5-MeO-MiPT

N-[2-(5-methoxy-1H-indol-3-yl)ethyl]-N-methylpropan-2-amine

Overview

5-MeO-MiPT belongs to Psychedelics / Tryptamines.

Key safety note: Human safety data for 5-MeO-MiPT are limited, though a first-in-human Phase 1 study (as MSD-001) reported no serious cardiovascular or psychiatric adverse effects across 0.5–10 mg.[4]
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.
  • Often described as only weakly hallucinogenic for a psychedelic, the 'least psychedelic' psychedelic tryptamine, with entactogen-like, MDMA-adjacent qualities
  • Greatly enhanced tactile sensation and eroticism at low doses
  • Heightened emotion, euphoria, relaxation and associative thinking, with minimal classical visuals or ego dissolution
  • A pronounced physical body load: tingling, tremor, mild motor impairment, appetite loss and insomnia
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. Shulgin's original oral range in TiHKAL was 4–6 mg. A Phase 1 study found the most consistent effects at 6–10 mg, while community sources report a wider spread up to ~15–20 mg. It is potent and carries a marked physical body load: start low and go slow.

Dose ranges

Threshold

~2–3 mg

Light

3–6 mg

Common

6–10 mg

Strong

10–15 mg

Duration

onset

20–40 min

peak

2–3 h

total

5–8 h

Chemical & Physical Properties
FormulaC15H22N2O
Molar mass246.35 g/mol
StateSolid (free base is a white-to-yellow crystalline powder, the hydrochloride and sulfate are the water-soluble salt forms)
Melting point162–163 °C (hydrochloride salt), free-base value not reliably reported
Boiling pointunavailable: true. reason: a crystalline solid that decomposes on strong heating rather than boiling. No reliable experimental boiling point is reported
Densityunavailable: true. reason: no reliable experimental value is reported for the solid
Vapor pressureNot reported
pKaNot reported
LogP2.3 (predicted, XLogP3)
SolubilityFree base: soluble in ethanol, DMSO, DMF (≈30 mg/mL), chloroform, ether and acetone. Insoluble in water, Hydrochloride and sulfate salts: water-soluble, insoluble in organic solvents
Refractive indexNot reported
Identifiers & Synonyms
CAS96096-55-8
CAS (enantiomer)
PubChem CID2763156
InChIKeyHEDOODBJFVUQMS-UHFFFAOYSA-N
InChIInChI=1S/C15H22N2O/c1-11(2)17(3)8-7-12-10-16-15-6-5-13(18-4)9-14(12)15/h5-6,9-11,16H,7-8H2,1-4H3
SMILESCC(C)N(C)CCC1=CNC2=C1C=C(C=C2)OC

Synonyms

  • Moxy
  • Moxie
  • 5-Methoxy-N-methyl-N-isopropyltryptamine
  • 5-methoxy-N-isopropyl-N-methyltryptamine
  • MSD-001
Pharmacodynamics & Biochemistry

Serotonergic tryptamine with mixed psychedelic and entactogen-like effects. A 5-HT2A agonist (the target most linked to psychedelic effects) but with notably higher affinity at 5-HT1A, plus activity at 5-HT2C, 5-HT7 and other serotonin subtypes. Also binds σ2, D4 and adrenergic receptors. Unusually for a psychedelic tryptamine it is often described as only weakly hallucinogenic: the 'least psychedelic' of the psychedelic tryptamines. Extensively metabolised by hepatic cytochrome P450 enzymes (notably CYP2D6). CYP2D6 poor metabolisers show higher and longer exposure.

Biological targets

  • 5-HT2A
  • 5-HT1A
  • 5-HT2C

Binding & functional measurements

TargetMeasurementSpecies
5-HT1A receptorKi 58 ± 10 nMHuman
5-HT7 receptorKi 20 nMHuman
5-HT1D receptorKi 23 nMHuman
σ2 receptorKi 90 nMHuman
5-HT2A receptorKi 163 ± 30 nMHuman
5-HT6 receptorKi 130 nMHuman
α2-adrenoceptorKi 5,300 ± 300 nMHuman
5-HT1B receptorKi 303 nMHuman
α2C-adrenoceptorKi 637 nMHuman
5-HT2C receptorKi 1,300 ± 300 nMHuman
I1 imidazoline receptorKi 879 nMHuman
5-HT5A receptorKi 953 nMHuman
D4 receptorKi 1,422 nMHuman
σ1 receptorKi 1,666 nMHuman
α2B-adrenoceptorKi 1,693 nMHuman
D3 receptorKi 2,470 nMHuman
Serotonin transporterKi 3,300 ± 300 nMHuman
5-HT1E receptorKi 3,496 nMHuman
H1 receptorKi 3,900 ± 500 nMHuman
5-HT1A receptorEC50 37 nM
Emax 108%		Human
5-HT1A receptorEC50 36 nM
Emax 101%		Mouse
5-HT2A receptorEC50 17 nM
Emax 94.8%		Human
5-HT2A receptorEC50 50 nM
Emax 96.4%		Mouse
5-HT2B receptorEC50 50 nM
Emax 87.9%		Human
5-HT2C receptorEC50 39 nM
Emax 115%		Human
Pharmacokinetics
BioavailabilityNot reported
TmaxNot reported
Half-life≈2–3 h
VdNot reported
Protein bindingNot reported
MetabolismExtensive hepatic phase I metabolism by cytochrome P450 (notably CYP2D6) via O- and N-demethylation, hydroxylation and N-oxidation. Metabolites include 5-HO-MiPT and 5-MeO-NiPT. CYP2D6 poor metabolisers show ~1.6–1.8× higher exposure and a longer half-life[3]
ExcretionNot reported
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.

Not reported

Human safety data for 5-MeO-MiPT are limited, though a first-in-human Phase 1 study (as MSD-001) reported no serious cardiovascular or psychiatric adverse effects across 0.5–10 mg. It is potent, active at only a few milligrams, so accurate low dosing is essential. Reported effects include a pronounced physical body load (tingling, tremor, mild motor impairment, nausea), appetite loss and insomnia, and uncomfortable overstimulation at higher doses. Preclinical work found apoptotic neurotoxicity and hypothermia at high doses in mice. As with all serotonergic drugs, combining it with MAOIs or other serotonergic agents raises the risk of serotonin toxicity. Limited data must never be read as evidence of safety.[4]

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

SSRIs, SNRIs, Lithium, Tramadol, Other serotonergic drugs Add to serotonergic load and can raise the risk of serotonin toxicity.
MAOIs May intensify and unpredictably prolong effects.
Stimulants (amphetamines, cocaine) Compound cardiovascular strain, anxiety and overstimulation, adding to an already heavy body load.
Strong CYP2D6 inhibitors (e.g. paroxetine, fluoxetine) Can raise and prolong exposure, as can being a CYP2D6 poor metaboliser.

Contraindications

Personal or family history of psychosis, schizophrenia or bipolar disorder
Cardiovascular disease, hypertension or arrhythmia significant or uncontrolled disease or hypertension.
Concurrent MAOI, SSRI/SNRI or other serotonergic medication MAOIs or other strongly serotonergic drugs.
Settings where impairment or dissociation risks injury (driving, water, heights) pronounced physical body load.
Usage & Context
  • Research.
  • Recreational.
Sources & Evidence

Further Information