NM-2-AI
N-methyl-2-aminoindane
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NM-2-AI (N-methyl-2-aminoindane) is a synthetic stimulant of the aminoindane class. It is a conformationally rigid structural analog of methamphetamine, distinguished by short duration and low potency. NM-2-AI is believed to act primarily as a norepinephrine releasing agent, producing its effects by reversing transporter function to flood synapses with norepinephrine.[1][2]
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NM-2-AI appeared on the research chemical market around 2009–2010, part of a wave of aminoindane derivatives marketed as legal alternatives to banned cathinones and MDMA.[3] It circulated briefly before fading from vendor catalogs, though forensic detections continued into the early 2020s.[4] It remains unscheduled under international drug control conventions.[5]
Subjective effects include physical stimulation, wakefulness, analysis enhancement, and mild euphoria. The experience is stimulant-forward — a driven, noradrenergic push toward alertness and focus without the empathogenic warmth of serotonin-releasing relatives like MDAI.[6] Compulsive redosing, post-acute irritability, and anxious overstimulation at higher doses are characteristic unsought effects.
Dependence potential is rated moderate by community consensus, and the toxic dose in humans is unknown — computational modeling predicts an 82% probability of cardiovascular toxicity.[7] One fatality has been documented in a polydrug context.[4] No controlled human study of any kind has been published — the entire pharmacological profile rests on structural analogy, one mouse study, and community reports.
History[edit]
History
Discovery
The 2-aminoindane scaffold was first explored pharmacologically in the 1970s–1980s for bronchodilating and analgesic applications.[3] Little and Rees demonstrated sympathomimetic activity for N-methyl-2-aminoindane on guinea-pig tissue preparations in 1980.[8] The compound's synthesis follows straightforwardly from standard N-methylation of 2-aminoindane, and no original publication documenting its first deliberate preparation has been identified.
Scientific significance
The aminoindane class gained pharmacological importance in the 1990s through David Nichols's program at Purdue University, which developed ring-substituted aminoindanes — most notably MDAI — as non-neurotoxic alternatives to MDMA. Nichols and colleagues showed that aminoindane derivatives retained MDMA-like behavioral properties in rats[9] while MDAI released serotonin without producing neurotoxicity.[10] This work established the rigid indane scaffold as a tool for separating entactogenic effects from neurotoxic liability.
Market emergence and surveillance
NM-2-AI surfaced on research chemical markets around 2009–2010, following the UK's ban on mephedrone and other synthetic cathinones.[3] Italian forensic laboratories identified the compound in seized materials during 2013–2015.[11] In May 2021, the US Drug Enforcement Administration issued a formal alert after NM-2-AI was confirmed in blood from a 2015 overdose death in Iowa, and the Pittsburgh Poison Center reported seven additional suspected exposures between 2020 and 2021.[4]
The name "NM-2-AI" is a shorthand chemical abbreviation: N-methyl (NM) at the 2-aminoindane (2-AI) position. The compound has no established street names. Tirri et al. described NM-2-AI as "briefly used in the illicit drug market",[6] and its reputation among research chemical users is that of a marginal stimulant — functional but unremarkable, overshadowed by more potent or more empathogenic alternatives in the aminoindane family.
Chemistry[edit]
Chemistry
Structural class
NM-2-AI belongs to the aminoindane chemical class within the broader phenethylamine family. The indane ring system — a cyclopentane ring fused to a benzene ring — bridges the alpha-carbon to the aromatic ring, locking what would be the methamphetamine backbone into a rigid bicyclic conformation. This restriction of rotational freedom fundamentally alters how the molecule interacts with monoamine transporters compared to open-chain amphetamines.
NM-2-AI is the N-methyl derivative of 2-aminoindane (2-AI), carrying a single methyl group on the nitrogen at the 2-position of the cyclopentane ring. The aromatic ring bears no additional substitution — a key distinction from ring-substituted aminoindanes like MDAI and 5-IAI, which carry methylenedioxy or iodo groups that shift pharmacological selectivity toward serotonin release.
