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    5-IAI molecular structure

    5-IAI Stats & Data

    Hdep-28 Ethylnaphthidate 5-iodo-2-aminoindan 5iai
    NPS DataHub
    MW259.09
    FormulaC9H10IN
    CAS132367-76-1
    IUPAC5-iodo-2,3-dihydro-1H-inden-2-amine
    SMILESNC1Cc2ccc(I)cc2C1
    InChIKeyBIHPYCDDPGNWQO-UHFFFAOYSA-N
    Phenethylamines; Aminoindanes; 2020/1. Von 2-Phenethylamin abgeleitete Verbindungen; 2021/1. Von 2-Phenethylamin abgeleitete Verbindungen; 2022/1. Von 2-Phenethylamin abgeleitete Verbindungen
    Psychoactive Class Psychedelic / Stimulant
    Half-Life Unknown in humans (no formal pharmacokinetic studies; apparent effect window ~2–6 h does not establish elimination half-life).

    Receptor Profile

    Receptor Actions

    Agonists
    5-HT1A receptor agonist
    5-HT2A receptor agonist
    5-HT2B receptor agonist
    5-HT2C receptor agonist
    Alpha-2 adrenergic receptor agonist
    Other
    Serotonin-dopamine-norepinephrine releasing agent (SNDRA)

    Effect Profile

    Curated
    Psychedelic 2.9

    Mild auditory effects with low body load, visuals, and headspace

    Visual Intensity×3
    2
    Headspace Depth×3
    2
    Auditory Effects×1
    4
    Body Load / Somatic Effects×1
    3
    Empathogen 5.9

    Strong sensory enhancement with moderate euphoria, mild empathy and stimulation

    Empathy / Social Openness×3
    5
    Euphoria / Mood Elevation×2
    7
    Stimulation×1
    4
    Sensory Enhancement×1
    8
    Stimulant 3.2

    Moderate anxiety/jitters with mild euphoria, low stimulation and focus

    Stimulation / Energy×3
    3
    Euphoria / Mood Lift×2
    5
    Focus / Productivity×2
    2
    Anxiety / Jitters×1
    7

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Unknown in humans (no formal pharmacokinetic studies; apparent effect window ~2–6 h does not establish elimination half-life).
    Addiction Potential
    Low–moderate. As a monoamine releaser it may encourage redosing within a session, but physical dependence is unlikely; compulsive patterns decrease with adequate spacing and sleep/nutrition support.

    Tolerance Decay

    Full tolerance 6h Half tolerance 14d Baseline ~35d

    Pattern extrapolated from MDMA‑like releasers and aminoindane reports: acute tachyphylaxis within a session, partial tolerance over 1–2 weeks, and return to near‑baseline by ~4–6 weeks with abstinence. Data quality low due to absence of controlled human studies.

    Cross-Tolerances

    MDMA
    70% ●○○
    6‑APB / 5‑APB / 5‑MAPB
    60% ●○○
    MDAI / MMAI (aminoindanes)
    60% ●○○

    Legal Status

    Country Status Notes
    Finland Scheduled in the "government decree on psychoactive substances banned from the consumer market".
    Sweden Sweden's public health agency suggested classifying 5-IAI as a hazardous substance, on September 25, 2019.

    Harm Reduction

    drugs.wiki

    • Identity uncertainty is a major risk: multiple forum analyses from 2010–2013 allege that products sold as “5‑IAI” were often inactive or different stimulants; treat all samples as unknown until reagent‑tested and, where available, lab drug checking confirms identity. This directly affects dose, onset, and safety planning.

    • Mechanistically, 5‑IAI behaves as a serotonin>norepinephrine≈dopamine releasing agent and substituted for MDMA in rodent discrimination studies, implying entactogenic effects with stimulant load; human data remain anecdotal.

    • Animal work found markedly less serotonergic neurotoxicity than para‑iodoamphetamine at comparable high doses, yet small decreases in serotonergic markers occurred; avoid high/repeated dosing.

    • A modern review notes affinity at 5‑HT2B among other 5‑HT receptors; while functional agonism is not fully characterized, conservative spacing is advised (valvulopathy is a theoretical risk across 5‑HT2B‑active entactogens).

    • Expect typical releaser risks: hyperthermia, tachycardia, and hyponatremia with overhydration or MDMA‑style water‑loading; use small, regular sips (~250 ml/hour in heat) and avoid alcohol‑induced dehydration. (General HR extrapolated to serotonergic releasers.)

    • Bruxism, muscle tension, and insomnia are common; magnesium may help bruxism for some but evidence is mixed; non‑drug measures (jaw rests, gum, warm compress) are lower‑risk first‑line.

    • Redosing yields diminishing returns and disproportionate side effects; plan a single dose, avoid stacking, and do not chase effects with stimulants. (Pattern observed across community reports.)

    • Space sessions generously (≥4–6 weeks) to allow serotonergic recovery and reduce mood after‑effects; shorter intervals correlate with more severe comedowns across releasers. (Best‑practice HR extrapolation.)

    • If on any serotonergic prescription (SSRI/SNRI/MAOI/triptan), avoid entirely due to elevated serotonin syndrome risk highlighted in HR lists and combo charts.

    • Non‑selective beta‑blockers during acute stimulation may worsen vasoconstriction; if chest pain, severe headache, hyperthermia, or confusion occur, seek emergency care rather than self‑medicating.

    • Prefer oral titration over insufflation/rectal to reduce local harm and dose overshoot; nasal use commonly reports irritation without clear benefit.

    • Because formal human PK is lacking, treat timing and interactions as uncertain; build extra buffers before driving, sleeping, or combining with any other psychoactives.

    References

    Data Sources

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