MDA

1-(1,3-benzodioxol-5-yl)propan-2-amine

Overview

MDA belongs to Entactogens/Empathogens / Phenethylamines.

Key safety note: MDA carries the same core risks as MDMA, generally at a longer duration and with a more dopaminergic, more hallucinogenic character.[5][2]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Euphoria, emotional warmth, empathy and closeness, increased introspection and self-acceptance, and stimulation/increased energy. MDA tends to feel more introspective and emotionally intense, and more psychedelic, than the more social, extroverted MDMA.
  • At higher doses perceptual changes are common: brightened colours, closed-eye imagery, occasional mild visuals and, rarely, mild hallucinations, without the full sensory disruption of a classical psychedelic.
  • Unwanted effects include jaw clenching and teeth grinding, dilated pupils, raised heart rate and temperature, anxiety or fear, insomnia, and a multi-day 'comedown' of low mood, irritability and fatigue as serotonin recovers.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral (the common route). The values below are for oral use. These are commonly cited recreational reference ranges (PsychonautWiki), not a safe dose. MDA is longer-acting and more stimulating and psychedelic than MDMA, and redosing worsens the neurotoxic and comedown burden: avoid it. Do not combine with MAOIs or other serotonergic drugs (serotonin-syndrome risk). Keep cool and take breaks to avoid overheating. Sip rather than gulp water, and remember that powders sold as 'MDA'/'sass' are often mis-sold or adulterated, so test the substance.

Dose ranges

Threshold

20 mg

Light

40–60 mg

Common

60–100 mg

Strong

100–145 mg

Heavy

145 mg +

Duration

onset

30–90 min

total

5–8 h

after effects

4–48 h comedown (low mood, fatigue, anxiety)

Chemical & Physical Properties
FormulaC10H13NO2
Molar mass179.22 g/mol
StateLiquid
Melting pointNot reported
Boiling point157 °C at 22 mmHg, 80–90 °C at 0.2 mmHg
DensityNot reported
Vapor pressureNot reported
pKa9.67 (25 °C)
LogP1.64
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS4764-17-4
CAS (enantiomer)
PubChem CID1614
InChIKeyNGBBVGZWCFBOGO-UHFFFAOYSA-N
InChIInChI=1S/C10H13NO2/c1-7(11)4-8-2-3-9-10(5-8)13-6-12-9/h2-3,5,7H,4,6,11H2,1H3
SMILESCC(CC1=CC2=C(C=C1)OCO2)N

Synonyms

  • 3,4-Methylenedioxyamphetamine
  • Tenamfetamine
  • Sass
  • Love drug
  • Sally
  • Sassafras
Pharmacodynamics & Biochemistry

MDA (3,4-methylenedioxyamphetamine) is an entactogen with mixed stimulant and psychedelic character, and is also the primary active metabolite of MDMA (MDMA is its N-methyl homologue). Like MDMA it acts mainly as a monoamine releaser: it is carried into the nerve terminal as a substrate by the serotonin (SERT), noradrenaline (NET) and dopamine (DAT) transporters, where it disrupts vesicular storage via VMAT2 and reverses transporter flow, driving serotonin, noradrenaline and dopamine out into the synapse rather than merely blocking their reuptake. Reported release potencies are fairly balanced across the three transporters (EC50 on the order of ~110–190 nM), so it produces both serotonergic entactogenic and catecholaminergic stimulant effects. It also has direct agonist activity at 5-HT2A (and 5-HT2B/2C) receptors, more so than MDMA, and this stronger direct serotonergic-receptor action is thought to give MDA its greater psychedelic/hallucinogenic quality (brightened colours, imagery, occasional mild visuals) layered on top of the empathogenic effects. The two enantiomers differ: R-(−)-MDA carries most of the psychedelic, LSD-like character, whereas S-(+)-MDA is the more potent transporter substrate and drives the stimulant and entactogenic effects. MDA is normally used as the racemate.

Biological targets

  • SERT
  • DAT
  • NET
  • 5-HT2A

Binding & functional measurements

TargetMeasurementSpecies
Dopamine transporterEC50 106 ± 7.0 nM
Emax 104%
Rat
Noradrenaline transporterEC50 47 ± 7.0 nM
Emax 91%
Rat
Serotonin transporterEC50 162 ± 28 nM
Emax 109%
Rat
Pharmacokinetics
BioavailabilityOral, well absorbed
Tmax≈1–2 h
Half-life≈6–8 h
VdNot reported
Protein bindingNot reported
MetabolismHepatic CYP2D6 demethylenation. Also a metabolite of MDMA
ExcretionRenal
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

140 mg/kg (mouse, i.p.)

