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MDA

Group: Empathogens
Tags: Amphetamines
Nicknames: Sassafras, Sass, Sally, Medusa
Last reviewed: October 2026

Pharmacology

MDA belongs to the phenethylamine/amphetamine family and is structurally the N-desmethyl analogue of MDMA, essentially MDMA with one less methyl group, which accounts for much of the overlap, and difference, in their effects.

Two optical isomers of MDA exist. These are mirror image versions of the molecule. One version (the S-MDA) is more potent than the other (R-MDA), and possesses more psychoactive stimulant properties, similar to MDMA. S-MDA has greater affinity for the three monoamine transporters and generally considered the isomer responsible for MDA’s amphetamine like character. R- MDA is seen as milder and more psychedelic

Shulgin describes the effects of this version as ‘more peaceful and MDMA-like’ at lower doses. Generally, MDA is longer lasting than MDMA with expected effects between 6-8 hours. MDA acts on three transporter molecules in the brain, SERT, NET and DAT that cause an increase in the serotonin, norepinephrine (noradrenaline) and dopamine neurotransmitters, (an SNDRA), and is also an agonist at the serotonin 5-HT2A, 5-HT2B and 5-HT2C receptors, with additional affinity for several adrenergic and serotonin receptor subtypes. Serotonin release is thought to underlie its empathogenic/entactogenic effects, dopamine release its euphoric and reinforcing effects, and combined dopamine/norepinephrine release its stimulant effects, while direct 5-HT2A agonism is thought to drive its psychedelic effects. This direct receptor agonism is a key reason MDA's psychedelic component is more pronounced than MDMA's.

Onset of action of MDA is typically roughly 20–65 minutes, with peak effects around 2 hours after dosing. The elimination half-life is approximately 8–11 hours, with a duration of action of 5–8 hours (occasionally up to 10- notably longer than MDMA). Interestingly, this longer duration compared with MDMA appears to be a pharmacodynamic difference rather than a pharmacokinetic one as MDA's effects rely relatively more on 5-HT2A receptor agonism than on serotonin release itself, which is part of why it "feels" different rather than just "lasts longer" in a simple dose-response sense. Metabolism is hepatic, involving cytochrome P450 enzymes, with renal excretion.

There is some evidence of MDA producing serotonergic neurotoxic effects in animal studies, possibly due to its metabolism. This is similar to contested, dose dependent concerns raised about MDMA.

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