7-Hydroxymitragynine
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7-Hydroxymitragynine (7-HMG) — 7-OH — is a semi-synthetic opioid of the monoterpenoid indole alkaloid class. It is the primary active metabolite of mitragynine, the dominant alkaloid in kratom, with 13-fold greater analgesic potency than morphine.[1] 7-HMG is a partial agonist at µ-opioid receptors, producing its effects by activating G-protein pain-suppression pathways without recruiting β-arrestin.[2]
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No dose data on record for this route. The timings below are not a dose guide.
Isolated in 1994 from Thai kratom leaf material,[3] 7-HMG was reframed in 2019 as the metabolite responsible for most of mitragynine's analgesic activity.[4] Since 2023, concentrated semi-synthetic 7-HMG products have flooded gas stations and smoke shops.[5][6] The FDA recommended DEA scheduling of these products in July 2025.[7]
Subjective effects include analgesia, sedation, euphoria, and anxiolysis. The experience is opioid-typical — a dissolving warmth in which pain recedes and emotional tension quiets — with no psychedelic, dissociative, or hallucinogenic features documented at any dose. Nausea, constipation, and respiratory slowing are characteristic unsought effects.
7-HMG produces physical dependence with a classical opioid withdrawal, and its respiratory depression is 4.5 times more potent than morphine in animal models.[8] Tolerance develops with chronic use and is bidirectional with morphine;[9] multiple case reports document opioid use disorder from semi-synthetic 7-HMG products.[10] No controlled human trials of isolated 7-HMG have been conducted — dose-response relationships, therapeutic index, and drug interaction magnitude remain uncharacterized.
History[edit]
Discovery
7-Hydroxymitragynine was first isolated in 1994 from Thai kratom leaf by Ponglux and colleagues.[3] In 2002, Takayama's group demonstrated that this trace alkaloid was 13-fold more potent than morphine in functional assays — a finding that recast a traditional plant constituent as a compound of serious pharmacological interest.[1] By 2005, animal studies had confirmed that chronic 7-HMG administration produces tolerance, cross-tolerance with morphine, and naloxone-precipitable withdrawal — a classical opioid dependence profile.[9]
Scientific Reframing
Two developments in 2016 reshaped the field. Kruegel and colleagues established that 7-HMG is a G-protein-biased agonist at the μ-opioid — activating pain-suppression pathways without recruiting β-arrestin.[2] Separately, Lydecker documented suspected adulteration of commercial kratom products with elevated 7-HMG concentrations.[11] Then in 2019, the paradigm shifted again: Kruegel showed that mitragynine is converted to 7-HMG by liver enzymes, and that brain concentrations of 7-HMG after oral mitragynine are sufficient to account for most of kratom's analgesic effects.[4] A further complication emerged when 7-HMG was found to be unstable in human plasma, converting to the even more potent mitragynine pseudoindoxyl.[12]
Market Emergence and Regulatory Response
Between 2023 and 2025, concentrated semi-synthetic 7-HMG products proliferated in gas stations and online retailers, marketed as dietary supplements in the form of sublingual films, tablets, and nasal sprays.[5][6][13] The FDA issued warning letters to seven companies in June 2025 and formally recommended DEA scheduling on July 29, 2025.[7] As of May 2026, DEA rulemaking remains pending.
The abbreviation "7-OH" — from 7-hydroxymitragynine — became the dominant consumer-facing name as semi-synthetic products entered smoke shops and gas stations starting in 2023. The naming is notable: "7-OH" distances the product from kratom's botanical identity and frames it as a novel compound rather than a concentrated derivative of a traditional plant. Early commercial kratom products had already been documented with artificially elevated 7-HMG concentrations,[11] but the explicit branding of isolated 7-HMG as a standalone product category marked a commercial and pharmacological break from the kratom tradition.
Chemistry[edit]
Structural Class
7-Hydroxymitragynine belongs to the monoterpenoid indole alkaloid family, built on a 9-methoxy-Corynanthe-type scaffold.[14] It is derived from mitragynine by the addition of a hydroxyl group at the C-7 position — a single oxygen atom that transforms mitragynine from an opioid receptor antagonist into a partial agonist with 13-fold greater analgesic potency than morphine.