Molecular properties
| Molecular formula | C₁₀H₁₃N |
| Molecular weight | 147.22 g/mol |
Two CAS registry numbers appear in the literature — likely distinguishing the free base from the hydrochloride salt, or representing a registry duplication, as both map to the same chemical structure.[7][12]
Stereochemistry
NM-2-AI has a single chirality center at C-2 of the indane ring. No published data address enantioselective pharmacology or the enantiomeric composition of commercial preparations. The compound is presumed to circulate as a racemic mixture.citation needed
Physical properties
NM-2-AI is typically encountered as a white powder or crystals in the hydrochloride salt form, with an approximate melting point of 230°C.citation needed No published stability or degradation pathway data exist for the compound under storage conditions.
Pharmacology[edit]
Pharmacology
Mechanism of action
NM-2-AI functions as a substrate-type monoamine releasing agent. It enters neurons through monoamine transporters and reverses their normal direction, causing norepinephrine to flood the synapse without the usual trigger of an action potential. This mechanism is shared with amphetamines, but the rigid indane scaffold alters which transporters the molecule prefers.
No in vitro study has directly measured NM-2-AI's potency at individual transporters. The pharmacological profile is inferred from the parent compound 2-aminoindane (2-AI), which acts primarily at the NET (NET) with weaker activity at the DAT (DAT) and minimal involvement of the SERT (SERT).[1] The parent compound also binds with high affinity to α2-adrenergic receptors.[2] Pinterova et al. noted in 2017 that "there is currently no scientific information available about these compounds" regarding NM-2-AI specifically.[3]
A classification conflict exists in the literature. Some sources describe NM-2-AI as a dopamine and serotonin releaser, but the available evidence points toward norepinephrine dominance.[1] Ring substitution — as in MDAI or MMAI — is what shifts aminoindane selectivity toward serotonin release; unsubstituted compounds like NM-2-AI and 2-AI lack this feature.[2] Tirri et al. documented entactogenic-like behavior in mice given NM-2-AI,[6] but whether this reflects low-level serotonin activity or a non-serotonergic mechanism remains unresolved. Liechti noted that aminoindanes as a class "predominantly enhance serotonin release," though this applies most strongly to ring-substituted members.[13]
The most defensible classification based on current evidence: primary norepinephrine releasing agent with possible secondary dopamine transporter activity; serotonin release not established.
Pharmacokinetics
No human pharmacokinetic data exist for NM-2-AI. Half-life, bioavailability, and clearance are uncharacterized in humans.
The primary metabolic pathway is N-demethylation to 2-aminoindane (2-AI), which is itself pharmacologically active — Tirri et al. identify it as "the main active metabolite".[6] In laboratory studies using human liver preparations, NM-2-AI also forms hydroxylated metabolites.[14] In rat urine, seven metabolites have been identified, including 2-AI and several hydroxylated derivatives.[15]
A clinically relevant variable: the 2-AI metabolite undergoes acetylation via NAT2, an enzyme that is genetically variable across the population. Individuals with the slow acetylator phenotype may experience prolonged exposure to active 2-AI.[14]
Community reports indicate onset at 30–60 minutes oral and total duration of 2–4 hours, though no controlled measurement has confirmed these values.
Neuroscience[edit]
Neuroscience
No direct neuroimaging, electrophysiology, or neurochemical measurement data exist for NM-2-AI in any species. The following mechanisms are inferred from its presumed norepinephrine-releasing pharmacology.
Where it acts
As a NET-preferring releasing agent, NM-2-AI is expected to amplify noradrenergic signaling from the locus coeruleus to the prefrontal cortex, amygdala, and hypothalamus. Moderate norepinephrine elevation in prefrontal circuits sharpens attention and working memory — consistent with the focus and analysis enhancement reported by users. Excessive noradrenergic tone tips this into anxiety, cardiovascular activation, and restless overstimulation.
If secondary DAT activity is present,[2] it would engage the mesolimbic mesolimbic pathway, accounting for the mild euphoria and compulsive redosing urge described in community reports.
Why it matters
NM-2-AI's profile illustrates the "wanting vs. liking" distinction in reward neuroscience. A NET-dominant compound with secondary dopamine activity enhances arousal and motivation (wanting) without the hedonic warmth (liking) that serotonin-releasing entactogens provide. Community descriptions of NM-2-AI as stimulating but emotionally shallow are consistent with this framework. Tirri et al. noted that its behavioral effects in mice "appear atypical and less intense with respect to those induced by classic stimulants"[6] — a pattern that may reflect this unusual transporter balance.
