Mitragynine
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Mitragynine is a naturally-occurring opioid of the indole alkaloid class. It is the principal psychoactive constituent of kratom (Mitragyna speciosa), a Southeast Asian tree in the coffee family. Mitragynine is a partial agonist at µ-opioid receptors, producing its effects primarily through a liver-generated active metabolite.[1]
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First isolated in 1921 by Ellen Field at the University of Edinburgh,[2] mitragynine remained a pharmacological curiosity until the discovery that it activates opioid receptors without recruiting the signaling pathway most responsible for respiratory depression.[3][4] It is unscheduled at the United States federal level and under active clinical investigation as an opioid use disorder therapeutic.
Subjective effects include stimulation, enhanced focus, analgesia, sedation, and mood elevation. The experience is defined by a bimodal dose-response — low doses produce coffee-like alertness and sociability, while higher doses shift toward warm opioid sedation and pain suppression. Nausea, constipation, and cognitive dulling are characteristic unsought effects.
Physical dependence develops with regular use, though withdrawal is rated milder than classical opioid withdrawal.[5] The primary acute danger is poly-substance combination: 87% of kratom-associated deaths involve co-exposure to other drugs,[6] and liver injury is a recognized adverse effect.[7] Phase 1 clinical data are emerging, but no definitive human toxicity thresholds have been established.
History[edit]
Discovery
Mitragyna speciosa was first described botanically by Pieter Willem Korthals in 1839. Traditional use of the plant — fresh leaves chewed or brewed as tea for fatigue, pain, and opium substitution — was documented throughout nineteenth-century Southeast Asia.[8] Mitragynine was isolated as a discrete compound in 1921 by Ellen Field at the University of Edinburgh, with its chemical structure established by Beckett, Shellard, and Tackie in 1965.[2]
Scientific significance
The landmark 2004 review by Takayama identified 7-hydroxymitragynine as more potent than mitragynine itself in animal pain models, reframing kratom pharmacology around a minor alkaloid rather than the abundant parent compound.[9] Kruegel et al. confirmed in 2019 that mitragynine is converted to 7-hydroxymitragynine in the liver, and that this metabolite accounts for most opioid-mediated analgesia in mice.[1] The discovery that mitragynine activates opioid receptors through G-protein signaling without recruiting β-arrestin-2 — the pathway behind respiratory depression — positioned it as a potential lead for safer analgesics.[4][3]
Regulation and modern use
The DEA announced emergency scheduling of mitragynine and 7-hydroxymitragynine in August 2016, drawing unprecedented opposition: 51 members of Congress objected, over 23,000 public comments were submitted, and the notice was withdrawn in October 2016.[10] Thailand — where kratom had been controlled since 1943 — reversed course in 2021, legalizing domestic cultivation and use. The WHO Expert Committee on Drug Dependence concluded that same year that insufficient evidence existed to recommend international scheduling.[10] An estimated 1.9 million Americans have used kratom,[11] and the first FDA-IND Phase 1 study of pure mitragynine is underway.
The name Mitragyna was assigned by Korthals, who noted that the plant's stipules resembled a bishop's mitre. In Southeast Asian labor culture, kratom occupied a niche comparable to betel nut and tea — a work-enhancing plant integrated into daily routine rather than consumed recreationally. In Western markets, kratom arrived primarily through online vendors in the 2000s and rapidly became associated with self-managed opioid withdrawal, a use pattern that continues to shape both its user community and its regulatory trajectory.
Chemistry[edit]
Structural class
Mitragynine is a Corynanthe-type monoterpenoid indole alkaloid built on a pentacyclic indole-fused quinolizidine scaffold — the same core architecture found in the related kratom alkaloids speciogynine, speciociliatine, and paynantheine.[9] The indole and quinolizidine ring systems derive biosynthetically from tryptamine and secologanin, placing mitragynine within the broader alkaloid family that includes yohimbine and corynantheine.
