NM-2-AI
N-methyl-2-aminoindane
Studies and references cited across this article, graded by evidence strength.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
oraltrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 5 mg | 5 mg | low |
| Low | 50–100 mg | 50–100 mg | low |
| Common | 100–150 mg | 100–150 mg | low |
| Strong | 150–200 mg | 150–200 mg | low |
| Heavy | 200+ mg | 200+ mg | low |
| Editorial | All dose values from existing DB / community consensus (PsychonautWiki confirmed matching data). No controlled human dosing study exists for NM-2-AI. The threshold value (5 mg) has an unusually large gap to light range (50 mg) and may be inaccurate — flagged for editorial review. Dose values are safety-critical and entirely unvalidated by clinical data. | ||
ReasoningReasoningAll dose values from existing DB / community consensus (PsychonautWiki confirmed matching data). No controlled human dosing study exists for NM-2-AI. The threshold value (5 mg) has an unusually large gap to light range (50 mg) and may be inaccurate — flagged for editorial review. Dose values are safety-critical and entirely unvalidated by clinical data. Evidence basis: community_consensus_large | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | Onset 30–60 minutes from existing DB / community consensus (PsychonautWiki). No controlled human PK data. Community reports indicate onset at 30–60 minutes, suggesting rapid absorption and N-demethylation. | ||
ReasoningReasoningOnset 30–60 minutes from existing DB / community consensus (PsychonautWiki). No controlled human PK data. Community reports indicate onset at 30–60 minutes, suggesting rapid absorption and N-demethylation. Evidence basis: community_consensus_large | |||
| Come uptrace | 15–30 minutes | 15–30 minutes | low |
| Editorial | Come-up phase proposed by Phase 1 at 15–30 minutes based on stimulant class norms and total duration constraint (2–4 hours). No published data for this phase. | ||
ReasoningReasoningCome-up phase proposed by Phase 1 at 15–30 minutes based on stimulant class norms and total duration constraint (2–4 hours). No published data for this phase. Evidence basis: structural_analogy | |||
| Peaktrace | 45–90 minutes | 45–90 minutes | low |
| Editorial | Peak duration proposed by Phase 1 at 45–90 minutes based on total duration (2–4 hours) and stimulant class temporal profile. No published data for this phase. | ||
ReasoningReasoningPeak duration proposed by Phase 1 at 45–90 minutes based on total duration (2–4 hours) and stimulant class temporal profile. No published data for this phase. Evidence basis: structural_analogy | |||
| Offsettrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | Offset proposed by Phase 1 at 30–60 minutes based on total duration and stimulant class rapid offset pattern. Community reports describe rapid decline, consistent with short-acting stimulant profile. | ||
ReasoningReasoningOffset proposed by Phase 1 at 30–60 minutes based on total duration and stimulant class rapid offset pattern. Community reports describe rapid decline, consistent with short-acting stimulant profile. Evidence basis: structural_analogy | |||
| Totaltrace | 2–4 hours | 2–4 hours | low |
| Editorial | Total duration 2–4 hours from existing DB / community consensus (PsychonautWiki). This represents subjective experience duration, not pharmacological half-life. No controlled human data. | ||
ReasoningReasoningTotal duration 2–4 hours from existing DB / community consensus (PsychonautWiki). This represents subjective experience duration, not pharmacological half-life. No controlled human data. Evidence basis: community_consensus_large | |||
| After effectstrace | 2–6 hours | 2–6 hours | low |
| Editorial | Aftereffects proposed by Phase 1 at 2–6 hours based on stimulant comedown/fatigue pattern. Post-acute depression, irritability, cognitive fatigue, and insomnia are class-typical for monoamine releasing agents. | ||
ReasoningReasoningAftereffects proposed by Phase 1 at 2–6 hours based on stimulant comedown/fatigue pattern. Post-acute depression, irritability, cognitive fatigue, and insomnia are class-typical for monoamine releasing agents. Evidence basis: structural_analogy | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | moderate | moderate | low |
| Chronic | low | low | low |
| Organs Affected | cardiovascular, pulmonary, hepatic | cardiovascular, pulmonary, hepatic | low |
| Editorial | Acute toxicity rated moderate per work-notes based on in silico predictions (Jurowski & Frydrych 2026) and one polydrug fatality. Chronic toxicity proposed as low (discounted from work-notes 'no data' per evidence discount rule — MDAI hepatotoxicity in HepG2 is the closest analog data but may not translate due to different ring substitution). All values are computational predictions or structural analogy to MDAI, not experimental measurements for NM-2-AI. | ||