The core unanswered question is whether NM-2-AI has any meaningful SERT activity. The mild entactogenic quality some users report could reflect low-level SERT activity undetected in vitro, noradrenergic modulation of oxytocin release, or simple misattribution.
Subjective Effects[edit]
Subjective Effects
The experience of NM-2-AI is stimulant-forward: a noradrenergic push toward physical activation, wakefulness, and cognitive sharpening, without the empathogenic depth characteristic of serotonin-releasing aminoindanes. At lower doses, users describe focused stimulation and mild mood lift. At higher doses, the driven quality intensifies into restless overstimulation and anxiety, with the short duration (2–4 hours oral) and rapid offset creating persistent pressure to redose. Set and setting modulate the balance — social environments may draw out mild prosocial effects, while solitary use amplifies the jittery, task-oriented quality of noradrenergic activation.
Relative to MDMA, NM-2-AI produces substantially less emotional connection, sensory enhancement, and empathic warmth — it functions closer to a low-potency stimulant than a true entactogen. Compared to its parent compound 2-ai, the N-methyl group appears to increase potency and central nervous system penetration while maintaining a similar qualitative character.[6]
Effect Grid
At 100–150 mg oral, NM-2-AI delivers its core stimulant profile: pronounced wakefulness, physical stimulation, and noticeable thought acceleration. Appetite suppression becomes reliable. Mild euphoria emerges, though attenuated compared to dopamine-dominant stimulants. Some users report faint prosocial warmth at the upper end of this range, but empathogenic depth remains limited.
Physical effects include increased heart rate, mild bruxism, excessive sweating, and dehydration sensation. Cardiovascular activation is perceptible. Nausea may occur during onset but typically resolves as stimulation builds.
The short duration (2–4 hours) creates pressure toward compulsive redosing. Post-acute cognitive fatigue, low mood, and irritability are common as effects wane.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Sound sensitivity · Visual processing acceleration · Color enhancement
Pupil dilation · Appetite suppression · Body high · Dry mouth · Muscle tension · Excessive sweating · Dehydration sensation · Heart rate perception changes · Insomnia · Physical fatigue · Restlessness · Spontaneous body sensations · Tactile euphoria · Bruxism · Bodily lightness · Breathing alteration · Respiratory stimulation · Tingling / electric sensations · Vibrations / buzzing · Nausea · Sexual arousal suppression · Dizziness · Headache · Involuntary body movements · Laughter fits · Sexual arousal enhancement · Nystagmus (eye wobbles) · Trembling · Vomiting
Muscle tension · Excessive sweating · Dehydration sensation · Heart rate perception changes · Insomnia · Physical fatigue · Restlessness · Spontaneous body sensations · Tactile euphoria · Bruxism · Bodily lightness · Breathing alteration · Respiratory stimulation · Tingling / electric sensations · Vibrations / buzzing · Nausea · Sexual arousal suppression · Dizziness · Headache · Involuntary body movements · Laughter fits · Sexual arousal enhancement · Nystagmus (eye wobbles) · Trembling · Vomiting
Openness enhancement · Motivation enhancement · Analysis enhancement · Aesthetic enhancement · Cognitive flexibility · Conceptual thinking · Focus enhancement · Humor enhancement · Immersion enhancement · Information processing enhancement · Introspection enhancement · Novelty enhancement · Pattern recognition enhancement · Thought connectivity · Creativity enhancement · Language enhancement · Thought organization · Motivation suppression · Cognitive dysphoria · Increased nature relatedness · Memory replays · Memory enhancement · Thought deceleration
Cognitive flexibility · Conceptual thinking · Focus enhancement · Humor enhancement · Immersion enhancement · Information processing enhancement · Introspection enhancement · Novelty enhancement · Pattern recognition enhancement · Thought connectivity · Creativity enhancement · Language enhancement · Thought organization · Motivation suppression · Cognitive dysphoria · Increased nature relatedness · Memory replays · Memory enhancement · Thought deceleration
Irritability · Anxiety · Anxiety suppression · Emotional lability · Simultaneous emotions · Anhedonia · Catharsis · Dysphoria · Emotional suppression · Empathy suppression · Paranoia
Emotional lability · Simultaneous emotions · Anhedonia · Catharsis · Dysphoria · Emotional suppression · Empathy suppression
Communication enhancement · Sociability enhancement · Craving · Emotional susceptibility · Flow state · Ego inflation · Depersonalization · Derealization · Boundary dissolution
Flow state · Ego inflation · Depersonalization · Derealization · Boundary dissolution
Timeline
Gradual stimulant awareness emerges — subtle alertness increase, possible mild nausea. Cardiovascular activation is not yet perceptible.