The core architecture consists of fused indole and quinolizidine ring systems with five stereogenic centers. Key functional groups include the C-7 hydroxyl (the structural distinction from mitragynine), a C-8 methoxy group, and an (E)-configured methoxycarbonyl vinyl substituent.
| Molecular formula | C₂₃H₃₀N₂O₅ |
| Molecular weight | 414.5 g/mol |
Stereochemistry
The naturally occurring and pharmacologically active form possesses (2S,3S,7aS,12bS) absolute configuration. Enantioselective total synthesis was achieved by Kruegel and colleagues in 2016,[2] and structure-activity studies on mitragynine confirmed that receptor binding is stereospecific — the opposite enantiomer is substantially weaker.
Stability
No published characterization of melting point, aqueous solubility, or solid-state stability exists for 7-HMG. The compound is notably unstable in human plasma, converting to mitragynine pseudoindoxyl — a transformation that proceeds far more rapidly in human blood than in other tested species.[12] This species-dependent instability has significant consequences for interpreting animal studies.
Natural Occurrence
7-HMG occurs as a trace constituent in Mitragyna speciosa leaves, typically less than 2% of total alkaloid content.[15] Most systemic 7-HMG exposure in kratom users comes from the liver converting ingested mitragynine into 7-HMG.[4] Semi-synthetic products are manufactured by controlled oxidation of extracted mitragynine.[16]
Pharmacology[edit]
Mechanism of Action
7-Hydroxymitragynine is a partial agonist at the µ-opioid receptor and a competitive antagonist at kappa- and delta-opioid receptors.[2][17] This mixed profile — activating one opioid receptor subtype while blocking the other two — distinguishes it from most clinical opioids.
At the µ-opioid receptor, 7-HMG activates G-protein signaling pathways with partial efficacy while producing no measurable β-arrestin recruitment.[18][2] This G-protein-biased signaling was originally predicted to reduce adverse effects like respiratory depression. Animal data challenge that prediction: 7-HMG depresses breathing with 4.5-fold greater potency than morphine in rats, fully reversible by naloxone.[8]
The frequently cited "13-fold more potent than morphine" figure refers to whole-animal pain tests, not receptor binding strength.[19] 7-HMG shows high selectivity for opioid receptors and does not bind significantly to adrenergic receptors — unlike mitragynine, which has adrenergic activity.[20][21]
Pharmacokinetics
7-HMG occupies a dual role: it is both an active metabolite of mitragynine and a precursor to the even more potent mitragynine pseudoindoxyl.
Formation: When kratom is consumed orally, the liver converts mitragynine into 7-HMG via CYP3A enzymes.[4] In healthy volunteers given kratom tea, 7-HMG reached peak blood levels at roughly 1.8 hours, with total exposure approximately 20% of the parent mitragynine.[22] Co-administration of the CYP3A4 inhibitor itraconazole cut 7-HMG peak levels by 56%, directly confirming this enzyme-dependent formation in humans.[22]
Elimination: In the largest human pharmacokinetic study, 7-HMG showed dose-proportional increases across the tested range.[23] The single-dose half-life was approximately 4.7 hours, but this extended to 24.7 hours with repeated dosing — indicating the compound accumulates with regular use. Steady state was reached at approximately 7 days.[23]
Downstream conversion: 7-HMG is unstable in human blood, converting to mitragynine pseudoindoxyl — a compound more potent than either mitragynine or 7-HMG at the µ-opioid receptor.[12] This conversion happens far more extensively in human plasma than in other species, meaning animal studies may systematically underestimate how strong 7-HMG is in humans.[12]
Route effects: semi-synthetic 7-HMG products formulated for sublingual or nasal delivery bypass liver metabolism entirely, increasing the amount that reaches the bloodstream and accelerating onset.[5] No published bioavailability data for isolated 7-HMG exist in humans by any route.