ReasoningReasoningAcute toxicity rated moderate per work-notes based on in silico predictions (Jurowski & Frydrych 2026) and one polydrug fatality. Chronic toxicity proposed as low (discounted from work-notes 'no data' per evidence discount rule — MDAI hepatotoxicity in HepG2 is the closest analog data but may not translate due to different ring substitution). All values are computational predictions or structural analogy to MDAI, not experimental measurements for NM-2-AI. Evidence basis: structural_analogy | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | low | low | low |
| Psychological | moderate | moderate | low |
| Compulsive Redosing | high | high | low |
| Dose Escalation | moderate | moderate | low |
| Editorial | Work-notes specify physical dependence low-to-moderate, psychological moderate, compulsive redosing moderate-to-high. Proposed physical as 'low' and compulsive redosing as 'high' to capture the short-duration redosing driver emphasized in both work-notes and article prose. MDAI conditioned place preference in mice (Gatch et al. 2016) confirms abuse potential in the aminoindane class. No published NM-2-AI dependence studies exist — all values from community consensus. | ||
ReasoningReasoningWork-notes specify physical dependence low-to-moderate, psychological moderate, compulsive redosing moderate-to-high. Proposed physical as 'low' and compulsive redosing as 'high' to capture the short-duration redosing driver emphasized in both work-notes and article prose. MDAI conditioned place preference in mice (Gatch et al. 2016) confirms abuse potential in the aminoindane class. No published NM-2-AI dependence studies exist — all values from community consensus. Evidence basis: community_consensus_large | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | mild | mild | low |
| Symptoms | fatigue, depression, hypersomnia, irritability, cognitive fog, increased appetite | fatigue, depression, hypersomnia, irritability, cognitive fog, increased appetite | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | No published withdrawal data for NM-2-AI. Withdrawal existence marked true based on class-level stimulant withdrawal profile (fatigue, depression, hypersomnia). Severity rated mild — stimulant withdrawal is typically not medically dangerous. All parameters inferred from stimulant class norms. | ||
ReasoningReasoningNo published withdrawal data for NM-2-AI. Withdrawal existence marked true based on class-level stimulant withdrawal profile (fatigue, depression, hypersomnia). Severity rated mild — stimulant withdrawal is typically not medically dangerous. All parameters inferred from stimulant class norms. Evidence basis: community_consensus_large | |||
Tolerance Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Buildup | moderate | moderate | low |
| Half-life | 5 days | 5 days | low |
| Full Reset | 10 days | 10 days | low |
| Cross-tolerances | dopaminergic stimulants, other monoamine releasing agents | dopaminergic stimulants, other monoamine releasing agents | low |
| Editorial | Tolerance half-life (~5 days) and full reset (~1.5 weeks / 10 days) from existing DB / community consensus. Buildup rated moderate per work-notes. Cross-tolerances expanded from seed data 'dopamine, stimulant' to explicit 'dopaminergic stimulants, other monoamine releasing agents'. Mechanism inferred from stimulant class — no published NM-2-AI tolerance data. | ||
ReasoningReasoningTolerance half-life (~5 days) and full reset (~1.5 weeks / 10 days) from existing DB / community consensus. Buildup rated moderate per work-notes. Cross-tolerances expanded from seed data 'dopamine, stimulant' to explicit 'dopaminergic stimulants, other monoamine releasing agents'. Mechanism inferred from stimulant class — no published NM-2-AI tolerance data. Evidence basis: community_consensus_large | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| other Concurrent MAOI usetrace | absolute | absolute | medium |
| Editorial | Class-level absolute contraindication for all monoamine releasing agents. No NM-2-AI-specific case data, but mechanism is well-established pharmacologically. | ||
ReasoningReasoningClass-level absolute contraindication for all monoamine releasing agents. No NM-2-AI-specific case data, but mechanism is well-established pharmacologically. | |||
| cardiovascular Uncontrolled hypertensiontrace | absolute | absolute | medium |
| Editorial | Class-level contraindication for all NET-releasing stimulants. NM-2-AI's inferred NET-dominant pharmacology makes this particularly relevant. No substance-specific data. | ||
ReasoningReasoningClass-level contraindication for all NET-releasing stimulants. NM-2-AI's inferred NET-dominant pharmacology makes this particularly relevant. No substance-specific data. | |||
| cardiovascular Severe cardiovascular diseasetrace | absolute | absolute | low |