Rising stimulation with increasing heart rate awareness and mood elevation. Appetite suppression begins. Physical energy builds noticeably.
Maximum stimulation and mild euphoria. Thought acceleration, wakefulness, and cardiovascular activation at their strongest. Bruxism and sweating most pronounced.
Rapid decline in stimulation. Emerging fatigue, irritability, and low mood as monoamine stores deplete. Compulsive redosing urge is strongest during this phase.
Post-acute fatigue, cognitive fog, possible depressed mood, and appetite return. Residual insomnia may persist.
⚠ Do not drive or operate heavy machinery for at least 4 hours after dosing due to residual cognitive impairment and potential fatigue.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 10 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- High
- Dose escalation
- Moderate
- Cross-tol.
- dopaminergic stimulants · other monoamine releasing agents
Toxicity
No experimentally derived lethal dose, safe dose ceiling, or maximum tolerated dose has been established for NM-2-AI in any species. The exact toxic dose in humans is unknown.
Predicted toxicity
Computational modeling provides the only toxicity estimates available. Jurowski and Frydrych published predicted oral LD50 values in rats ranging from approximately 113 to 560 mg/kg across multiple modeling platforms.[7] The same models predict an 82% probability of cardiovascular toxicity and a 65% probability of pulmonary involvement. Predicted heart rhythm disruption risk (hERG channel inhibition) appears low at anticipated recreational concentrations, though this has not been validated experimentally.[7]
Genotoxicity modeling returned a 66.3% probability of mutagenicity — higher than the parent compound 2-AI (58.7%), suggesting the N-methyl group increases this risk.[7]
Structural analog toxicology
MDAI, the closest aminoindane with experimental toxicity data, showed strong liver toxicity potential in human liver cells (exceeding MDMA) and caused fatal blood clotting abnormalities with brain swelling in rats.[16][17][18] At least one human death involved MDAI (blood level 2.09 mg/L in a polydrug context).[19] Whether NM-2-AI shares these specific toxicity patterns is unknown — its lack of ring substitution may produce a different organ toxicity profile.
Human forensic cases
One confirmed fatality involving NM-2-AI: Sioux City, Iowa, 2015 — NM-2-AI at 95.4 ng/mL in whole blood alongside the synthetic cannabinoid MAB-CHMINACA (2.7 ng/mL).[4] The polydrug context prevents definitive attribution. Seven additional suspected exposures were reported by the Pittsburgh Poison Center between 2020 and 2021.[4]
Overheating risk
MDAI produced dangerous body temperature elevation in group-housed rats, amplified by social and warm conditions.[16] NM-2-AI's norepinephrine-dominant pharmacology can independently raise body temperature through sympathetic activation, even without the serotonin release that drives hyperthermia with entactogens.
Psychological Risks
No controlled data on psychological adverse effects exist. Based on pharmacology and community reports:
- Anxiety and agitation: Norepinephrine excess is inherently anxiety-producing. Restlessness and overstimulation are reported at higher doses.
- Compulsive redosing: The short duration and rapid offset create strong pressure to redose, a pattern consistently noted in community reports.
- Post-acute depression and irritability: Expected from monoamine depletion following release, a class-typical effect.
- Psychosis: No published case reports, but stimulant psychosis is a class-level risk at high doses or with prolonged use.
Tolerance & Dependence
No published data on NM-2-AI tolerance, dependence, or withdrawal exist.
Tolerance develops with repeated use. Community sources estimate full reset at approximately 1.5 weeks, with cross-tolerance reported to other dopaminergic stimulants.inferred
Dependence potential is rated moderate by community consensus — described as "moderately addictive with a high potential for abuse." No published study has confirmed this for NM-2-AI specifically.safety citation needed MDAI produced reward-seeking behavior in mice at low doses,[17] confirming abuse potential exists across the aminoindane class.