Key structural features distinguishing mitragynine from its congeners include a methoxy group on the indole ring, an ethyl substituent at C3, and an E-configured acrylate side chain whose geometry influences receptor binding orientation.[12]
Molecular properties
| Molecular formula | C₂₃H₃₀N₂O₄ |
| Molecular weight | 398.5 g/mol |
Stereochemistry
Mitragynine has three chirality centers with absolute configuration (2S,3S,12bS). Three natural diastereomers co-occur in M. speciosa: speciogynine, speciociliatine, and mitraciliatine.[13][12]
The stereochemistry has measurable pharmacokinetic consequences. The 3S alkaloid series (mitragynine, speciogynine, paynantheine) reaches peak blood levels faster and persists longer than the 3R series (speciociliatine, mitraciliatine), differences attributed to differential metabolism and tissue distribution.[13]
Natural occurrence
Mitragynine is the dominant alkaloid in kratom leaves, typically comprising 40–66% of total alkaloid content.[9] Over 40 related indole alkaloids have been identified in the plant.[8] Alkaloid concentrations vary with geographic origin (Thai vs. Malaysian chemotypes), harvest season, leaf maturity, and processing method.
Pharmacology[edit]
Mechanism of action
Mitragynine is a partial agonist at the µ-opioid receptor, meaning it activates the receptor but with a lower maximum effect than full agonists like morphine.[14] Its opioid activity is largely metabolism-dependent: the liver converts mitragynine to 7-hydroxymitragynine (7-HMG), a much more potent opioid receptor activator that accounts for most of the analgesic effect in animal models.[1] The parent compound itself binds the µ-opioid receptor weakly,safety citation needed so the route of administration — and whether the substance passes through the liver — critically determines opioid effect intensity.
Both mitragynine and 7-HMG activate the receptor through G-protein signaling without recruiting β-arrestin-2.[3][4] This distinction matters because β-arrestin-2 recruitment is the pathway primarily responsible for respiratory depression, constipation, and rapid tolerance with conventional opioids.
Beyond opioid receptors, mitragynine blocks κ-opioid and δ-opioid receptors.[15] κ-Opioid blockade is relevant because κ activation produces dysphoria and aversion — its antagonism may contribute to mitragynine's mood-elevating properties. Additional activity at adrenergic receptors[16][17] likely drives the stimulant-like effects at low doses, a quality absent from classical opioids.
Interactions with serotonin receptors and calcium channels have been reported but not systematically characterized.[18][19]
Pharmacokinetics
Mitragynine is rapidly absorbed after oral administration, reaching peak blood levels within approximately one hour.[20][21][13] The compound distributes extensively into tissues,[20] and virtually all of it is metabolized by the liver — less than 0.2% is excreted unchanged in urine.[20]
The half-life is unusually long: roughly 23 hours after a single dose in chronic users,[20] extending to approximately 44 hours in opioid-naive individuals and up to 68 hours with repeated daily dosing.[21] The active metabolite 7-HMG appears in blood within 1–2 hours, and its half-life increases from about 5 hours (single dose) to 25 hours (multiple doses).[21] Steady state takes 8–9 days for mitragynine and roughly 7 days for 7-HMG.[21]
Mitragynine inhibits the liver enzyme CYP3A in a time-dependent manner, meaning its interaction potential increases with continued use.[22] It also inhibits P-glycoprotein, a transport protein that controls drug absorption and brain penetration.[23] These properties create significant drug interaction potential, detailed in the Safety section.
Oral bioavailability of pure mitragynine has not been directly measured in humans. Computational predictions suggest absorption exceeding 75%,[24] but human confirmation is lacking.
Neuroscience[edit]
Where it acts
Mitragynine's opioid activity engages the mesolimbic mesolimbic pathway — µ-opioid receptor activation in the ventral tegmental area releases dopamine in the nucleus accumbens, producing reinforcing and mood-elevating effects. The partial agonist ceiling predicts lower dopamine release than full agonists, consistent with milder euphoria and lower abuse potential.[25] Concurrent κ-opioid receptor blockade may further enhance positive mood by removing the dysphoric opposition that κ activation normally provides.[15]
Pain relief operates through descending modulation, where opioid receptor activation in the brainstem suppresses pain signals at the spinal level. Because this analgesia depends on liver conversion to 7-hydroxymitragynine,[1] individual differences in liver enzyme activity produce variable analgesic responses.
Why it matters
The low-dose stimulant effects — alertness, energy, focus — likely reflect adrenergic receptor activity rather than opioid mechanisms.[17][16] This dual opioid-adrenergic pharmacology is distinct from classical opioids and explains the bimodal dose-response that defines the mitragynine experience.
The absence of β-arrestin-2 recruitment is predicted to slow receptor adaptation and reduce tolerance development. Preclinical evidence supports this: kratom alkaloids produce less withdrawal than morphine at equivalent doses.[26] Chronic use does, however, produce heightened pain sensitivity in animal models, indicating compensatory changes occur independently of the arrestin pathway.[26]
No neuroimaging studies of mitragynine's effects on the human brain have been published — the neural basis of the bimodal dose-response remains uncharacterized in humans. Whether individuals with low CYP3A enzyme activity experience predominantly stimulant effects with attenuated opioid activity has not been studied. The compound's effects on brain structure and long-term synaptic changes are unknown.
