generation run 2026-05-11
60 min completedmodel pipeline-v5plan not recordedrun/1e06c7cd…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
- safety_data_unverified
- structural_inference
Reproduce
- inputs
- 20 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
19 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | NM-2-AI / N-methyl-2-aminoindane | 1 | 1 | Core chemical identity confirmation for seed data verification |
| 2 | PubMed | 2-aminoindane N-methyl pharmacology stimulant | 14 | 3 | Early aminoindane pharmacology papers and MDMA-analog drug discrimination studies provide mechanistic class context |
| 3 | PubMed | aminoindane new psychoactive substance forensic detection | 10 | 4 | NM2AI-specific metabolism data; MDAI human pharmacology as closest structural analog; forensic market data showing NM2AI in seized materials |
| 4 | PubMed | NM-2-AI aminoindane | 2 | 2 | Both directly about NM-2-AI; primary sources for toxicology and metabolism |
| 5 | WebSearch | NM-2-AI UK Psychoactive Substances Act scheduling US analog act | 10 | 2 | Jurisdiction-specific legal status |
| 6 | PubChem | CID 15023225 N-methyl-2-aminoindane | 1 | 1 | Chemical identity verification |
| 7 | WebSearch | NM-2-AI case report intoxication forensic death adverse event | 10 | 2 | Critical safety and forensic case data |
| 8 | OpenAlex | aminoindane monoamine releasing pharmacology new psychoactive substance | 10 | 2 | High-citation review papers providing context for aminoindane pharmacology class |
| 9 | ClinicalTrials.gov · absence | aminoindane NM-2-AI 2-aminoindane | 0 | — | No trials to report |
| 10 | PubMed | aminoindane MDAI monoamine transporter releasing agent SERT DAT NET | 1 | 1 | Key pharmacology data on aminoindane class NET/SERT/DAT selectivity |
| 11 | UNODC | — | 1 | 1 | International scheduling status |
| 12 | PubMed | NM2AI N-methyl aminoindane behavioral pharmacokinetics mice 2023 | 1 | 1 | Only direct in vivo behavioral/PK study of NM2AI |
| 13 | PubMed | Halberstadt 2-aminoindan ring-substituted monoamine transporters alpha2 adrenergic 2019 | 1 | 1 | Definitive pharmacology data on 2-AI and ring-substituted derivatives with Ki values |
| 14 | WebSearch | NM-2-AI N-methyl-2-aminoindane legal status scheduling UK US EU 2026 | 10 | 3 | Legal status in key jurisdictions |
| 15 | UNODC | — | 1 | 2 | Chemical identity confirmation and CAS discrepancy flag |
| 16 | WebFetch | — | 1 | 2 | Key finding establishing research gap timeline |
| 17 | WebSearch | NM-2-AI case report intoxication forensic death adverse event | 10 | 2 | Forensic case documentation |
| 18 | Multiple | NM-2-AI pharmacological classification cross-reference | 5 | 2 | Critical pharmacological discrepancy needing expert editorial review |
| 19 | WebSearch | NM-2-AI pharmacology norepinephrine selective monoamine releasing transporter | 10 | 2 | Key pharmacological discrepancy requiring flagging |
69 claims by section — every cited sentence, checked against its source
pharmacology17 · 15 ok
Simmler et al. (2014) characterized 2-AI at human monoamine transporters in HEK293 cells, demonstrating primary interaction with the norepinephrine transporter (NET) with substantially less involvement of the serotonin transporter (SERT) or dopamine transporter (DAT)supported
2-AI interacted with NET. All substances were monoamine transporter inhibitors with marked differences in DAT vs SERT inhibition profiles. j.bcp.2014.01.024
Halberstadt et al. (2019) confirmed that 2-AI acts as a substrate for both NET and DAT, and further identified high-affinity binding at alpha-2 adrenergic receptor subtypes: alpha-2C (Ki = 41 nM), alpha-2A (Ki = 134 nM), and alpha-2B (Ki = 211 nM).supported
2-AI is a substrate for NET and DAT. High alpha2C receptor affinity (Ki=41 nM), alpha2A (Ki=134 nM), alpha2B (Ki=211 nM). s00213-019-05207-1
Secondary sources describe NM-2-AI as a highly selective norepinephrine releasing agent that does not release serotonin or dopamine at concentrations up to 100 micromolar; however, this claim is not traceable to a specific primary publication and appears to derive from extrapolation of 2-AI data with the assumption that N-methylation enhances NET selectivitysupported
