Orally and parenterally active psychotropic tryptamine derivatives

Based on McKenna & Towers [1984]
Texts from Petrus Pennanen, Michael from Melbourne.
Huge amounts of HTML formatting and referencing by dimitri
Much of this document is available in other formats at Hyperreal and Hyperspace


Data compiled from Kantor et al [1980]; Shulgin [1976], [1982]; Shulgin & Carter [1980]
Name of compound R1 R2 R3 R4 R5 Dosage (mg) Route (Oral/Par)
tryptamine H H H H H 1001 par/oral?
DMT (dimethyltryptamine) CH3 CH3 H H H 60 par
DET C2H5 C2H5 H H H 60 par/oral
DPT n-prop n-prop H H H 60 par/oral
DAT C3H5 C3H5 H H H 30 par/oral
DIPT i-prop i-prop H H H 30 oral
5-MeO-DIPT i-prop i-prop H H OCH3 12 oral
5-MeO-DMT CH3 CH3 H H OCH3 6 par
psilocin CH3 CH3 H OH H 122 oral
CZ-74 C2H5 C2H5 H OH H 152 oral
5-hydroxytryptamine (serotonin) H H H H OH 1003 oral
bufotenine CH3 CH3 H H OH 164 par
IT-290 H H CH3 H H 30 oral
4-hydroxy-alfa-methyl-tryptamine H H CH3 OH H 203 oral
MP-809 H H CH3 H CH3 605 oral
5-fluoro-alfa-methyl-tryptamine H H CH3 H F 256 oral
5-methoxy-alfa-methyl-tryptamine H H CH3 H OCH3 3 oral
4-hydroxy-diisopropyl-tryptamine i-prop i-prop H OH H 126 oral
i-prop CH3 H OH H 66 oral
N-t-butyl-tryptamine H t-butylH H H ? 7 par?
H H H ? ? ? ?
5-alfa-DMT CH3 CH3 CH3 H H ? ?
1 Autonomic symptoms; little central activity.
2 The phosphate esters are psilocybin and CEY-19, respectively; both are stoichiometrically equivalent to the 4-hydroxy isomers.
3 Cardiovascular and autonomic symptoms; little central activity.
4 A pressor amine rather than a hallucinogen in man.
5 An antidepressant rather than a hallucinogen in man.
6 Based on anonymous reports in the lay press. No clinical studies have been published.
7 No oral activity with doses up to 20 mg, may be parenterally active.
Other potentially psychedelic tryptamines include:
6-fluoro-alfa-methyltryptamine, 7-methyltryptamine, 5-methyltryptamine
5-fluorotryptamine, 6-fluorotryptamine and 5- and 6-fluorotryptophans.

Synthesis of DMT derivatives

Tryptamine derivatives and beta-carbolines have been detected as endogenous metabolites in mammals, including humans. Methyl transferases that catalyze the synthesis of tryptamines, including DMT, 5-MeO-DMT and bufotenine, are found in human lung, brain, cerebrospinal fluid, liver and heart (McKenna & Towers [1984]). In the pineal gland MAO is the primary inactivation pathway of serotonin, a neurotransmitter synthesized from the amino acid tryptophan. If MAO is blocked by harmine, harmaline or other MAO inhibitors serotonin can be converted by the methyltransferase enzymes HIOMT and INMT into psychedelic tryptamines (5-HT -(HIOMT)-> 5-MeOT -(2*INMT)-> 5-MeO-DMT).

So, ingesting l-tryptophan to increase serotonin levels, a candy bar to increase the amount of tryptophan getting to your brain and natural plant material containing 25-50 mg harmine/harmaline to block MAO, all at the same time, might cause your pineal gland to synthesize substantial amounts of 5-MeO-DMT (Most [1986]). This is extremely dangerous for persons with existing amine imbalance or schizophrenia. For normal, healthy people possible consequences are bad.

A potent inhibitor of INMT, which is a necessary enzyme for the synthesis of DMT and 5-MeO-DMT, is found in particularly high concentrations in the pineal gland. A bypassing or inhibition of the synthesis of this inhibitor might be responsible for trances and other psychedelic states achieved "without drugs" (Strassman [1990]). See Strassman's article for more information and speculation about the pineal gland.