Subjective Effects[edit]
Mitragynine delivers an experience unusual among opioid compounds: a clear bimodal arc in which stimulant and opioid qualities exist on a single dose-dependent continuum. At lower doses, the dominant character is activating — heightened focus, physical energy, talkativeness — with warmth and mild mood elevation in the background. As dose increases, the opioid dimension ascends: sedation deepens, pain dissolves, and the stimulant edge softens into heavy-limbed calm. Individual liver enzyme activity shapes where this transition occurs, making the crossover point variable between users. Set and setting exert moderate influence, particularly around the boundary where stimulant and opioid qualities compete.
Relative to classical opioid analgesics such as morphine or oxycodone, mitragynine produces a more stimulant-inflected, less sedating experience at low doses, with a ceiling on euphoria imposed by partial agonist pharmacology. Compared to buprenorphine — another partial µ-opioid agonist — mitragynine's adrenergic activity contributes a distinctive activating quality absent from buprenorphine's profile.
Effect Grid
Common doses (15–40 mg mitragynine) represent the transition zone between stimulant-dominant and opioid-dominant effects. Analgesia begins to emerge alongside continued mood elevation. Cognitive euphoria becomes more pronounced, and anxiety suppression is frequently reported. Sociability may persist or begin yielding to a more inward, relaxed state.
Physical effects shift noticeably: warmth and body high develop, muscle relaxation appears, and some users experience nausea at the upper end of this range. Pupil constriction becomes detectable. Appetite suppression typically persists. Mild dizziness is possible.
This range corresponds to approximately 2–5 grams of dried leaf. The balance between stimulation and sedation is strongly influenced by individual CYP3A metabolizer status, which determines the rate of conversion to the more potent opioid metabolite 7-hydroxymitragynine.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Vestibular distortion · Visual acuity suppression · Tinnitus
Constipation · Muscle relaxation · Nausea · Sedation · Stimulation · Bodily heaviness · Diarrhea · Dizziness · Wakefulness · Appetite suppression · Breathing alteration · Dry mouth · Excessive sweating · Insomnia · Muscle tension · Physical fatigue · Restlessness · Tactile euphoria · Trembling · Vomiting · Yawning · Brain zaps · Headache · Heart rate perception changes · Sexual arousal suppression · Watery eyes · Nystagmus (eye wobbles) · Pain enhancement
Stimulation · Bodily heaviness · Diarrhea · Dizziness · Wakefulness · Appetite suppression · Breathing alteration · Dry mouth · Excessive sweating · Insomnia · Muscle tension · Physical fatigue · Restlessness · Tactile euphoria · Trembling · Vomiting · Yawning · Brain zaps · Headache · Heart rate perception changes · Sexual arousal suppression · Watery eyes · Nystagmus (eye wobbles) · Pain enhancement
Cognitive fatigue · Cognitive impairment · Focus suppression · Information processing enhancement · Information processing suppression · Thought deceleration · Confusion · Motivation suppression
Information processing suppression · Thought deceleration · Confusion · Motivation suppression
Emotional suppression · Anhedonia · Dysphoria
Timeline
Initial awareness of effects — subtle stimulation, mild alertness shift, or faint warmth depending on dose. Sub-threshold at the lowest doses.
Effects build steadily. Low doses develop stimulant clarity and sociability; higher doses begin to introduce opioid warmth and emerging analgesia. Mild nausea possible at upper dose ranges.
Maximum intensity plateau. Low-dose peak: focused stimulation, mood elevation, wakefulness. High-dose peak: sedation, strong analgesia, opioid-type euphoria, bodily heaviness, pupil constriction.
Gradual diminution of primary effects. Residual warmth, relaxation, or mild stimulation persists. Nausea typically resolves.
Mild residual effects — lingering mood elevation, subtle fatigue, or gentle relaxation. Pharmacological activity persists well beyond subjective experience due to the 23–67 hour elimination half-life.