2-AI interacted with NET. All substances were monoamine transporter inhibitors with marked differences in DAT vs SERT inhibition profiles. j.bcp.2014.01.024
Secondary sources describe NM-2-AI as a highly selective norepinephrine releasing agent that does not release serotonin or dopamine at concentrations up to 100 micromolar; however, this claim is not traceable to a specific primary publication and appears to derive from extrapolation of 2-AI data with the assumption that N-methylation enhances NET selectivitysupported
2-AI is a substrate for NET and DAT. Ring substitution increases SERT selectivity. s00213-019-05207-1
Pinterova et al. (2017) explicitly noted that "there is currently no scientific information available about these compounds" regarding NM-2-AI.supported
Specifically notes that as of 2017 'there is currently no scientific information available about NM-2-AI.' fpsyt.2017.00236
Little and Rees (1980) confirmed sympathomimetic properties for the N-methyl-2-aminoindane derivative in vitro on guinea-pig ileum, consistent with noradrenergic releasing activity.supported
In vitro actions of 2-aminoindane and N-methyl/N,N-dimethyl derivatives on guinea-pig ileum. N-methyl derivative inhibited responses to electrical stimulation. Sympathomimetic properties. pmid:6110722
The parent 2-AI shows primary NET selectivity, unsubstituted aminoindanes favor NET/DAT over SERT as a structure-activity principle, and ring substitution (as in MDAI, MMAI) is required to shift selectivity toward serotonin releasesupported
5-IAI and MDAI preferentially inhibited SERT and NET and released 5-HT. 2-AI interacted with NET. j.bcp.2014.01.024
The parent 2-AI shows primary NET selectivity, unsubstituted aminoindanes favor NET/DAT over SERT as a structure-activity principle, and ring substitution (as in MDAI, MMAI) is required to shift selectivity toward serotonin releasesupported
2-AI is a substrate for NET and DAT. Ring substitution increases SERT selectivity. s00213-019-05207-1
Tirri et al. (2023) describe NM-2-AI as possessing "entactogenic activity" in mice, which may reflect in vivo serotonergic contributions not captured in vitro, activity of the 2-AI metabolite, or non-serotonergic mechanisms underlying the entactogenic phenomenologysupported
Demonstrated entactogenic activity, mild hallucinogenic effect (PPI disruption). Main active metabolite is 2-aminoindane (2-AI). ijms24031882
Liechti (2015) notes that aminoindanes as a class "predominantly enhance serotonin release," but this characterization applies most strongly to ring-substituted compounds rather than unsubstituted or N-methyl analogs.supported
Notes aminoindanes predominantly enhance serotonin release. smw.2015.14043
Claim in pharmacology — not_supportednot supportedworking →
The primary metabolic pathway is N-demethylation to 2-aminoindane (2-AI), which is itself pharmacologically active — Tirri et al. (2023) identify 2-AI as "the main active metabolite"supported
Main active metabolite is 2-aminoindane (2-AI). ijms24031882
In pooled human liver microsomes (pHLM), NM-2-AI forms a hydroxylamine and diastereomers from beta-hydroxylationsupported
NM-2-AI formed a hydroxylamine and diastereomers from beta-hydroxylation in pHLM. dta.2699
In rat urine, seven main metabolites were identified by LC-HRMS: 2-AI, two hydroxy-2-AI isomers, and four hydroxy-NM-2-AI isomers, with hydroxylated metabolites also present as sulfate conjugatespartially supported
In silico and in vivo (mice) NM2AI metabolism study. Seven main metabolites in urine: 2-AI, two hydroxy-2-AI, four hydroxy-NM2AI; conjugation in some. bkaa111
The 2-AI metabolite undergoes acetyl conjugation via N-acetyltransferase isoform 2 (NAT2), which is polymorphically expressed in humans — slow acetylator phenotype individuals may experience prolonged exposure to active 2-AIsupported
NAT acetylation isoform characterization. dta.2699
