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Human dose:
 150-200 mg/ iv Usdin & Efron 1979 citing Pennes & Hoch 1957
 300-400 mg/ p.o. Usdin & Efron 1979 citing Clarke 1969
Orally active at 8 mg/ kg; Intravenously at 2 mg/ kg. Naranjo 1967 and Ott 1993
When smoked, far smaller amounts (even normally trivial) produce a discernible interaction with tryptamines and/or LSD.
Shredded B. caapi bark saturated with between 20-50% DMT (w/w) makes an amazing smoking blend.


3-4 [to ?] hours. [I can find no solid answers on this. See comments under metabolism]
Gracie & Zarkov reported a much longer effect when smoking around 50 mg of isolated alkaloid (which was very likely contaminated with Harman).


Hallucinogenic. Usdin & Efron 1979 citing Pennes & Hoch 1957 (Also in Clarke's citing no one) We would suggest that the claims purporting hallucinogenicity bear a bit closer examination.
Not hallucinogenic. Usdin & Efron 1979 citing Turner et al. 1955
MAOI. Usdin & Efron 1979 citing Burger & Nara 1965
[Highly selective and reversible action.]
Thought to be specific for MAOI-A but may also affect MAOI-B weakly.
IC₅₀ as an MAOI is ~1.25 x 10^-8 M
EC₅₀ as an MAOI is 1.4 x 10^-5 M
       McKenna et al. 1998]
Therapeutic category: Central stimulant [Note 1] Merck Index
Sedative. Ott 1993 See this book. Also considered a sedative by Naranjo 1967 and by Leuner & Schlichtung 1989
Vasodilator. Raymond-Hamet 1941
At 3 mg/ kg or above (intramuscular in humans) causes sleep disturbances, tremors and nausea. Sax & Lewis 1989

Gunn 1935 reported a clonic convulsant action followed by a depressant action
See also Green & Slotkin 1973
Increases memory & intellectual faculties.
Shows action as a local anaesthetic (0.4% solution is said to be equivalent to 0.2% cocaine hydrochloride) Perrot & Raymond-Hamet 1927
The most recent thought is that this substance MAY be a hallucinogen at near toxic dosage levels.

Harmine has seen a variety of medical uses, all of which have fallen into disuse; including after-care for encephalitis victims and as a treatment for Parkinson' disease (harmine's effectiveness in this latter case was limited by how far the disease had progressed). It has also seen experimental use as a light activated cytotoxic agent. The largest reason for harmine's lack of modern development is its non-patentable nature.


Toxicity : [Note 2]
MLD [minimum lethal dose] 200 mg per kg subcutaneously in rats. Merck Index Ninth Edition entry # 4471
LD50: 200 mg./ kg./ subcutaneous/ rat
      Usdin & Efron (1979) citing Merck Seventh
Rat: LDLo intravenous 10 mg/kg
Mouse: LD50 subcutaneous 243 mg/kg
LDLo intravenous 50 mg/kg
Rabbit: LDLo subcutaneous 200 mg/kg
LDLo intravenous 60 mg/kg
Guinea pig: LDLo subcutaneous 100 mg/kg
Frog: LDLo subcutaneous 300 mg/kg
      Sax & Lewis 1989
Perrot & Raymond-Hamet 1927 reported 200 mg/kg to be a lethal dose but did not include the route.
In the rabbit the lethal dose of harmine was said to be 60 mg/kg iv by Fuentes & Longo 1971

(Said to emit toxic NO_X fumes when heated to decomposition. Sax & Lewis 1989)

Death is due to a paralysis of respiration.
      Perrot & Raymond-Hamet 1927

Harmine showed very strong inhibition of the motility of Trypanosoma lewisii Kent (in vitro) Hopp et al. 1976

Harmine was shown to have antibacterial activity against gram-positive and gram-negative bacteria. Ahmad 1992 (Ross et al. 1980 claimed harmine was inactive but their study apparently showed poor methodology with regards to evaluating harmine. Al-Shamma et al. 1981 reported harmine active as an antimicrobial agent; see also Al-Shamma & Mitscher 1979.)


Merck Index cited Slotkin & DiStefano 1970
See also Ho 1977
Metabolism in mice: Tweedie & Burke 1987
Rats excrete as glucuronide conjugate. Slotkin & DiStefano 1970

Metabolism may vary widely between different species. Half-life in rats is 6 hours.
Harmine (and its metabolites) show a 3 hour half-life in humans (however, the half-life of harmine in humans given ayahuasca orally was reported to be less than two hours according to McKenna et al. 1998 Maximum plasma levels were reached 102 minutes after ingestion.)
Harmine will noticeably interact with free base tryptamines or orally activate tryptamines for only up to around 4 hours after its ingestion. This refers to harmine pre-administered rather than concurrently taken.
Harmaline and tetrahydroharmine are likely to have a slightly longer duration and be handled and processed differently, if observations from other species can be considered an indicator.
Detailed human pharmacological data is apparently only now beginning to be generated.


Cmax (average) 114.8 ± 61.7 ng/ml
Tmax (average) 102.0 ± 58.3 min.
T1/2 (average) 115.6 ± 60.1 min.

(Dosage of 3.4 mg/kg oral)
     Callaway et al. 1999