⚠ Do not drive or operate heavy machinery for several hours after subjective effects resolve, as motor coordination may remain subtly impaired due to mitragynine's long elimination half-life.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 21 days
- Physical
- Moderate
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- morphine · oxycodone · heroin
Toxicity
No human lethal dose for mitragynine has been established. The largest mortality analysis — 156 kratom-associated deaths — found that 87% involved co-exposure to other substances.[6] Only 23% of cases identified mitragynine as the sole intoxicant. Postmortem blood concentrations in fatal cases range from 0.19 to 1.9 mg/L, but these do not represent established toxic thresholds given confounding poly-substance exposure.safety citation needed
Liver injury
Mitragynine is a probable cause of drug-induced liver injury. A scoping review identified multiple case reports and regulatory database entries documenting a predominantly cholestatic pattern.[7][27] Mean time from use to symptom onset is 21 days (range 2–49 days). Common symptoms include abdominal discomfort, yellowing of the skin, itching, and dark urine. The mechanism is unclear — direct toxicity, immune-mediated injury, and contaminant effects are all under investigation.[28]
Heart and circulation
Case reports describe blood pressure instability, heart muscle damage, and abnormal heartbeat associated with kratom use.[29] Surgical patients with kratom use history present specific concerns including blood pressure instability and agitation.[11]
Respiratory effects
Mitragynine's signaling profile predicts reduced respiratory depression relative to classical opioids, and animal data confirm significantly less breathing suppression than morphine at equivalent pain-relieving doses.[30] Fatal respiratory depression has nonetheless been reported, primarily alongside other sedating substances.
Seizures
Seizure events have been reported in association with kratom use, including a case involving kratom with modafinil.[15] Multiple reviews cite seizures as a recognized adverse event.[19]
Neonatal effects
Kratom use during pregnancy can produce neonatal abstinence syndrome. Three published case reports document withdrawal symptoms in newborns born to mothers using kratom, including oral intolerance, restlessness, irritability, and vomiting.[31][32][33] Perceived safety as a "natural" herb does not confer safety in pregnancy.[34]
Kidney injury
Acute kidney injury has been documented in severe overdose complicated by muscle breakdown.[29] No data on chronic kidney effects are available.
Psychological risks
Systematic data on psychological adverse effects are limited. In the only controlled human study, 40 mg mitragynine produced increased ratings of memory suppression and mild psychological symptoms, though clinical significance at this dose is unclear.[35]
User surveys describe anxiety, irritability, and depressed mood as dose-dependent or withdrawal-associated phenomena.[36] Chronic heavy use has been linked to cognitive complaints in observational studies, though controlled evaluations are lacking.citation needed No published data address psychosis risk, persisting perceptual changes, or psychiatric destabilization in vulnerable populations.
Tolerance & dependence
Tolerance to mitragynine's opioid effects develops with repeated use, and cross-tolerance to morphine has been documented.[37] Physical dependence develops with regular use — consumption exceeding approximately 4 glasses of kratom tea per day (76–115 mg/day mitragynine equivalent) is associated with higher withdrawal severity.[5]
Withdrawal symptoms include muscle and joint pain, watery eyes, runny nose, yawning, insomnia (46% report increased sleep problems), diarrhea, feverish sensations, appetite suppression, tremors, and nausea.[5] Psychological withdrawal includes depressed mood (81% report mild depression), anxiety (70% report mild anxiety), restlessness, irritability, and tension.[36]
Withdrawal severity is rated milder than classical opioid withdrawal in user reports,[5] consistent with preclinical findings that kratom alkaloids produce less withdrawal than morphine at equivalent doses.[26]
Treatment most commonly employs buprenorphine-naloxone (Suboxone) for both acute detoxification and maintenance.[37] Alternative protocols include intravenous clonidine with oral dihydrocodeine and lofexidine.[37]
Drug interactions
Mitragynine's interaction risk arises from three converging mechanisms: liver enzyme inhibition, transport protein inhibition, and additive effects with other sedating drugs.
CYP3A substrates
The most clinically significant interaction class. Mitragynine's time-dependent CYP3A inhibition increases exposure to CYP3A-metabolized drugs with narrow safety margins.[22] At-risk medications include midazolam, triazolam, certain immunosuppressants (tacrolimus, cyclosporine), and some antiretrovirals. Modelling predicts midazolam exposure increases of 2.2–2.7×.[38]
A fatal case possibly attributable to CYP-mediated potentiation of quetiapine has been reported.[39]
CYP3A inhibitors (azole antifungals, macrolide antibiotics, ritonavir) reduce 7-HMG formation from mitragynine, potentially attenuating opioid effects while increasing parent compound exposure.[38]
CNS depressants
Co-administration with opioids, benzodiazepines, alcohol, or sedating antihistamines poses the highest acute fatality risk. The majority of kratom-associated deaths involved concurrent sedating substances.[6][40][41][42]
P-glycoprotein substrates
Mitragynine inhibits P-glycoprotein transport,[23] relevant for drugs dependent on this transporter for absorption or brain exclusion (digoxin, dabigatran, certain chemotherapy agents).
