Harmine half life: The plasma elimination half-life is on the order of 1–3 hours.

Urine Samples. Urine was collected in fractions of 0 to 8 h, 8 to 16 h, and 16 to 24 h in plastic containers with 3 ml of 6 N HCl and kept in the refrigerator during the 0- to 24-h collection period. Volunteers took home the two plastic containers corresponding to the 8- to 16-h and 16- to 24-h periods. Volume of each fraction was recorded and pH was adjusted to 2 to 4 with 6 N HCl, and two 50-ml aliquots were frozen at –20°C and stored at –80°C until analysis. The following monoamine metabolites, VMA, HVA, 5-HIAA, metanephrine, and normetanephrine were quantified by means of HPLC with coulometric detection following previously validated procedures (Soldin and Hill, 1980; Parker et al., 1986; Gamache et al., 1993). The limit of quantification was 3 mg/l for VMA, HVA, and 5-HIAA, 0.05 mg/l for metanephrine, and 0.10 mg/l for normetanephrine.

Harmol glucuronide and harmol sulfate have been described as the main urine metabolites of harmine following its i.v. administration in humans (Slotkin et al., 1970).

Alternative routes of administration like suppository, intravenous, intramuscular, inhalational aerosol, transdermal and sublingual avoid the first-pass effect because they allow drugs to be absorbed directly into the systemic circulation. Note that the intravenous route also avoids the absorption phase.

Pharmacokinetics are also dose-dependent. So the if you want similar looking curves for smoked harmalas, compare it with similar oral doses.

Can one assume that the graph for harmine can be scaled proportionally to the dose consumed?

Would you say that this way of thinking could be correct. Or would you say this is plain wrong?

I wouldn't say it's plain wrong. My understanding is that the shape of your curve looks good, but in the end I wouldn't bet money on it. The curve could also peak at 40ng/ml, because the lung may absorb harmalas much better.

Are you worried about drug interactions, a drug test, or just curious?

Yes. I understand this. Thank you.

Ok. I see. For me...to become certain...I might have to bite the bullet and swallow some dmt after a certain ammount of time and see if something happens.

This wouldnt work im afraid as the mao in your stomach is unaffected (or barely affected) when you smoke it.

Abstract
The activity of both isozymes of monoamine oxidase (MAO) is reduced by 50% in the brain of human smokers. We hypothesized that this is not an epiphenomenon, but should bring about potentiation of the action of psychostimulant drugs. To test this hypothesis, we carried out serial positron emission tomography (PET) studies in Göttingen miniature pigs to measure the binding of the MAO-A ligand [11C]harmine and to measure the changes in [11C]raclopride binding evoked by a low dose of amphetamine (0.7 mg/kg as free base, i.v.), first in a baseline condition, and, one month later, after acute treatment with pargyline (2 x 3 mg/kg as free base, i.m.). In the baseline, the distribution volume of [11C]harmine relative to the arterial input (V(d), ml g(-1)) ranged from 74 ml g(-1) in cerebellum to 139 ml g(-1) in the medial hypothalamus. Pargyline treatment reduced the magnitude of V(d) globally to 34-54 ml g(-1). Nearly complete displacement of [11C]harmine binding was detected in neocortex and striatum, but there was evidence for pargyline-resistant binding in the pituitary gland and diencephalon. In the baseline condition, the low dose of amphetamine evoked a 14% decline in the binding potential (BP) (pB) of [11C]raclopride in striatum (P = 0.026). After pargyline treatment, the amphetamine effect was of similar magnitude (-11%), although not statistically significant (P = 0.054). However, the second amphetamine challenge evoked a 24% reduction in [11C]raclopride pB relative to the original baseline condition (P = 0.01. Present results do not strongly support our hypothesis that MAO inhibition should potentiate the amphetamine-evoked dopamine release as measured in the [11C]raclopride competition paradigm.

This study quantifies blood and urinary levels of harmine and its urinary metabolites (harmol, harmol glucuronide and harmol sulfate) in man and rats after the i. v. administration of 0.5 mg of harmine per kg (man and rats) and 5 mg of harmine per kg (rats). Metabolites were analyzed by paper chromatography, enzymatic hydrolysis and fluorometry. Within two minutes after administration, 10% of the dose was found in the blood of either species; after four hours, ≤1%. Both species excreted the same urinary metabolites. After 48 hours, total urinary excretion was about the same, although the excretion rate was higher in man. Urinary harmine and harmol concentrations were insignificant. Harmol sulfate was the primary conjugate in rats; harmol glucuronide excretion predominated in man. The ratio of the rate of harmol glucuronide excretion to the rate of harinol sulfate excretion (G/S) increased with time in rats given 5 mg of harmine per kg, but was relatively constant in rats and humans given 0.5 mg of harmine per kg. Administration of Na2SO3 to rats given 5 mg of harmine per kg prevented this rise in G/S, suggesting that 3'-phosphoadenosine 5'-phosphosulfate plays a limiting role in the formation of harmol sulfate.