciferine Ibogaine Last updated: April 2026. This article is for informational purposes only and does not constitute medical advice. Not a medicinal product. Always consult qualified medical professionals regarding health-related questions.

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Mesembrine — Compound Profile

Mesembrine 2D structure of Mesembrine (C17H23NO3) — source: PubChem CID 394162 Chemistry CID: 394162 · PubChem Formula: C17H23NO3 Molecular weight: 289.4 g/mol IUPAC: (3aS,7aS)-3a-(3,4-dimethoxyphenyl)-1-methyl-2,3,4,5,7,7a-hexahydroindol-6-one CAS: 24880-43-1 Family & pharmacology Family: Sceletium alkaloid (mesembrane-type tricyclic) Pharmacological class: Serotonin reuptake inhibitor (SRI) and phosphodiesterase type 4 (PDE4) inhibitor. Mesembrine inhibits the serotonin transporter (SERT) with potency comparable to SSRIs, increasing synaptic serotonin availability. The concurrent PDE4 inhibition — which raises intracellular cAMP — is a mechanistic feature not found in conventional SSRIs and may contribute to anxiolytic and cognitive effects observed in preclinical and clinical studies. Mesembrine does not exhibit monoamine oxidase inhibition at relevant concentrations. Natural source: Mesembrine is the primary alkaloid in Sceletium tortuosum (kanna), a small succulent plant native to the semi-arid regions of South Africa, particularly the Western Cape and Northern Cape provinces. The plant contains at least four major alkaloids (mesembrine, mesembrenone, mesembrenol, and mesembranol); mesembrine typically predominates in fermented preparations (called kougoed). Total alkaloid content varies significantly between chemotypes and growing conditions. Historical context Sceletium tortuosum has one of the longest documented histories of use of any psychoactive plant. The earliest written account was by Jan van Riebeeck, the Dutch VOC commander who established the Cape Colony, who recorded Khoisan use of kanna in his diary in 1662. Subsequent colonial-era accounts describe kanna as a valuable trade commodity between Khoisan groups, sometimes used in lieu of tobacco or exchanged for livestock. Mesembrine as an alkaloid was first isolated in 1898 by German pharmacologists Bodendorf and Krieger from dried Sceletium material. Its full chemical structure was elucidated over the following decades, with the mesembrane carbon skeleton fully described by the mid-20th century. Modern pharmacological characterisation of its serotonergic mechanism was established in the 1990s. Traditional use Khoisan and early Cape Coloured communities chewed, smoked, or used fermented kanna (kougoed) as snuff for mood elevation, sociality, and pain relief Hunters used kanna to suppress hunger and thirst on long treks; it was also used for toothache and intestinal complaints Kanna functioned as an important trade good between Khoisan groups across the Cape, sometimes commanding high barter value Fermentation (kougoed preparation) involved burying plant material and allowing it to ferment over days, which transforms alkaloid ratios — increasing mesembrenone relative to mesembrine and affecting potency Modern research context Scientific interest in mesembrine and Sceletium extracts accelerated from the 2000s. The commercial extract Zembrin® (a standardised 2:1 extract of Sceletium tortuosum) has been evaluated in multiple clinical studies. Harvey et al. published the first randomised controlled trial in humans in 2011 (J Ethnopharmacol 2011, PMID 22234675), demonstrating anxiolytic effects and improved cognitive flexibility in healthy volunteers. A subsequent randomised double-blind crossover trial (Nell et al. 2013) found that Zembrin attenuated threat-related amygdala reactivity in healthy subjects — a finding consistent with anxiolytic activity. The dual SRI+PDE4 mechanism distinguishes mesembrine from classic SSRIs, and its relatively rapid onset of effect (hours rather than weeks, as reported in qualitative user accounts) has been a subject of mechanistic interest. PDE4 inhibition alone (as seen in roflumilast) has antidepressant-like effects in animal models, potentially synergising with SERT blockade. Safety Mesembrine and Sceletium tortuosum preparations are generally considered to have a benign safety profile at low-to-moderate doses. Reported adverse effects include mild headache, nausea, and initial sedation. The most significant pharmacological interaction risk is with other serotonergic agents: co-administration of Sceletium preparations with SSRIs, SNRIs, or MAOIs raises the theoretical risk of serotonin syndrome and should be avoided. Case reports of serotonin syndrome with kanna have appeared in the literature. Sceletium has no meaningful cardiovascular or hepatotoxic risk profile at doses used traditionally or in clinical studies. It is not considered habit-forming in the classical sense, though tolerance and mild psychological dependence are plausible with regular high-dose use. It is not recommended during pregnancy or lactation in the absence of safety data. Legal status in Germany As of 2026, mesembrine and Sceletium tortuosum are not scheduled in the German Narcotics Act (BtMG, Anlagen I–III) or the New Psychoactive Substances Act (NpSG). The plant, its extracts, and mesembrine as an isolated alkaloid are legal to possess, sell, and purchase in Germany. Kanna and Sceletium extracts are openly available in health supplement and botanical retail channels in Germany and the EU. Related content Plant Extracts at amama Mitragynine — Compound Profile Muscimol — Compound Profile