Neuroscience[edit]
Where It Acts
7-HMG's primary neural actions occur in the brain's reward and pain-control circuits. In pain modulation, it activates µ-opioid receptors along the descending pathway from the periaqueductal gray through the brainstem to the spinal cord, suppressing pain signals at both spinal and supraspinal levels.[24] In reward circuitry, it produces a distinctive biphasic pattern: low doses increase dopamine release in the nucleus accumbens while high doses decrease it.[25] This differs from classical opioids like morphine, which produce dose-dependent dopamine increases. 7-HMG also depresses brainstem respiratory centers with 4.5-fold greater potency than morphine.[8]
Why It Matters
7-HMG's G-protein-biased signaling[2] was predicted to reduce adverse effects mediated by β-arrestin pathways, including respiratory depression. Animal data undercut this prediction for breathing[8] but may still be relevant to tolerance and gut effects. More broadly, the discovery that mitragynine's analgesic effects are actually mediated by its metabolite 7-HMG[4] — which itself converts to the more potent pseudoindoxyl in human blood[12] — establishes a multi-step activation chain that makes animal-to-human translation unreliable.
The therapeutic index in humans — the gap between an effective analgesic dose and a dangerous one — has not been measured. Controlled respiratory dose-response data in humans do not exist. The relative contribution of 7-HMG versus its downstream metabolite mitragynine pseudoindoxyl to human effects is unknown, because the plasma conversion rate differs dramatically between species.[12] The mechanism behind the biphasic dopamine response[25] — facilitation at low doses, suppression at high doses — remains unexplained.
Subjective Effects[edit]
The 7-HMG experience is opioid in character: a spreading warmth that blunts physical pain and quiets emotional distress, accompanied by heavy sedation and a narrowing of mental activity. At lower exposures — typical of traditional kratom use, where 7-HMG forms gradually via liver metabolism — the onset is gentle, the sedation moderate, and mild stimulation may coexist with analgesic warmth. At higher exposures from concentrated semi-synthetic products, the opioid qualities dominate: deeper sedation, stronger euphoria, and pronounced respiratory slowing. No psychedelic, dissociative, or hallucinogenic features have been reported at any dose. Set and setting modulate the experience less than they do for psychedelics — the pharmacology is the primary driver.
Relative to morphine, 7-HMG produces qualitatively similar analgesia and euphoria through partial rather than full µ-opioid receptor activation. All human experiential data come from kratom preparations containing the full alkaloid mixture, not from isolated 7-HMG — the precise boundary between this compound's contribution and that of co-administered kratom alkaloids remains undrawn.
Effect Grid
Common doses produce the characteristic opioid experience: substantial pain suppression, pronounced euphoria and cognitive euphoria, and marked anxiety suppression. A warm body high and tactile euphoria dominate the physical experience. Sedation becomes prominent, with a heavy, comfortable bodily heaviness and strong muscle relaxation.
Nausea is common, particularly on the come-up. Constipation, pupil constriction, and respiratory depression are pharmacologically expected at this level. Spontaneous body sensations including itching may occur. Dry mouth and appetite suppression are typical. Motor control impairment and thought deceleration are functionally significant.
Compulsive redosing urge may emerge. Duration of effects is expected to last several hours. Emotional suppression and dreaming suppression are likely with evening dosing.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Muscle relaxation · Pain suppression · Bodily heaviness · Constipation · Nausea · Spontaneous body sensations · Tactile euphoria · Breathing alteration · Dizziness · Physical fatigue · Appetite suppression · Dry mouth · Sexual arousal suppression · Vomiting · Yawning · Excessive sweating · Temperature dysregulation · Bodily dissociation
Constipation · Nausea · Spontaneous body sensations · Tactile euphoria · Breathing alteration · Dizziness · Physical fatigue · Appetite suppression · Dry mouth · Sexual arousal suppression · Vomiting · Yawning · Excessive sweating · Bodily dissociation
Cognitive impairment · Focus suppression · Information processing suppression · Thought deceleration · Memory suppression · Motivation suppression · Confusion
Memory suppression · Motivation suppression · Confusion
Timeline
Gradual emergence of first effects as mitragynine undergoes hepatic CYP3A oxidation to 7-HMG. Subtle warmth and mild anxiolysis may be the earliest perceptible shifts.
Opioid-typical warmth, analgesia, and sedation reach maximum intensity. Euphoria, muscle relaxation, and pupil constriction are prominent. Nausea most likely during early peak.
Gradual decline of analgesic and euphoric effects consistent with single-dose elimination half-life of 4. 7 hours. Sedation and bodily heaviness may persist longer than mood effects.