NM-2-AI and 2-AI were detected in hair and blood in mouse studiessupported
NM2AI and 2-AI detected in hair and blood. bkaa111
Claim in pharmacology — inconclusiveinconclusiveworking →
safety13 · 13 ok
Jurowski and Frydrych (2026) published the first comprehensive toxicity profile of NM-2-AI using multiple computational platforms:supported
This study provides the first toxicity profile of two aminoindane-based NPS: 2-AI and NM-2-AI, using a multi-method in silico approach. j.tiv.2025.106149
Predicted hERG inhibition IC50: 126.9 micromolar — suggesting low risk of QT prolongation at anticipated recreational concentrations, though this prediction has not been validated experimentally.supported
hERG IC50 = 126.9 µM j.tiv.2025.106149
Skin irritation probability: 60%; eye irritation: predicted non-irritant.supported
Skin irritation less probable (60%). Non-irritant to eye. j.tiv.2025.106149
MDAI provides the closest available experimental toxicology data for the aminoindane class: * LD50 in rats: 28.33 mg/kg subcutaneous, 35 mg/kg intravenous; not established up to 40 mg/kg oral * Cause of death: disseminated intravascular coagulopathy (DIC) with brain edema * Lethality at 100 mg/kg intraperitoneal in all 8 mice tested * Strong cytotoxic potential in human HepG2 hepatocyte cells, exceeding MDMA * Fatal human case: blood MDAI 2.09 mg/L (polydrug, alongside 5-EAPB 6.45 mg/L)supported
MDAI LD50 = 28.33 mg/kg sc and 35 mg/kg iv in rats. Not established up to 40 mg/kg oral. Disseminated intravascular coagulopathy (DIC) with brain edema as cause of death. j.pnpbp.2016.04.004
MDAI provides the closest available experimental toxicology data for the aminoindane class: * LD50 in rats: 28.33 mg/kg subcutaneous, 35 mg/kg intravenous; not established up to 40 mg/kg oral * Cause of death: disseminated intravascular coagulopathy (DIC) with brain edema * Lethality at 100 mg/kg intraperitoneal in all 8 mice tested * Strong cytotoxic potential in human HepG2 hepatocyte cells, exceeding MDMA * Fatal human case: blood MDAI 2.09 mg/L (polydrug, alongside 5-EAPB 6.45 mg/L)supported
MDAI LD50 = 28.33 mg/kg sc and 35 mg/kg iv in rats. Not established up to 40 mg/kg oral. Disseminated intravascular coagulopathy (DIC) with brain edema as cause of death. j.pnpbp.2016.04.004
MDAI provides the closest available experimental toxicology data for the aminoindane class: * LD50 in rats: 28.33 mg/kg subcutaneous, 35 mg/kg intravenous; not established up to 40 mg/kg oral * Cause of death: disseminated intravascular coagulopathy (DIC) with brain edema * Lethality at 100 mg/kg intraperitoneal in all 8 mice tested * Strong cytotoxic potential in human HepG2 hepatocyte cells, exceeding MDMA * Fatal human case: blood MDAI 2.09 mg/L (polydrug, alongside 5-EAPB 6.45 mg/L)supported
Lethality in 8/8 mice at 100 mg/kg. fbp.0000000000000237
MDAI provides the closest available experimental toxicology data for the aminoindane class: * LD50 in rats: 28.33 mg/kg subcutaneous, 35 mg/kg intravenous; not established up to 40 mg/kg oral * Cause of death: disseminated intravascular coagulopathy (DIC) with brain edema * Lethality at 100 mg/kg intraperitoneal in all 8 mice tested * Strong cytotoxic potential in human HepG2 hepatocyte cells, exceeding MDMA * Fatal human case: blood MDAI 2.09 mg/L (polydrug, alongside 5-EAPB 6.45 mg/L)supported
MDAI showed strong cytotoxic potential in HepG2 cells compared to moderate effects for MDMA and other NPS. j.toxlet.2018.11.007
MDAI provides the closest available experimental toxicology data for the aminoindane class: * LD50 in rats: 28.33 mg/kg subcutaneous, 35 mg/kg intravenous; not established up to 40 mg/kg oral * Cause of death: disseminated intravascular coagulopathy (DIC) with brain edema * Lethality at 100 mg/kg intraperitoneal in all 8 mice tested * Strong cytotoxic potential in human HepG2 hepatocyte cells, exceeding MDMA * Fatal human case: blood MDAI 2.09 mg/L (polydrug, alongside 5-EAPB 6.45 mg/L)supported
Blood: MDAI 2.09 mg/L, 5-EAPB 6.45 mg/L. Cause of death attributed to NPS consumption. j.forsciint.2019.03.023