| Editorial | In silico cardiovascular toxicity prediction (82%) combined with class-level sympathomimetic mechanism. The 82% figure is a computational model output, not experimental measurement. | ||
ReasoningReasoningIn silico cardiovascular toxicity prediction (82%) combined with class-level sympathomimetic mechanism. The 82% figure is a computational model output, not experimental measurement. | |||
| neurological Seizure disorderstrace | relative | relative | low |
| Editorial | Class-level relative contraindication for all stimulant/monoamine releasing agents. No NM-2-AI-specific seizure case reports exist. | ||
ReasoningReasoningClass-level relative contraindication for all stimulant/monoamine releasing agents. No NM-2-AI-specific seizure case reports exist. | |||
| hepatic Hepatic impairmenttrace | relative | relative | low |
| Editorial | Class-level relative contraindication based on hepatic metabolism pathway and MDAI hepatotoxicity data. MDAI cytotoxicity may not translate to NM-2-AI due to different ring substitution. | ||
ReasoningReasoningClass-level relative contraindication based on hepatic metabolism pathway and MDAI hepatotoxicity data. MDAI cytotoxicity may not translate to NM-2-AI due to different ring substitution. | |||
| psychiatric Bipolar disordertrace | relative | relative | low |
| Editorial | Class-level relative contraindication for stimulant/monoamine releasing agents. No NM-2-AI-specific psychiatric case data exist. | ||
ReasoningReasoningClass-level relative contraindication for stimulant/monoamine releasing agents. No NM-2-AI-specific psychiatric case data exist. | |||
| psychiatric Psychosis spectrum disorderstrace | relative | relative | low |
| Editorial | Class-level relative contraindication for dopamine-releasing stimulants. No NM-2-AI-specific psychosis case reports, but stimulant psychosis is a well-established class risk. | ||
ReasoningReasoningClass-level relative contraindication for dopamine-releasing stimulants. No NM-2-AI-specific psychosis case reports, but stimulant psychosis is a well-established class risk. | |||
| pregnancy breastfeeding Pregnancytrace | absolute | absolute | medium |
| Editorial | Class-level absolute contraindication for all sympathomimetic vasoconstrictors in pregnancy. No substance-specific reproductive data. | ||
ReasoningReasoningClass-level absolute contraindication for all sympathomimetic vasoconstrictors in pregnancy. No substance-specific reproductive data. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 1800–3600 sec(i=0.05) | 1800–3600 sec(i=0.05) | low |
| Editorial | Onset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. | ||
ReasoningReasoningOnset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. Evidence basis: community_consensus_large | |||
| Come uptrace | 900–1800 sec(i=0.40) | 900–1800 sec(i=0.40) | low |
| Editorial | Onset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. | ||
ReasoningReasoningOnset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. Evidence basis: community_consensus_large | |||
| Peaktrace | 2700–5400 sec(i=1.00) | 2700–5400 sec(i=1.00) | low |
| Editorial | Onset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. | ||
ReasoningReasoningOnset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. Evidence basis: community_consensus_large | |||
| Resolutiontrace | 1800–3600 sec(i=0.30) | 1800–3600 sec(i=0.30) | low |
| Editorial | Onset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. | ||
ReasoningReasoningOnset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. Evidence basis: community_consensus_large | |||
| Afterglowtrace | 7200–21600 sec(i=0.10) | 7200–21600 sec(i=0.10) | low |
| Editorial | Onset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. | ||
ReasoningReasoningOnset (30–60 min) and total (2–4 h) from existing DB / community consensus. Come-up (15–30 min), peak (45–90 min), offset (30–60 min), and aftereffects (2–6 h) proposed by Phase 1 based on stimulant class norms and total duration constraints. No controlled human pharmacokinetic data exist for NM-2-AI. All phase durations are community estimates or class-level inferences. Evidence basis: community_consensus_large | |||
Dose Tier Summaries
At 50–100 mg oral, NM-2-AI produces mild stimulation and increased wakefulness. Cognitive effects include subtle thought acceleration and a slight sharpening of focus, though below the threshold for productive enhancement. A faint mood lift may be perceptible, but entactogenic warmth is absent at this range. Physical effects are modest: mild appetite suppression, slight increase in heart rate awareness, and a subtle energizing body feeling. Bruxism and excessive sweating are unlikely at this level. Duration remains short (2–4 hours total), and aftereffects are mild. Functional impairment is minimal, though sleep may be delayed if dosed in the evening.