CYP2D6 substrates
Mitragynine inhibits CYP2D6 in laboratory studies, though clinical effects at typical kratom doses appear minimal.[22] Higher doses or sensitive CYP2D6 substrates may present interaction risk.[23]
Serotonergic drugs
Mitragynine interacts with serotonin pathways, creating theoretical serotonin syndrome risk with SSRIs, SNRIs, and MAOIs. No published case reports of serotonin syndrome from mitragynine combinations were identified.safety citation needed
Other interactions
A seizure case has been reported with kratom–modafinil co-administration.[15] Standard opioid urine drug screens do not reliably detect mitragynine or 7-HMG; specific laboratory methods are required.[43]
Contraindications
Pregnancy: Mitragynine crosses the placenta. Neonatal abstinence syndrome has been documented.[31][32][33]
Liver disease: Pre-existing liver conditions increase risk of drug-induced liver injury and impair clearance of both mitragynine and its active metabolite.[7]
Concurrent sedating substances: Co-administration with opioids, benzodiazepines, alcohol, or gabapentinoids carries risk of additive respiratory depression. The majority of kratom-associated fatalities involve poly-substance exposure.[6]
CYP3A-metabolized medications with narrow safety margins: Mitragynine's enzyme inhibition can raise co-administered drug levels to toxic concentrations.[22]
Kidney disease: Acute kidney injury has been documented in severe overdose.[29] No safety data exist for pre-existing kidney disease.
Surgical patients with kratom use history require specific clinical attention due to risks of blood pressure instability, agitation, pain management difficulty, and withdrawal.[11]
Harm Reduction[edit]
Forms & Identification
Kratom's highly variable alkaloid content means that even plain leaf powder from different vendors — or different batches from the same vendor — can produce substantially different effects at the same weight. Extract products concentrate mitragynine and may contain elevated 7-hydroxymitragynine, making dosing unpredictable without tested potency information.
Products marketed as "enhanced" or "7-OH" contain semi-synthetic 7-hydroxymitragynine, which is pharmacologically distinct from kratom leaf — a near-full opioid agonist with significantly higher potency and risk. Treat any 7-HMG product as a different substance class from plain leaf.
Guidelines
- Start with low doses of any new batch or product, as alkaloid content varies considerably between sources
- Measure doses by weight rather than volume — a kitchen scale accurate to 0.1 g is sufficient for powder
- Allow at least 45–60 minutes before redosing, as peak effects can be delayed
- Avoid daily use to reduce dependence risk — even short tolerance breaks of 2–3 days help
- Stay hydrated; kratom can produce dry mouth and reduced thirst awareness
- Inform medical providers of kratom use before surgery or when prescribed new medications, particularly CYP3A-metabolized drugs
Set & Setting
Mitragynine's bimodal dose-response means that context matters most at the boundary between stimulant and sedating doses. Low doses are compatible with work and social settings. Higher sedating doses are best taken in a safe, comfortable environment where the ability to rest is available. Avoid driving or operating machinery at any dose above the stimulant range.
Aftercare & integration. Mitragynine's long half-life (up to 24–68 hours depending on use pattern[21]) means residual effects and drug interactions may persist well beyond the subjective experience. Avoid other sedating substances for at least 24 hours after a high dose.
After regular use, even brief cessation may produce mild withdrawal symptoms including muscle aches, sleep disruption, and low mood. These typically peak 2–3 days after the last dose and resolve within a week. Maintaining hydration, light exercise, and consistent sleep schedules supports recovery during this period.
Recovery & Support
Physical dependence on kratom develops with regular use and is a physiological adaptation, not a moral failure. Withdrawal is milder than classical opioid withdrawal but nonetheless uncomfortable, and medical support can substantially ease the process.
Buprenorphine-naloxone (Suboxone) is the most commonly used treatment for kratom dependence.[37] Medical detoxification is advisable for anyone using high daily doses or experiencing significant withdrawal symptoms. Online communities — including kratom-specific recovery forums — provide peer support and practical guidance for tapering and cessation.