Subclinical residual effects including mild sedation, reduced anxiety, and possible rebound irritability. With chronic dosing, the elimination half-life extends to 24. 7 hours, significantly prolonging aftereffects.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- Severe
- Tolerance buildup
- moderate
- Tolerance reset
- —
- Physical
- High
- Psychological
- High
- Compulsive redosing
- High
- Dose escalation
- High
- Cross-tol.
- morphine · mu-opioid agonists (class)
Toxicity
Acute Toxicity
The primary lethal risk from 7-HMG is respiratory depression — suppressed breathing — which is 4.5-fold more potent than morphine in animal models.[8] This respiratory depression is fully reversed by naloxone.[8] No lethal dose has been established in any species. No controlled human toxicity data exist. safety citation needed
Fatalities
Most published fatality data report mitragynine rather than 7-HMG blood concentrations. An epidemiological study of 156 kratom-associated deaths found 80% were male (mean age 32.3 years), with polysubstance use in 87% of cases.[26] The largest case-control study identified 38 single-substance kratom fatalities with autopsy findings including fluid in the lungs (55.6%), enlarged liver (47.4%), and enlarged heart (47.4%).[27]
safety citation needed The role of 7-HMG versus its metabolite mitragynine pseudoindoxyl in fatal toxicity is unknown. Postmortem 7-HMG concentrations are rarely measured separately.
Liver Injury
Kratom use has been associated with liver injury in multiple case reports, including bile duct blockage[28] and severe liver damage resembling autoimmune patterns.[29][30] Whether 7-HMG itself is responsible or whether other kratom alkaloids drive liver injury has not been determined.
Muscle Breakdown
Severe muscle breakdown requiring surgical intervention has been reported following kratom overdose, though other substances were also involved.[31]
Neonatal Risk
No published data on neonatal withdrawal from gestational 7-HMG exposure exist. Risk is expected based on its µ-opioid receptor activity. safety citation needed
Psychological Risks
No psychedelic, dissociative, or hallucinogenic effects have been documented. Psychological risks are opioid-class:
- Compulsive redosing — documented with semi-synthetic 7-HMG products[5][32]
- Opioid use disorder — multiple case reports document DSM-5 criteria met with 7-HMG products[10]
- Dose escalation — progressive escalation from kratom to 7-HMG to mitragynine pseudoindoxyl documented clinically[33]
Tolerance and Dependence
Tolerance develops with chronic use, following the same pattern as morphine.[9] Bidirectional cross-tolerance with morphine is established: tolerance to one produces tolerance to the other.[9] Clinical case reports describe rapid dose escalation, including one case documenting progression to mitragynine pseudoindoxyl at doses of 9 × 20 mg daily including nocturnal use.[33]
Physical dependence produces a classical opioid withdrawal syndrome. In animal models, naloxone-precipitated withdrawal was qualitatively similar to morphine withdrawal.[9] Human case evidence confirms opioid-type withdrawal including medically managed inpatient withdrawal,[32] acute withdrawal after high-dose chronic cessation,[34] and severe early-onset withdrawal following escalation to pseudoindoxyl.[33]
Abuse liability: 7-HMG (but not mitragynine) substituted for morphine in animal self-administration studies, and its reinforcement were mediated by µ and delta receptors.[21] Prior 7-HMG exposure increased subsequent morphine intake, while prior mitragynine exposure decreased it[21] — suggesting 7-HMG may sensitize reward pathways.