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Muscimol — Compound Profile

Muscimol 2D structure of Muscimol (C4H6N2O2) — source: PubChem CID 4266 Chemistry CID: 4266 · PubChem Formula: C4H6N2O2 Molecular weight: 114.1 g/mol IUPAC: 5-(aminomethyl)-1,2-oxazol-3-one CAS: 2763-96-4 Family & pharmacology Family: Isoxazole (not an indole alkaloid) Pharmacological class: GABA-A receptor full agonist — binds selectively and potently at the GABA-binding site (orthosteric site) of GABA-A receptors, producing sedative, hypnotic, anxiolytic, and at higher doses dissociative/psychedelic effects. Unlike benzodiazepines (which act allosterically), muscimol is a direct agonist and therefore active even in the absence of endogenous GABA. It does not act on serotonergic (5-HT₂A) or dopaminergic pathways. Natural source: Muscimol is the primary psychoactive constituent of Amanita muscaria (fly agaric) and related Amanita species including A. pantherina and A. regalis. It is formed in vivo and during drying/cooking by decarboxylation of ibotenic acid, a structural precursor also present in fresh fruiting bodies. The ratio of ibotenic acid to muscimol is highly variable and depends on drying temperature and time. Historical context Muscimol was first isolated in 1964 by Swiss chemist Conrad Hans Eugster and colleagues at the University of Zurich, who also elucidated its structure and confirmed its GABAergic mechanism. Interest in Amanita muscaria as a psychoactive agent long predates isolation: ethnomycologist R. Gordon Wasson proposed in 1968 (Soma: Divine Mushroom of Immortality) that fly agaric was the identity of Soma, the sacred beverage described in the Rigveda — a hypothesis that remains debated among ethnobotanists and classicists. Siberian and Eurasian accounts of fly agaric use — particularly among Koryak, Chukchi, and Evenki reindeer herders — were documented by European travellers from the 18th century onward. The anthropologist Jochen Gartz and others have argued that the reindeer–Amanita relationship (reindeer actively seeking fly agaric) has contributed to shamanic iconography including the Santa Claus myth. Traditional use Siberian shamanic ritual: fly agaric dried and consumed by shamans to induce visionary states; urine recycling (muscimol is excreted largely unchanged) was documented in several ethnohistorical sources Reindeer herding communities in northeastern Siberia consumed fly agaric to reduce fatigue and pain on long journeys Not documented in significant traditional use contexts in Central or Western Europe, despite widespread occurrence of A. muscaria Modern research context Contemporary research interest in muscimol centres on its GABA-A agonism as a tool compound to map receptor subunit specificity, and on potential therapeutic applications in anxiety and epilepsy. Muscimol's selectivity profile differs from benzodiazepines and barbiturates, and unlike many GABA-A modulators it does not require a specific subunit combination, making it a useful research probe. Muscimol shows anticonvulsant effects in animal models and has been investigated for neuroprotective properties in ischemia models. It is important to note that muscimol has no serotonergic activity — its experiential profile (sedation, dreamlike states, body effects) differs substantially from classical psychedelics (psilocybin, LSD). Clinical research in humans remains limited; most data derive from animal pharmacology. Safety Muscimol is potent at low doses (effective dose range reported in the single-digit milligram range in experienced users). Fresh Amanita muscaria fruiting bodies contain predominantly ibotenic acid, which must be converted to muscimol by decarboxylation (typically via controlled drying at 50–70 °C). Ibotenic acid is a neuroexcitatory NMDA receptor agonist that contributes to nausea and dysphoria. Improperly prepared material therefore carries higher risk than preparations where decarboxylation is complete. Dose–response is steep and highly variable between specimens. Adverse effects include nausea, vomiting, excessive salivation, confusion, and ataxia. There is no specific antidote; supportive care is standard. Combining muscimol with alcohol or other CNS depressants significantly increases the risk of respiratory depression. Not appropriate for unsupervised use. Legal status in Germany As of 2026, muscimol is not scheduled in the German Narcotics Act (BtMG, Anlagen I–III) and is not listed in the New Psychoactive Substances Act (NpSG). Amanita muscaria mushrooms and muscimol-containing preparations are legal to possess, purchase, and sell in Germany. There is no medicinal-use restriction comparable to that affecting ibogaine or psilocybin. Amanita muscaria extracts and dried fruiting bodies are openly traded as botanical specimens. Related content Plant Extracts at amama Ibogaine — Compound Profile Mitragynine — Compound Profile

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