MDAI produced hyperthermia in group-housed rats (social conditions amplifying thermoregulatory disruption)supported
Hyperthermia in group-housed rats. j.pnpbp.2016.04.004
Structural analog context: MDAI produced conditioned place preference in mice at 0.3–10 mg/kg, confirming abuse potential in the aminoindane classsupported
Conditioned place preference 0.3-10 mg/kg. fbp.0000000000000237
Serotonin syndrome risk: Liechti (2015) notes that aminoindanes as a class are associated with acute serotonin syndrome risk at high doses or in combination with serotonergic agentssupported
Reviews relative serotonergic vs dopaminergic activity as predictor of effects and toxicity. smw.2015.14043
Pharmacokinetic interactions: The NAT2 polymorphism affecting 2-AI acetylation introduces a variable: CYP inhibitors or NAT2 competitive substrates could prolong active metabolite exposuresupported
NAT acetylation isoform characterization. dta.2699
Absolute contraindications (class-level inference): * Concurrent MAOI use: Risk of hypertensive crisis and serotonin syndrome * Uncontrolled hypertension: Noradrenergic activation elevates blood pressure; pre-existing hypertension compounds cardiovascular risk * Severe cardiovascular disease: Predicted 82% cardiovascular toxicity probability makes pre-existing cardiac pathology a high-risk factorsupported
Cardiovascular toxicity probability 82% for NM-2-AI; hERG IC50 = 126.9 µM j.tiv.2025.106149
pharmacokinetic-detail8 · 5 ok
Manier et al. (2020) incubated NM-2-AI with pooled human liver microsomes (pHLM) and pooled human liver S9 fraction (pS9): * N-demethylation to 2-aminoindane (2-AI) — the primary metabolic pathway * Hydroxylamine formation — detected in both pHLM and pS9 * Beta-hydroxylation producing diastereomeric products (pHLM) * N-acetylation of the 2-AI metabolite via NAT2 (N-acetyltransferase isoform 2)supported
NM-2-AI formed a hydroxylamine and diastereomers from beta-hydroxylation in pHLM. In pS9 merely a hydroxylamine. NAT acetylation isoform characterization. dta.2699
Mestria et al. (2021) characterized metabolites in rat urine following NM-2-AI administration, identifying seven main metabolites by LC-HRMS: * 2-AI (N-demethylation product) * Two hydroxy-2-AI isomers * Four hydroxy-NM-2-AI isomers * Sulfate conjugates of hydroxylated metabolitespartially supported
In silico and in vivo (mice) NM2AI metabolism study. Seven main metabolites in urine: 2-AI, two hydroxy-2-AI, four hydroxy-NM2AI; conjugation in some. bkaa111
Both NM-2-AI and 2-AI were detected in mouse hair and blood samples, establishing relevance for forensic detection in chronic exposure scenarios.supported
NM2AI and 2-AI detected in hair and blood. bkaa111
Tirri et al. (2023) confirmed 2-AI as "the main active metabolite" in their behavioral pharmacokinetic study in mice, establishing that the pharmacological activity of NM-2-AI in vivo is a composite of parent compound and active metabolite effects.supported
Main active metabolite is 2-aminoindane (2-AI). Pharmacokinetics characterized. ijms24031882
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Manier et al. (2020) and Mestria et al. (2021) developed validated LC-HRMS analytical methods for NM-2-AI and its metabolites in urine, blood, and hair matricessupported
LC-HRMS method developed. bkaa111
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
comparative-pharmacology7 · 7 ok
MDAI at 180–228 mg produces subjective effects comparable to 125 mg MDMA in humans, with pronounced prosocial and empathogenic qualitiessupported
MDAI produced effects comparable with 125 mg MDMA. Increased blood pressure similar to MDMA; no increase in heart rate or body temperature. dta.3622
MDAI carries established hepatotoxic risk (strong cytotoxic potential in HepG2 cells, exceeding MDMA) and a documented LD50 in rats (28.33 mg/kg subcutaneous)supported
MDAI showed strong cytotoxic potential in HepG2 cells compared to moderate effects for MDMA and other NPS. j.toxlet.2018.11.007
MDAI carries established hepatotoxic risk (strong cytotoxic potential in HepG2 cells, exceeding MDMA) and a documented LD50 in rats (28.33 mg/kg subcutaneous)supported
