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Kratom (Mitragynine)

Opioidoral · inferred

Primary alkaloid of Mitragyna speciosa (kratom). Partial agonist at mu-opioid receptors with dose-dependent effects: stimulant at low doses (1-3g), opioid-like analgesia/sedation at higher doses (5-15g). Hepatically metabolized to 7-hydroxymitragynine (13x more potent at MOR) and mitragynine pseudoindoxyl. Also interacts with serotonin (5-HT2C/5-HT7), dopamine (D2), and alpha-2 adrenergic receptors. Terminal half-life ~23h but highly variable (3-43h depending on preparation and dose).

Projected serum levels — 3 g (leaf) (≈ 45 mg), as needed (shown daily)

Kratom (Mitragynine)
Kratom (Mitragynine) modeled serum levels, 3 g (leaf) (≈ 45 mg) as needed (shown daily) over 15 days Population-based pharmacokinetic estimate. Steady state reached after approximately 2 days. 0 6.3 12.5 18.8 25 Day 0 Day 4 Day 8 Day 11 Day 15 Time on a regular schedule ≈ steady state · day 2
Kratom (Mitragynine) modeled serum levels with a loading dose of 4.5 g (leaf), then 3 g (leaf) (≈ 45 mg) as needed (shown daily) The first dose is larger so levels approach steady state faster. 0 6.3 12.5 18.8 25 Day 0 Day 4 Day 8 Day 11 Day 15 Time on a regular schedule

Maintenance schedule: 3 g (leaf) (≈ 45 mg) as needed (shown daily) (oral).

Loading schedule: 4.5 g (leaf) on day 1, then 3 g (leaf) (≈ 45 mg) as needed (shown daily) — reaching therapeutic levels sooner.

Modeled steady state after ~2 days: peak ≈ 22.0 mg, trough ≈ 9.2 mg body load. Population-based estimate over 15 days for a reference dose at a 70 kg reference body mass — the interactive app scales curves to your doses, timing, and body mass.

Key facts

Category
Opioid
Route modeled
Oral
Model confidence
inferred
Half-life
15 h
Common dose
3 g (leaf) (≈ 45 mg)
Reference dose range
1.5–6 g (leaf) (single dose)
Suggested cadence
as needed (shown daily)

Documented interactions

  • contraindicated
    Efavirenz (Sustiva) + Kratom (Mitragynine) CYP induction

    Efavirenz (Sustiva) inducer of CYP3A4 predicted to change Kratom (Mitragynine) AUC by ~0.18x

  • contraindicated
    Rifampin + Kratom (Mitragynine) CYP induction

    Rifampin inducer of CYP3A4 predicted to change Kratom (Mitragynine) AUC by ~0.18x

  • danger
    1P-LSD (1-Propionyl-LSD) + Kratom (Mitragynine) Serotonin risk

    1P-LSD (1-Propionyl-LSD) and Kratom (Mitragynine) both have serotonergic activity. Risk of serotonin syndrome (hyperthermia, rigidity, autonomic instability, altered mental status).

  • danger
    25I-NBOMe + Kratom (Mitragynine) Serotonin risk

    25I-NBOMe and Kratom (Mitragynine) both have serotonergic activity. Risk of serotonin syndrome (hyperthermia, rigidity, autonomic instability, altered mental status).

  • danger
    2C-I (2,5-Dimethoxy-4-iodophenethylamine) + Kratom (Mitragynine) Serotonin risk

    2C-I (2,5-Dimethoxy-4-iodophenethylamine) and Kratom (Mitragynine) both have serotonergic activity. Risk of serotonin syndrome (hyperthermia, rigidity, autonomic instability, altered mental status).

  • danger
    2C-B (4-Bromo-2,5-dimethoxyphenethylamine) + Kratom (Mitragynine) Serotonin risk

    2C-B (4-Bromo-2,5-dimethoxyphenethylamine) and Kratom (Mitragynine) both have serotonergic activity. Risk of serotonin syndrome (hyperthermia, rigidity, autonomic instability, altered mental status).

Serum checks 482 modeled interaction pairings for kratom (mitragynine) across your whole stack — absorption conflicts, enzyme inhibition, and nutrient depletion included.

Research behind this entry

  1. Pharmacokinetics of mitragynine in man Trakulsrichai S et al. · Drug Design, Development and Therapy, 2015 DOI

    First human pharmacokinetic study of mitragynine in 10 chronic kratom users. Established terminal half-life of 23.24 +/- 16.07 hours with oral two-compartment model, Tmax ~0.83h, and linear pharmacokinetics.

  2. 7-Hydroxymitragynine Is an Active Metabolite of Mitragynine and a Key Mediator of Its Analgesic Effects Kruegel AC et al. · ACS Central Science, 2019 DOI

    Demonstrated that mitragynine is hepatically converted to 7-hydroxymitragynine, which acts as the primary mediator of analgesic effects. This metabolic activation is critical to understanding kratom pharmacology and…

  3. Kratom Alkaloids: Interactions With Enzymes, Receptors, and Cellular Barriers Basiliere S, Bhowmik S et al. · Frontiers in Pharmacology, 2021 DOI

    Comprehensive review of kratom alkaloid interactions with CYP enzymes (CYP3A4, CYP2D6), opioid receptors, serotonin receptors, and P-glycoprotein. Highlights drug interaction potential and complex polypharmacology.

3 published studies referenced in the app, each with a plain-language summary.