Published treatment approaches include buprenorphine[10][35] and methadone.[36] A systematic review concluded that while animal evidence consistently shows abuse liability, clinical evidence remains insufficient for definitive characterization.[37]
Drug Interactions
CYP3A4 inhibitors (itraconazole, ketoconazole, grapefruit, ritonavir, clarithromycin) produce a complex interaction: they decrease 7-HMG formation from mitragynine while also decreasing 7-HMG clearance. In the only published human interaction study, itraconazole decreased 7-HMG peak levels by 56% when derived from oral kratom.[22] In rats, ketoconazole increased 7-HMG behavioral potency 9.7-fold.[38] The net effect in humans taking preformed 7-HMG products is unpredictable. safety citation needed
CNS depressants (opioids, benzodiazepines, alcohol, sleeping pills) produce additive or synergistic respiratory depression. The large majority of kratom-associated fatalities involve polysubstance use.[26][27]
Cannabidiol (CBD): Co-administration increases mitragynine exposure 2.8-fold in rats with delayed absorption, attributed to enzyme inhibition.[39]
CYP3A substrates (many benzodiazepines, statins, calcium channel blockers): kratom alkaloids can increase exposure to these drugs by inhibiting the enzyme that clears them.[40]
CYP2D6 substrates and P-glycoprotein substrates: Kratom alkaloids inhibit both CYP2D6 and P-glycoprotein, potentially increasing exposure to drugs metabolized or transported by these pathways.[41]
Serotonergic drugs: Serotonergic activity has been noted for kratom alkaloids,[42] but no cases of serotonin syndrome with 7-HMG have been reported. safety citation needed
Contraindications
Absolute contraindications:
- Concurrent CNS depressant use (opioids, benzodiazepines, barbiturates, alcohol, sleeping pills) — additive respiratory depression with established fatality risk[26][27]
- Severe liver disease — 7-HMG depends on liver enzymes for clearance; impaired function may cause unpredictable accumulation. Liver injury has been reported with kratom use[28][29]
- Severe respiratory disease — baseline breathing impairment increases vulnerability to opioid-mediated respiratory depression[8]
Relative contraindications:
- CYP3A4 inhibitor use — altered drug levels with unpredictable net effect[22][38]
- Pregnancy — no data on gestational exposure; neonatal withdrawal expected based on opioid receptor activity safety citation needed
- Active substance use disorder — 7-HMG maintains self-administration and increases subsequent morphine intake in animal models[21]
- Moderate liver disease — enzyme-dependent metabolism may be altered
Harm Reduction[edit]
Forms & Identification
7-HMG products span a wide range of formats — sublingual films, pressed tablets, liquid tonics, and nasal sprays — each with different onset speeds and bioavailability. Sublingual and nasal routes bypass liver metabolism, delivering more compound to the bloodstream faster than oral routes.[5] This means two products containing the same milligram amount of 7-HMG can produce very different effects depending on the delivery format.
Product labeling in this market is unreliable. Early kratom products were documented with artificially elevated 7-HMG concentrations,[11] and the current semi-synthetic market operates without standardized testing or manufacturing oversight.[13] Stated doses on packaging should not be assumed accurate.
Set & Setting
The opioid experience is less sensitive to set and setting than psychedelic states, but environment still matters. A safe, comfortable location with a sober companion present reduces risk during initial exposures. Because 7-HMG depresses breathing — the primary lethal mechanism — falling asleep alone after use is a specific danger. This risk escalates sharply with any co-ingested depressant.
Guidelines
- Start with the lowest available dose and wait for full onset before considering redosing — onset varies by route (sublingual and nasal are faster than oral)
- Never combine with other depressants — alcohol, benzodiazepines, other opioids, and sleeping pills produce additive respiratory depression
- Have naloxone available and ensure someone present knows how to administer it
- Avoid using alone, particularly with sublingual or nasal products that produce rapid-onset effects
- Do not drive or operate machinery — sedation and impaired reaction time are core effects
- Be aware of accumulation — 7-HMG's half-life extends from approximately 4.7 hours (single dose) to 24.7 hours with repeated use,[23] meaning effects can stack unexpectedly with daily dosing
- Avoid CYP3A4 inhibitors including grapefruit, which can unpredictably alter 7-HMG levels
Aftercare & Integration
7-HMG's extended half-life with repeated dosing[23] means residual effects can persist longer than expected. Allow a full recovery period before driving, working, or making significant decisions. Hydration, light food, and rest support physical recovery.
The opioid warmth and emotional quieting produced by 7-HMG can create a strong pull toward re-use, particularly for those managing chronic pain or emotional distress. Honest self-assessment of the desire to redose — especially if the interval between uses is shortening — is the single most important aftercare practice.
Recovery & Support
7-HMG produces classical opioid dependence. If you are using daily, experiencing withdrawal symptoms between doses, or escalating your dose, medical support is available. Published treatment approaches include buprenorphine[10] and methadone,[36] both established medications for opioid use disorder.