Drug Interactions
Serotonin syndrome risk: Aminoindanes as a class carry acute serotonin syndrome risk at high doses or in combination with serotonergic agents.[13] Even with NM-2-AI's primary noradrenergic mechanism, combining it with SSRIs, SNRIs, MAOIs, tramadol, or other entactogens that raise serotonin levels creates danger. The active metabolite 2-AI may contribute serotonergic interactions not predicted from the parent compound alone.
Tramadol: Rated lethal in community interaction data. Tramadol blocks serotonin reuptake and lowers seizure threshold; combined with a monoamine releaser, the mechanisms for lethality include serotonin syndrome and seizures.safety citation needed
MDMA: Rated dangerous. Combining two monoamine releasers produces additive serotonin release, overheating risk, and cardiovascular overload.
MAOIs: Monoamine oxidase inhibitors combined with substrate-type releasers produce potentially fatal blood pressure crisis and serotonin syndrome through uncontrolled monoamine accumulation.
Pharmacokinetic interactions: The genetic variability in NAT2 (the enzyme that clears the active metabolite 2-AI) means that drugs competing for the same enzyme pathway could prolong active metabolite exposure.[14]
Contraindications
No substance-specific contraindication data have been published. The following are inferred from NM-2-AI's stimulant and monoamine-releasing pharmacologyinferred:
Absolute (class-level inference):
- Concurrent MAOI use: Risk of fatal blood pressure crisis and serotonin syndrome
- Uncontrolled high blood pressure: Noradrenergic activation elevates blood pressure further
- Severe heart condition: The 82% predicted cardiovascular toxicity probability[7] makes pre-existing cardiac disease a high-risk factor
Relative (class-level inference):
- Seizure disorders: Stimulants lower seizure threshold
- Liver impairment: NM-2-AI undergoes liver metabolism; impaired clearance could increase exposure
- Bipolar disorder or psychosis spectrum conditions: Stimulant activation may trigger mania or psychotic episodes
- Pregnancy: No reproductive data exist; stimulant vasoconstrictors are contraindicated as a class in pregnancy
Harm Reduction[edit]
Forms & Identification
NM-2-AI's simple chemical structure does not produce distinctive color changes with common reagent test kits (Marquis, Mecke, Mandelin), making field identification unreliable. A negative or ambiguous reagent result does not confirm identity — it only rules out some other substance classes. For NM-2-AI specifically, laboratory analysis (GC-MS or similar) is the only reliable confirmation method.
Because NM-2-AI originates entirely from unregulated synthesis, batch purity varies unpredictably. The compound has been found in forensic seizures alongside other novel psychoactive substances,[11] raising the possibility of contamination or mislabeling in vendor supply.
Guidelines
- Test substance identity with reagent kits to rule out dangerous substitutions, and ideally confirm with laboratory analysis
- Weigh doses with a milligram-precision scale — volumetric estimation of powders is unreliable
- Set a firm dose limit and timing plan before the session; do not carry extra material
- Start at the low end of the reported dose range and wait at least 90 minutes before considering a redose
- Stay hydrated but avoid overhydration — moderate sipping, not forced water intake
- Avoid use in hot environments or during intense physical activity
- Have a trusted person aware of what you have taken and when
- Do not combine with MAOIs, tramadol, MDMA, or other stimulants
Set & Setting
NM-2-AI's noradrenergic pharmacology produces a physically driven, alert state. Social environments may draw out mild prosocial effects; solitary use tends to amplify the restless, jittery quality. The short duration (2–4 hours) and abrupt offset create strong psychological pressure to redose — planning a firm dose limit before the session begins is more effective than deciding in the moment.
The stimulant body load (elevated heart rate, physical tension) can become uncomfortable in hot, crowded, or physically demanding settings. A calm environment with access to water and fresh air reduces physiological strain.
Aftercare & integration. The stimulant comedown from NM-2-AI involves monoamine depletion — expect fatigue, low mood, and irritability in the 12–48 hours following use. Sleep is the most effective recovery tool; if stimulant residue prevents sleep, a dark quiet room and avoidance of screens help more than additional substances.
Nutrient replenishment matters: eat a full meal within a few hours of the experience ending, prioritizing protein and complex carbohydrates. Magnesium supplementation may help with residual muscle tension.
If compulsive redosing occurred during the session, treat this as information — it reflects the compound's pharmacological profile, not personal failure, and it should factor into future decisions about use.
