7-Hydroxymitragynine

methyl (E)-2-[(2S,3S,7aS,12bS)-3-ethyl-7a-hydroxy-8-methoxy-1,2,3,4,6,7,7a,12b-octahydroindolo[2,3-a]quinolizin-2-yl]-3-methoxyprop-2-enoate

Overview

7-Hydroxymitragynine belongs to Opioids.

Key safety note: 7-Hydroxymitragynine is a genuine μ-opioid agonist and is the constituent responsible for kratom's opioid effects and its dependence potential.[2][4][5]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Classic μ-opioid effects: analgesia, euphoria, warmth, relaxation and sedation, with anxiolysis at lower doses.
  • Opioid adverse effects: nausea and vomiting, itching, constipation, pinpoint pupils, dizziness and, at higher doses or in combination, dangerous respiratory depression.
  • Repeated use produces rapid tolerance and physical dependence, with an opioid-type withdrawal syndrome (anxiety, aches, sweating, insomnia, gastrointestinal distress, craving) on cessation.
  • Concentrated 7-OH products can produce far stronger opioid effects than traditional kratom tea, with correspondingly greater overdose and dependence risk.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral. Not a recommendation. There are no controlled human dosing studies for isolated 7-hydroxymitragynine. It is a μ-opioid agonist, so opioid tolerance, dependence, overdose and respiratory-depression risks apply, and it should never be combined with other depressants. The critical hazard is that 'concentrated 7-OH' products are semi-synthetically enriched far above natural leaf levels, so per-serving amounts vary enormously between products and are frequently much stronger than they appear. Naloxone reverses its opioid effects.

Dose ranges

Marketed 7-OH product (per tablet/serving)

commonly ≈5–30 mg, highly variable, not a safe or recommended dose

Duration

onset

≈15–45 min (oral, approximate)

peak

Not well characterised

total

≈3–5 h (approximate, opioid-like)

Chemical & Physical Properties
FormulaC23H30N2O5
Molar mass414.49 g/mol
StateSolid
Melting pointNot reported
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP2.3 (predicted, XLogP3)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS174418-82-7
CAS (enantiomer)
PubChem CID44301524
InChIKeyRYENLSMHLCNXJT-CYXFISRXSA-N
InChIInChI=1S/C23H30N2O5/c1-5-14-12-25-10-9-23(27)20-17(7-6-8-19(20)29-3)24-21(23)18(25)11-15(14)16(13-28-2)22(26)30-4/h6-8,13-15,18,27H,5,9-12H2,1-4H3/b16-13+/t14-,15+,18+,23+/m1/s1
SMILESCC[C@@H]1CN2CC[C@]3(C(=NC4=C3C(=CC=C4)OC)[C@@H]2C[C@@H]1/C(=C\OC)/C(=O)OC)O

Synonyms

  • 7-OH-mitragynine
  • 7-hydroxymitragynine
  • Active kratom metabolite
  • 7-OH
Pharmacodynamics & Biochemistry

7-Hydroxymitragynine (7-OH) is an oxidative metabolite of mitragynine, the main alkaloid of kratom (Mitragyna speciosa), and is the principal opioid-active species behind kratom's μ-opioid effects. At the μ-opioid receptor (MOR) it is a partial agonist with markedly higher affinity than the parent alkaloid (Kᵢ ≈78 nM vs. ≈7,700 nM for mitragynine), with weaker activity at κ- and δ-opioid receptors. Functionally the two alkaloids differ sharply: in [³⁵S]GTPγS assays mitragynine behaves as an MOR antagonist while 7-OH is a partial agonist (Emax ≈41%). In rats 7-OH produces morphine-like antinociception, roughly an order of magnitude (≈13×) more potent than morphine, that is reversed by the opioid antagonist naltrexone, whereas mitragynine does not. 7-OH shows G-protein–biased signalling at MOR (relatively little β-arrestin-2 recruitment) in vitro. This was once hoped to mean safer opioids, but the clinical benefit of bias is now disputed, and 7-OH still carries the core opioid liabilities of tolerance, physical dependence, withdrawal and respiratory depression: especially in the semi-synthetically enriched 'concentrated 7-OH' products now on sale.

Biological targets

  • MOR
  • KOR
  • DOR

Binding & functional measurements

TargetMeasurementSpecies
MORKi 78 nMHuman/Rodent
KORKi 130 nMHuman/Rodent
DORKi 130 nMHuman/Rodent
Pharmacokinetics
BioavailabilityFormed in vivo from mitragynine, also present in kratom products
TmaxNot reported
Half-lifeEstimates limited, reported a few hours
VdNot reported
Protein bindingNot reported
MetabolismHepatic. Further glucuronidation
ExcretionRenal and biliary
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

7-Hydroxymitragynine is a genuine μ-opioid agonist and is the constituent responsible for kratom's opioid effects and its dependence potential. Like other opioids it can cause respiratory depression: the risk is greatest in opioid-naïve users, at high doses, and in combination with other depressants (opioids, benzodiazepines, alcohol, gabapentinoids), and it produces tolerance, physical dependence and an opioid withdrawal syndrome on stopping. The acute danger has risen sharply with the appearance of 'concentrated 7-OH' products (tablets, shots, gummies sold in shops and gas stations) that are semi-synthetically enriched to contain far more 7-OH than any natural kratom leaf, so a single marketed serving can deliver a substantial opioid dose to someone who believes they are taking a herbal supplement. Its opioid effects are reversible by naloxone. Because it is an opioid, overdose can be fatal. It should not be combined with other depressants, driven on, or used in pregnancy. Its earlier reputation as a 'safer', biased opioid is not established and must not be relied on.[2][4][5]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Opioids, Benzodiazepines, Alcohol, Gabapentinoids (gabapentin, pregabalin), GHB / GBL Additive respiratory depression, potentially fatal.[4]
CYP3A4 inhibitors (ritonavir, azole antifungals, macrolides, grapefruit) Raise 7-OH and mitragynine exposure and effect.[4]
SSRIs, SNRIs, MAOIs Kratom combinations have been implicated in adverse serotonergic events.[4]

Contraindications

Combining with alcohol or other CNS depressants concurrent opioids or other CNS depressants (respiratory-depression risk).[4]
Opioid-naive (no tolerance) no tolerance, and a higher overdose risk from concentrated products.[5]
Pregnancy or breastfeeding neonatal opioid withdrawal reported with kratom.[5]
History of stimulant or substance use disorder history of opioid use disorder or dependence.[4]
Respiratory disease or sleep apnoea[4]
Usage & Context
  • Naturally a minor kratom alkaloid and an active metabolite of mitragynine. Traditional kratom leaf/tea contains only trace amounts.
  • Since the mid-2020s sold as semi-synthetically enriched 'concentrated 7-OH' products (tablets, shots, gummies) in convenience stores and vape/smoke shops, marketed as wellness or supplement products: the focus of intense FDA/DEA concern.
  • Also used by some people to self-treat pain or to manage opioid withdrawal.
Sources & Evidence

Further Information