For anyone using kratom to manage opioid withdrawal independently, medical supervision is strongly recommended. Self-managed substitution carries risks of dose escalation and cross-dependence.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most kratom experiences, even uncomfortable ones, are not medical emergencies. Seek immediate help if any of the following occur: breathing becomes slow, shallow, or stops; lips or fingertips turn blue; the person becomes unresponsive or cannot be woken; seizure activity; severe chest pain; or yellowing of the skin or eyes (a sign of liver injury requiring urgent evaluation).
Immediate steps:
- 1. Call emergency services if breathing is compromised or the person is unresponsive
- 2. Place an unresponsive but breathing person in the recovery position (on their side, airway clear)
- 3. If opioid overdose is suspected and naloxone is available, administer it — naloxone reverses µ-opioid agonism from both mitragynine metabolites and any co-ingested opioids
- 4. Do not induce vomiting
- 5. Stay with the person until help arrives
What to tell the dispatcher: Name the substance (kratom / mitragynine), approximate amount, time of ingestion, and any other substances taken. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Reversal agent: Naloxone is effective against the µ-opioid component of mitragynine's effects. Keep naloxone accessible whenever using kratom alongside other opioids or at high doses.
Legal Status[edit]
Mitragynine is not scheduled under any UN international drug convention following the WHO Expert Committee on Drug Dependence's 2021 determination that insufficient evidence existed to recommend international scheduling.[10] Jurisdictional status ranges from unscheduled and commercially available to outright prohibition, reflecting deep disagreement about the balance of therapeutic potential and abuse risk.
In the United States, the DEA's 2016 emergency scheduling attempt was withdrawn following unprecedented congressional and public opposition. Mitragynine remains unscheduled at the federal level, though the FDA maintains import alerts and consumer advisories. Several states have enacted bans, while others have adopted the kratom Consumer Protection Act (KCPA), establishing quality standards and age restrictions rather than prohibition.
Legal status for mitragynine and kratom is evolving rapidly across jurisdictions. The information below reflects status as of early 2026 and may not capture recent legislative changes.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not federally scheduled | DEA "Drugs and Chemicals of Concern" list; FDA Import Alert 54-15; state-level bans in AL, AR, IN, RI, VT, WI; KCPA enacted in several states[10] |
| United Kingdom | Illegal | Banned under Psychoactive Substances Act 2016 |
| Australia | Schedule 9 (Prohibited Substance) | Complete ban on possession, sale, and use |
| Canada | Legal to possess | Sales for human consumption not permitted under Food and Drugs Act |
| Thailand | Decriminalized / legal for traditional use | Removed from narcotics list under Kratom Act 2021; commercial export regulations in development |
| Malaysia | Illegal | Controlled under Poisons Act 1952 |
| Ireland | Schedule 1 controlled drug | Scheduled since 2017 under Misuse of Drugs Act |
| France | Illegal | Banned since 2020 |
| Netherlands | Legal | Sold in smart shops; not scheduled |
| Denmark / Romania / Poland | Banned | Various national scheduling instruments |
references
- [1] ^abcdKruegel AC, Uprety R, Grinnell SG, Langreck C, Pekarskaya EA, et al. (2019) 7-Hydroxymitragynine Is an Active Metabolite of Mitragynine and a Key Mediator of Its Analgesic Effects — ACS Central Science doi:10.1021/acscentsci.9b00141
- [2]
- [3] ^abcTodd DA, Kellogg JJ, Wallace ED, Khin M, Flores-Bocanegra L, et al. (2020) Chemical composition and biological effects of kratom (Mitragyna speciosa): In vitro studies with implications for efficacy and drug interactions — Scientific Reports doi:10.1038/s41598-020-76119-w
- [4] ^abcVaradi A, Marrone GF, Palmer TC, Narayan A, Szabo MR, et al. (2016) Mitragynine/Corynantheidine Pseudoindoxyls As Opioid Analgesics with Mu Agonism and Delta Antagonism, Which Do Not Recruit beta-Arrestin-2 — Journal of Medicinal Chemistry doi:10.1021/acs.jmedchem.6b00748
- [5] ^abcdSingh D, Narayanan S, Vicknasingam BK, Prozialeck WC, et al. (2018) Severity of Pain and Sleep Problems during Kratom (Mitragyna speciosa Korth.) Cessation among Regular Kratom Users — Journal of Psychoactive Drugs doi:10.1080/02791072.2018.1443234
- [6] ^abcdCorkery J, Streete P, Claridge H, et al. (2019) Characteristics of deaths associated with kratom use — Journal of Psychopharmacology doi:10.1177/0269881119862530