MDAI LD50 = 28.33 mg/kg sc and 35 mg/kg iv in rats. j.pnpbp.2016.04.004
Both are NET-preferring substrates with secondary DAT activity and minimal SERT involvementsupported
2-AI interacted with NET. All substances were monoamine transporter inhibitors with marked differences in DAT vs SERT inhibition profiles. j.bcp.2014.01.024
Both are NET-preferring substrates with secondary DAT activity and minimal SERT involvementsupported
2-AI is a substrate for NET and DAT. Ring substitution increases SERT selectivity. s00213-019-05207-1
N-methylation is expected to increase lipophilicity and CNS penetration (by analogy with amphetamine→methamphetamine), potentially explaining the lower dose threshold for NM-2-AI relative to 2-AI in community reports. 2-AI additionally shows high affinity at alpha-2 adrenergic receptors (Ki = 41 nM at alpha-2C); whether NM-2-AI retains this affinity is untested.supported
High alpha2C receptor affinity (Ki=41 nM) s00213-019-05207-1
The 5-iodo substitution in 5-IAI shifts selectivity toward SERT similarly to MDAI, producing an entactogenic profile. 5-IAI shows preferential SERT and NET inhibition and 5-HT releasesupported
5-IAI and MDAI preferentially inhibited SERT and NET and released 5-HT. j.bcp.2014.01.024
history7 · 6 ok
Claim in history — inconclusiveinconclusiveworking →
Little and Rees published one of the earliest in vitro characterizations of the 2-aminoindane series — including the N-methyl and N,N-dimethyl derivatives — in 1980, demonstrating sympathomimetic activity on guinea-pig ileum preparationssupported
In vitro actions of 2-aminoindane and N-methyl/N,N-dimethyl derivatives on guinea-pig ileum. Sympathomimetic properties. pmid:6110722
Oberlender and Nichols (1990) demonstrated that N-methyl aminoindane derivatives retained MDMA-like discriminative stimulus properties in rats, while Johnson et al. (1991) confirmed that MDAI produced serotonin release without the neurotoxicity observed with MDMAsupported
MDAI and its N-methyl derivative both showed entactogen-like MBDB-substitution, demonstrating that N-methylation of aminoindanes preserves entactogenic discriminative stimulus properties. pmid:1979813
Oberlender and Nichols (1990) demonstrated that N-methyl aminoindane derivatives retained MDMA-like discriminative stimulus properties in rats, while Johnson et al. (1991) confirmed that MDAI produced serotonin release without the neurotoxicity observed with MDMApartially supported
MDAI studied as non-neurotoxic MDMA analogue. Combination of MDAI with S-amphetamine resulted in marked long-term decrease in cortical/hippocampal/striatal 5-HT, 5-HIAA, and 5-HT uptake sites. pmid:1726189
NM-2-AI emerged on the research chemical market as part of a broader wave of synthetic aminoindanes that appeared following the United Kingdom's ban on mephedrone and other synthetic cathinones in 2009–2010supported
Aminoindanes emerged on market after UK cathinone bans in 2009-2010. fpsyt.2017.00236
NM-2-AI was seized and identified in Italian forensic laboratory materials during the 2013–2015 period, and Tirri et al. (2023) describe the compound as "briefly used in the illicit drug market".supported
NM2AI (N-methyl-2-aminoindane) detected in seized materials in Italy 2013-2015. j.forsciint.2016.01.037
NM-2-AI was seized and identified in Italian forensic laboratory materials during the 2013–2015 period, and Tirri et al. (2023) describe the compound as "briefly used in the illicit drug market".supported
Title: 'Behavioral and Pharmacokinetics Studies of N-Methyl-2-Aminoindane (NM2AI) in Mice: An Aminoindane Briefly Used in the Illicit Drug Market.' ijms24031882
summary6 · 5 ok
Claim in summary — inconclusiveinconclusiveworking →
NM-2-AI first appeared in the research chemical market circa 2009–2010 as part of a wave of aminoindane derivatives marketed as alternatives to banned cathinones and MDMAsupported
Aminoindanes emerged on market after UK cathinone bans in 2009-2010. fpsyt.2017.00236