Withdrawal from 7-HMG resembles opioid withdrawal broadly: muscle aches, insomnia, anxiety, nausea, sweating, and restlessness. Medical management can substantially reduce discomfort.[32] If you are considering stopping, consult a healthcare provider experienced with opioid tapering — abrupt cessation after heavy chronic use carries risk of severe withdrawal.[33]
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Emergency Response
Recognizing an emergency:
7-HMG is an opioid — the emergency signs are opioid overdose signs. Watch for: breathing that slows, becomes irregular, or stops; blue or gray lips and fingertips; pinpoint pupils; unresponsiveness to loud voice or sternal rub; gurgling or snoring sounds in an unconscious person.
Immediate steps:
- 1. Call emergency services immediately if breathing is slow, irregular, or absent
- 2. Administer naloxone if available — intranasal or intramuscular, per packaging instructions
- 3. Place the person in the recovery position (on their side) if unconscious but breathing
- 4. Stay with them — naloxone wears off faster than 7-HMG, and breathing may stop again
- 5. Do NOT induce vomiting in an unconscious person
- 6. Do NOT leave them alone to "sleep it off"
What to tell the dispatcher:
Name the substance (7-hydroxymitragynine or "7-OH" — a kratom-derived opioid), the amount if known, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Reversal agent: Naloxone fully reverses 7-HMG respiratory depression.[8] A second dose may be required because naloxone's duration of action is shorter than 7-HMG's.
Legal Status[edit]
The regulatory landscape for 7-hydroxymitragynine is actively evolving, driven by the emergence of concentrated semi-synthetic products since 2023. Unlike traditional kratom leaf — which contains 7-HMG only as a trace alkaloid — these concentrated formulations have prompted specific regulatory action at both federal and state levels.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not scheduled (as of May 2026) | FDA recommended DEA scheduling of concentrated 7-OH products on July 29, 2025; DEA rulemaking pending. Warning letters issued to seven companies in June 2025[7] |
| United States (state) | Varies by state | Arizona, Oklahoma, Texas, and Utah restrict 7-HMG content to less than 2% of total alkaloid content in commercial products[43] |
| Australia | Schedule 9 (prohibited substance) | 7-HMG is listed as a prohibited substance[43] |
| United Kingdom | Not scheduled | Kratom and alkaloids not currently controlled under the Misuse of Drugs Act; concentrated 7-HMG products generating regulatory scrutinycitation needed |
| Canada | Not explicitly scheduled | Health Canada prohibited marketing of kratom for oral use in 2020; 7-HMG as isolated compound not specifically listed under the Controlled Drugs and Substances Actcitation needed |
| Thailand | Decriminalized (personal use) | Kratom decriminalized for personal use in 2021; regulatory nuances may apply to isolated alkaloidscitation needed |
| Malaysia | Controlled | Kratom possession and sale prohibited under the Poisons Actcitation needed |
| European Union | Not scheduled at EU level | Regulation varies by member state; no EU-wide scheduling of kratom alkaloidscitation needed |
references
- [1] ^abTakayama H, Ishikawa H, Kurihara M, Kitajima M, Aimi N, Ponglux D, Koyama F, Matsumoto K, Moriyama T, Yamamoto L, Watanabe K, Murayama T, Horie S (2002) Studies on the Synthesis and Opioid Agonistic Activities of Mitragynine-Related Indole Alkaloids: Discovery of Opioid Agonists Structurally Different from Other Opioid Ligands. — Journal of Medicinal Chemistry doi:10.1021/jm010576e
- [2] ^abcdefKruegel AC, Gassaway MM, Kapoor A, Varadi A, Majumdar S, Filizola M, Javitch JA, Sames D (2016) Synthetic and Receptor Signaling Explorations of the Mitragyna Alkaloids: Mitragynine as an Atypical Molecular Framework for Opioid Receptor Modulators. — Journal of the American Chemical Society doi:10.1021/jacs.6b00360
- [3]
- [4]
- [5]
- [6] ^abHill K, Boyer EW, Grundmann O, Smith KE (2025) De facto opioids: Characterization of novel 7-hydroxymitragynine and mitragynine pseudoindoxyl product marketing. — Drug and Alcohol Dependence doi:10.1016/j.drugalcdep.2025.112701