Recovery & Support
NM-2-AI's moderate dependence potential and compulsive redosing profile mean that patterns of escalating use can develop without the dramatic withdrawal seen with stronger stimulants. If use has become more frequent than intended, or if obtaining and using the substance occupies increasing mental bandwidth, these are early signals worth taking seriously.
Peer support communities, including online harm reduction forums and local mutual aid groups, provide non-judgmental spaces to discuss stimulant use patterns. Professional support through a substance use counselor is appropriate when self-regulation efforts have not been effective. SAMHSA's National Helpline (1-800-662-4357) offers free, confidential referral in the United States.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Chest pain or pressure
- Seizure or convulsions
- Body temperature so high it can be felt through clothing
- Loss of consciousness or unresponsiveness
- Severe confusion, paranoia, or self-harm behavior
An elevated heart rate and mild anxiety alone do not constitute an emergency — chest pain, seizure, and extreme body temperature do.
Immediate steps:
- 1. Call emergency services if any of the above signs are present
- 2. Move the person to a cool, quiet area
- 3. If unconscious but breathing, place in the recovery position (on their side)
- 4. Do not restrain a conscious person unless there is immediate danger of self-harm
- 5. Do not induce vomiting
- 6. Stay with the person until help arrives
What to tell the dispatcher: Name the substance (NM-2-AI / N-methyl-2-aminoindane), the estimated amount taken, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
Legal Status
NM-2-AI is not controlled under any international drug control convention. The UNODC confirms that no aminoindanes are internationally scheduled.[5] National-level controls vary and are primarily enacted through blanket new psychoactive substance (NPS) legislation rather than specific scheduling of NM-2-AI by name.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| International | Not controlled | Not scheduled under 1961, 1971, or 1988 UN conventions[5] |
| United States | Unscheduled (federal) | Not on DEA controlled substance schedules. May be subject to Federal Analogue Act as structural analog of methamphetamine if intended for human consumption. DEA issued formal alert May 2021[4] |
| United Kingdom | Illegal | Covered under Psychoactive Substances Act 2016 (blanket ban on psychoactive substances effective 26 May 2016) |
| Germany | Controlled | Regulated under Neue-psychoaktive-Stoffe-Gesetz (NpSG), effective 26 November 2016 |
| Switzerland | Controlled | Listed specifically under Verzeichnis E |
| China | 2-AI controlled (October 2015) | NM-2-AI status not specifically confirmed; 2-AI scheduling may encompass derivativescitation needed |
| Canada | Not specifically scheduled | May be subject to analog provisions under the Controlled Drugs and Substances Actcitation needed |
| Australia | Not specifically confirmed | Scheduling status not identified in reviewed literaturecitation needed |
Analog act considerations
In the United States, the Federal Analogue Act permits prosecution of substances "substantially similar" to Schedule I or II controlled substances when intended for human consumption. NM-2-AI's structural relationship to methamphetamine (Schedule II) — as a conformationally restricted analog — creates potential liability under this provision. The DEA's 2021 formal alert[4] signals active surveillance interest that may precede future scheduling action.
references
- [1] ^abcSimmler LD, Rickli A, Schramm Y, Hoener MC, Liechti ME (2014) Pharmacological profiles of aminoindanes, piperazines, and pipradrol derivatives. — Biochemical Pharmacology doi:10.1016/j.bcp.2014.01.024
- [2] ^abcdHalberstadt A, Brandt S, Walther D, Baumann M (2019) 2-Aminoindan and its ring-substituted derivatives interact with plasma membrane monoamine transporters and alpha2-adrenergic receptors — Psychopharmacology doi:10.1007/s00213-019-05207-1
- [3] ^abcdPinterova N, Horsley RR, Palenicek T (2017) Synthetic Aminoindanes: A Summary of Existing Knowledge. — Frontiers in Psychiatry doi:10.3389/fpsyt.2017.00236
- [4]
- [5]
- [6] ^abcdefgTirri M, Corli G, Arfe R, Marchetti B, Bilel S, Bernardi T, Boccuto F, Odoardi S, Mestria S, Strano-Rossi S, Marti M (2023) Behavioral and Pharmacokinetics Studies of N-Methyl-2-Aminoindane (NM2AI) in Mice: An Aminoindane Briefly Used in the Illicit Drug Market. — International Journal of Molecular Sciences doi:10.3390/ijms24031882