Light range (50–100 mg) from existing DB / community consensus. Effects described by analogy with stimulant class norms at sub-common doses. No controlled human data.
ReasoningReasoning
Light range (50–100 mg) from existing DB / community consensus. Effects described by analogy with stimulant class norms at sub-common doses. No controlled human data.
Evidence basis: community_consensus_large
At approximately 5 mg, NM-2-AI produces sub-perceptual stimulant awareness. Effects at this level are minimal — a possible faint increase in alertness or slight physiological activation, but no meaningful psychoactive response. Most users report no discernible subjective change. This dose range serves primarily for allergy testing and individual sensitivity assessment. No cognitive enhancement, mood elevation, or physical stimulation is expected. The gap between threshold (5 mg) and light (50 mg) is unusually large and may reflect inaccurate threshold data rather than a genuine pharmacological plateau. Conservative titration through this range is advisable.
Threshold value (5 mg) from existing DB / community consensus (PsychonautWiki). No controlled dosing studies exist. The unusually large gap between threshold and light dose was flagged by Phase 1 as potentially inaccurate.
ReasoningReasoning
Threshold value (5 mg) from existing DB / community consensus (PsychonautWiki). No controlled dosing studies exist. The unusually large gap between threshold and light dose was flagged by Phase 1 as potentially inaccurate.
Evidence basis: community_consensus_large
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.
Common range (100–150 mg) from existing DB / community consensus. Effects profile assembled from seed effect data, community reports, and class-level stimulant/entactogen norms. No controlled human study.
ReasoningReasoning
Common range (100–150 mg) from existing DB / community consensus. Effects profile assembled from seed effect data, community reports, and class-level stimulant/entactogen norms. No controlled human study.
Evidence basis: community_consensus_large
At 150–200 mg oral, stimulation intensifies markedly. Euphoria becomes more pronounced, alongside strong thought acceleration, heightened motivation, and analysis enhancement. The compulsive redosing urge is prominent at this level — the rapid offset strongly drives re-administration. Cardiovascular effects escalate: abnormal heartbeat perception, elevated blood pressure, pronounced bruxism, and excessive sweating are expected. Restlessness and anxiety may emerge, particularly in stimulant-sensitive individuals or anxiogenic settings. Temperature dysregulation becomes a consideration. Post-acute depression, irritability, and cognitive fatigue are more likely and more intense than at common doses. Sleep disruption extends well beyond the subjective duration. Risk-benefit ratio narrows significantly at this tier.
Strong range (150–200 mg) from existing DB / community consensus. Adverse effect escalation inferred from stimulant class dose-response and community reports. In silico cardiovascular toxicity prediction (82%) supports caution.
ReasoningReasoning
Strong range (150–200 mg) from existing DB / community consensus. Adverse effect escalation inferred from stimulant class dose-response and community reports. In silico cardiovascular toxicity prediction (82%) supports caution.
Evidence basis: community_consensus_large
Doses exceeding 200 mg enter territory with no established safety ceiling. All stimulant adverse effects are amplified — severe cardiovascular strain, intense anxiety and agitation, pronounced bruxism, and excessive sweating. At these levels, the risk of stimulant-induced paranoia or psychotic features increases, particularly with repeated dosing within a session. Physically, sympathomimetic overload presents the primary danger: hypertensive emergency, cardiac arrhythmia, and hyperthermia are all plausible at extreme doses, though no human dose-toxicity relationship has been established. No controlled data exist for this range. One polydrug fatality has been documented (NM-2-AI 95.4 ng/mL alongside MAB-CHMINACA). The exact toxic dose in humans remains unknown.
Heavy threshold (200+ mg) from existing DB / community consensus. Adverse effect descriptions from class-level stimulant toxicology and the documented polydrug fatality (DEA 2021). No controlled data at any dose level.
ReasoningReasoning
Heavy threshold (200+ mg) from existing DB / community consensus. Adverse effect descriptions from class-level stimulant toxicology and the documented polydrug fatality (DEA 2021). No controlled data at any dose level.
Evidence basis: community_consensus_large
History
+ Aminoindanes (UNODC Substance Group Details) (2015)
− Details for Aminoindanes (2017)
publish Oct 2, 2026 · by agent-psx
backfill Jun 4, 2026
Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.
Sources
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Claim Verification
No claim verification has run for this version.