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Harmine Facts

Psychedelic; Indole alkaloid; Monoamine oxidase inhibitor

Description

Harmine (7-methoxy-1-methyl-β-carboline) is a naturally-occurring alkaloid of the β-carboline class. It blocks the enzyme that destroys serotonin and dietary tryptamines in the gut and liver.[1]

Subjective effects include mood elevation, enhanced introspection, and vivid visual imagery — though these are documented primarily in combination with DMT.[2] Harmine's standalone character is largely unknown — in most contexts it enables the experience rather than drives it.

No abuse liability has been established, and no controlled human dose data for harmine alone exist. The dominant risk is serotonin syndrome: combining harmine with antidepressants forces two serotonin-raising mechanisms at once, causing dangerous overheating, muscle rigidity, and seizure.[3]

Dose and durationby route · individual sensitivity varies

Oral(mg)
Threshold< 50 mgLight50 – 100 mgCommon100 – 200 mgStrong200 – 400 mgHeavy400+ mg

Starts in 30 – 60 minLasts 4 – 6 hoursAfter-effects 4 – 24 hours

Body and dependence

Acute toxicity
Low
Chronic toxicity
Low
Physical dependence
None
Psychological dependence
Negligible
Withdrawal
None recorded
Compulsive redosing
Negligible

Tolerance

Builds
None
Fully resets after
Not recorded
Carries over to
moclobemide

Effectslikely at a common dose

Body
none likely · 8 possible, including Nausea, Dizziness, Trembling

Who shouldn't take it

Absolute
Concurrent SSRI/SNRI use; Concurrent irreversible MAOI use; Pregnancy and lactation
Relative
Cardiovascular instability; Hepatic impairment; CYP2D6 poor metabolizer status; Concurrent tryptamine use without dose titration; Concurrent sympathomimetic use; High-tyramine foods at significant MAOI doses

Combinations60 recorded

Lethal (6)
Amphetamines; MDMA, Amphetamines; MDMA, MDA; Psychedelics; SNRIs; Stimulants
Dangerous (28)
5-HTP, Tryptophan; Alpha-2 adrenergic receptor antagonist; Buspirone; Ephedrine, Pseudoephedrine; Local anesthetics; NDRIs (Wellbutrin); NRIs; Opioids; SSRIs; Antihistamines; Antipsychotics; Benzodiazepines, Barbiturates; Caffeine; Cannabis; Clonidine, Guanfacine; Dopamine agonists; DXM; GHB, Baclofen; GHB, GBL; Ibogaine; Ketamine, DXM, PCP; L-Tyrosine; Naltrexone; NSAIDs; and 4 more, see full page
Caution (20)
See full page: psychedex.org/substances/harmine
Not graded (6)
Not listed never means safe.

Seek help immediately if

Most difficulty is psychological (intense fear, panic, confusion) and passes with calm support — the signs below mean seek emergency help:

  • Very high body temperature; hot, dry skin
  • Seizures
  • Chest pain; fast or irregular heartbeat
  • Severe muscle rigidity, tremor, or twitching (possible serotonin syndrome)
  • Cold, pale, or blue fingers/toes — severe vasoconstriction (notably NBOMe / DOx)
  • Persistent vomiting; unconsciousness; uncontrollable agitation or risk of self-harm

What to do

  1. Stay calm and reassure — remind them they took a drug and the effect will pass
  2. Move to a calm, quiet, safe space with low light; reduce noise and sensory input
  3. Keep them from harm — they may act on fear or confusion; stay with them, don't leave them alone
  4. Talk them down gently; don't grab or restrain unless they're in danger
  5. For the medical signs above (overheating, seizure, chest pain, vasoconstriction, unresponsive) call emergency services
  6. If overheating, cool the body; be ready to give rescue breaths / CPR

The experience is time-limited and usually resolves with calm reassurance in a safe setting — psychological first aid, not medication. Serious physical harm is uncommon for classic psychedelics (LSD, psilocybin) but real for some potent phenethylamines (NBOMe, DOx), where hyperthermia, seizures, and vasoconstriction warrant emergency care.

988 Suicide & Crisis LifelineFireside Project: 62-FIRESIDE

Version r1.a1 · Not medical advice

References

  1. [1]
    ^Kim H, Sablin SO, Ramsay RR (1997) Inhibition of monoamine oxidase A by beta-carboline derivatives — Archives of Biochemistry and Biophysics PMID:8990278
  2. [2]
    ^Riba J, Valle M, Urbano G, Yritia M, Morte A, Barbanoj MJ (2003) Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokinetics — Journal of Pharmacology and Experimental Therapeutics PMID:12660312
  3. [3]
    ^Finberg JPM, Rabey JM (2016) Inhibitors of MAO-A and MAO-B in Psychiatry and Neurology — Frontiers in Pharmacology doi:10.3389/fphar.2016.00340
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