MDA carries the same core risks as MDMA, generally at a longer duration and with a more dopaminergic, more hallucinogenic character. The main acute dangers are serotonergic and thermal: dangerous overheating (hyperthermia), especially when dancing in a hot, crowded space, and serotonin syndrome when combined with other serotonergic drugs: MAOIs are especially dangerous and the combination can be fatal. It raises heart rate, blood pressure and body temperature and strains the cardiovascular system. Deaths are usually from cardiovascular collapse or hyperthermia and its complications. As with MDMA, high or repeated doses are linked to serotonergic neurotoxicity in animals, and heavy use is followed by a serotonin-depletion 'comedown' of low mood, anxiety and fatigue lasting days. MDA tends to produce more anxiety, fear and stimulation than MDMA. Drinking too much water while unable to excrete it can cause dangerous hyponatraemia (low blood sodium). It should not be combined with MAOIs, other stimulants, or other serotonergic drugs, and material sold as 'MDA' or 'sass' is frequently mis-sold or adulterated.[5][2]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

MAOIs Risk of hypertensive crisis and severe, potentially fatal serotonin syndrome, never combine.[5]
SSRIs, SNRIs, Tramadol, Triptans, Lithium Serotonin-syndrome risk. SSRIs also blunt the desired effects by blocking the transporter MDA works through.[5]
Stimulants (amphetamines, cocaine) Additive cardiovascular strain and hyperthermia.[5]
Strong CYP2D6 inhibitors (e.g. paroxetine, fluoxetine) Can raise exposure (some SSRIs, ritonavir, or CYP2D6 deficiency), MDA is a CYP2D6 substrate and the active metabolite of MDMA.[2][5]

Contraindications

Cardiovascular disease, hypertension or arrhythmia hypertension or arrhythmia.[5]
Concurrent MAOI, SSRI/SNRI or other serotonergic medication concurrent MAOI or other serotonergic medication.[5]
Personal or family history of psychosis, schizophrenia or bipolar disorder[5]
Pregnancy or breastfeeding[5]
Hot, dehydrating environments (overheating risk) hot, dehydrating settings raise the hyperthermia risk.
Usage & Context
  • A recreational entactogen/psychedelic ('Sass', 'Sally', and sometimes sold as or alongside 'sassafras'), used for euphoria, empathy, emotional openness and mild psychedelic effects: mainly in dance, festival and psychonaut settings.
  • It is also the primary active metabolite of MDMA, so part of MDMA's effect and harm profile reflects MDA exposure.
  • It has no accepted medical use and is a Schedule I / Class A / Anlage I controlled substance. It was studied in mid-20th-century research (including unethical secret experiments) before being prohibited.
Sources & Evidence
  1. PubChem: 3,4-MDA (CID 1614) — identifiers & computed properties
  2. de la Torre R, Farré M, Navarro M, et al. (2004). Clinical pharmacokinetics of amfetamine and related substances: monitoring in conventional and non-conventional matrices. Clin Pharmacokinet 43:157-85.

    PMID 14871155 · doi:10.2165/00003088-200443030-00002

  3. Johnson MP, Hoffman AJ, Nichols DE (1986). Effects of the enantiomers of MDA, MDMA and related analogues on [3H]serotonin and [3H]dopamine release from superfused rat brain slices. Eur J Pharmacol 132:269-76.

    PMID 2880735 · doi:10.1016/0014-2999(86)90615-1

  4. Nash JF, Roth BL, Brodkin JD, et al. (1994). Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors. Neurosci Lett 177:111-5.

    PMID 7824160 · doi:10.1016/0304-3940(94)90057-4

  5. Wikipedia: 3,4-Methylenedioxyamphetamine (MDA) — pharmacology (monoamine release & 5-HT2 agonism), enantiomers, effects & legal status CC BY-SA 4.0
  6. PsychonautWiki: MDA — recreational dosage, duration & subjective effects CC BY-SA 4.0
  7. DEA Diversion Control Division: Controlled Substance Schedules (MDA is Schedule I)
  8. GOV.UK: Controlled drugs list — MDA is Class A (Misuse of Drugs Act 1971) OGL v3.0
  9. Anlage I BtMG — Betäubungsmittelgesetz (Gesetze im Internet): MDA (Tenamfetamin) ist nicht verkehrsfähig
  10. Brandt SD, Walters HM, Partilla JS, et al. (2020). The psychoactive aminoalkylbenzofuran derivatives, 5-APB and 6-APB, mimic the effects of 3,4-methylenedioxyamphetamine (MDA) on monoamine transmission in male rats. Psychopharmacology (Berl) 237:3703-3714.

    PMID 32875347 · doi:10.1007/s00213-020-05648-z

Further Information