The sole direct behavioral study — conducted in mice — confirmed in vivo entactogenic activity and identified the N-demethylated metabolite 2-aminoindane as the primary active metabolitesupported
First in vivo study of NM2AI in mice (IP 1-100 mg/kg). Demonstrated entactogenic activity. Main active metabolite is 2-aminoindane (2-AI). ijms24031882
The pharmacological mechanism is inferred primarily from the parent compound 2-aminoindane (2-AI), which acts as a substrate-type releaser at the norepinephrine transporter (NET) with secondary dopamine transporter (DAT) activity and minimal serotonin transporter (SERT) involvementsupported
2-AI interacted with NET. All substances were monoamine transporter inhibitors with marked differences in DAT vs SERT inhibition profiles. j.bcp.2014.01.024
The pharmacological mechanism is inferred primarily from the parent compound 2-aminoindane (2-AI), which acts as a substrate-type releaser at the norepinephrine transporter (NET) with secondary dopamine transporter (DAT) activity and minimal serotonin transporter (SERT) involvementsupported
2-AI is a substrate for NET and DAT. Ring substitution increases SERT selectivity. s00213-019-05207-1
In silico modeling predicts cardiovascular toxicity probability of 82% and elevated genotoxicity relative to the parent 2-AIpartially supported
Cardiovascular toxicity probability 82% for NM-2-AI; genotoxicity probability 66.3% (Ames test). j.tiv.2025.106149
neuroscience4 · 4 ok
If secondary DAT activity is present (as suggested by the parent 2-AI pharmacology), mesolimbic dopamine pathway potentiation (ventral tegmental area projections to nucleus accumbens) would underlie the euphoria, motivation enhancement, and compulsive redosing urge described in community reportssupported
2-AI is a substrate for NET and DAT. s00213-019-05207-1
Tirri et al. (2023) documented behavioral changes in mice consistent with entactogenic activity — including sensorimotor modulation and nociceptive alterations — while noting effects "appear atypical and less intense with respect to those induced by classic stimulants"supported
Demonstrated entactogenic activity, mild hallucinogenic effect (PPI disruption). ijms24031882
Does the 2-AI metabolite significantly contribute to the overall effect? Tirri et al. (2023) identify 2-AI as the main active metabolite, but the relative contribution of parent NM-2-AI vs. metabolite 2-AI to the subjective experience is unquantified.supported
Main active metabolite is 2-aminoindane (2-AI). ijms24031882
What is the alpha-2 adrenergic receptor activity of NM-2-AI? The parent 2-AI shows Ki = 41 nM at alpha-2C — whether NM-2-AI retains this affinity could significantly modulate its cardiovascular and CNS effects.supported
High alpha2C receptor affinity (Ki=41 nM) s00213-019-05207-1
receptor-pharmacology4 · 2 ok
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Halberstadt et al. (2019) confirmed 2-AI as a substrate at both NET and DAT and additionally characterized alpha-2 adrenergic receptor binding:supported
2-AI is a substrate for NET and DAT. High alpha2C receptor affinity (Ki=41 nM), alpha2A (Ki=134 nM), alpha2B (Ki=211 nM). s00213-019-05207-1
Ring substitution at the 5,6-position (as in MDAI) shifts selectivity dramatically toward SERT, producing entactogenic rather than stimulant profilessupported
Ring substitution increases SERT selectivity. s00213-019-05207-1
Claim in receptor-pharmacology — not_supportednot supportedworking →
chemistry1 · 1 ok
Two CAS registry numbers appear in the literature: 24445-44-1 (cited in Jurowski and Frydrych 2026) and 10408-85-2 (UNODC substance record)supported
N-Methyl-2-aminoindane (NM-2-AI, CAS: 24445-44-1) j.tiv.2025.106149
clinical-evidence1 · 1 ok
Angerer et al. (2024) administered MDAI (180–228 mg oral) to six healthy volunteers in a crossover design comparing effects to 125 mg MDMA:supported
MDAI (3.0 mg/kg, range 180-228 mg) in six healthy volunteers. MDAI produced effects comparable with 125 mg MDMA. dta.3622
effects-overview1 · 0 ok
Claim in effects-overview — not_supportednot supportedworking →