Methiopropamine
Studies and references cited across this article, graded by evidence strength.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
insufflatedtrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 5 mg | 5 mg | low |
| Low | 5–20 mg | 5–20 mg | low |
| Common | 20–40 mg | 20–40 mg | low |
| Strong | 40–60 mg | 40–60 mg | low |
| Heavy | 60+ mg | 60+ mg | low |
| Editorial | Values from existing DB / community consensus for threshold through strong tiers. Heavy tier (60+ mg) proposed by analogy to oral heavy dose. No controlled human dose-finding study exists for any insufflated tier. All values are safety-critical and unverified. | ||
ReasoningReasoningValues from existing DB / community consensus for threshold through strong tiers. Heavy tier (60+ mg) proposed by analogy to oral heavy dose. No controlled human dose-finding study exists for any insufflated tier. All values are safety-critical and unverified. Evidence basis: community_consensus_large | |||
oraltrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 10 mg | 10 mg | low |
| Low | 20–30 mg | 20–30 mg | low |
| Common | 30–50 mg | 30–50 mg | low |
| Strong | 50–60 mg | 50–60 mg | low |
| Heavy | 60+ mg | 60+ mg | low |
| Editorial | Values from existing DB / community consensus. No controlled human dose-finding study exists. Consistent with MPA being approximately 5× less potent than methamphetamine in rodent locomotor assays (Tuv et al. 2021). All dose values are safety-critical and unverified against published clinical sources. | ||
ReasoningReasoningValues from existing DB / community consensus. No controlled human dose-finding study exists. Consistent with MPA being approximately 5× less potent than methamphetamine in rodent locomotor assays (Tuv et al. 2021). All dose values are safety-critical and unverified against published clinical sources. Evidence basis: community_consensus_large | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | From existing DB / community consensus. No published controlled study. | ||
ReasoningReasoningFrom existing DB / community consensus. No published controlled study. Evidence basis: community_consensus_large | |||
| Offsettrace | 2–3 hours | 2–3 hours | low |
| Editorial | From existing DB / community consensus. No published controlled study. | ||
ReasoningReasoningFrom existing DB / community consensus. No published controlled study. Evidence basis: community_consensus_large | |||
| After effectstrace | 1–2 hours | 1–2 hours | low |
| Editorial | From existing DB / community consensus. No published controlled study. | ||
ReasoningReasoningFrom existing DB / community consensus. No published controlled study. Evidence basis: community_consensus_large | |||
| Come uptrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | Not in seed data. Proposed based on oral stimulant class norms and the 30-60 min onset suggesting a similar come_up window. | ||
ReasoningReasoningNot in seed data. Proposed based on oral stimulant class norms and the 30-60 min onset suggesting a similar come_up window. Evidence basis: structural_analogy | |||
| Peaktrace | 2–4 hours | 2–4 hours | low |
| Editorial | From existing DB / community consensus. No published controlled study. | ||
ReasoningReasoningFrom existing DB / community consensus. No published controlled study. Evidence basis: community_consensus_large | |||
| Totaltrace | 6–10 hours | 6–10 hours | low |
| Editorial | From existing DB / community consensus. No published controlled study. | ||
ReasoningReasoningFrom existing DB / community consensus. No published controlled study. Evidence basis: community_consensus_large | |||
insufflated
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 5–15 minutes | 5–15 minutes | low |
| Editorial | Proposed by analogy to insufflated stimulant class norms (methamphetamine, methylphenidate). No published insufflated duration data for MPA. | ||
ReasoningReasoningProposed by analogy to insufflated stimulant class norms (methamphetamine, methylphenidate). No published insufflated duration data for MPA. Evidence basis: structural_analogy | |||
| Peaktrace | 1–2 hours | 1–2 hours | low |
| Editorial | Proposed by analogy to insufflated stimulant class norms, adjusted for MPA's lower potency. No published data. | ||
ReasoningReasoningProposed by analogy to insufflated stimulant class norms, adjusted for MPA's lower potency. No published data. Evidence basis: structural_analogy | |||
| Offsettrace | 1–2 hours | 1–2 hours | low |
| Editorial | Proposed by analogy to insufflated stimulant class norms. No published data. | ||
ReasoningReasoningProposed by analogy to insufflated stimulant class norms. No published data. Evidence basis: structural_analogy | |||
| Totaltrace | 3–6 hours | 3–6 hours | low |
| Editorial | Proposed by analogy to insufflated stimulant class norms and expected shorter duration vs. oral route. No published data. Reference compound: methamphetamine insufflated. | ||
ReasoningReasoningProposed by analogy to insufflated stimulant class norms and expected shorter duration vs. oral route. No published data. Reference compound: methamphetamine insufflated. Evidence basis: structural_analogy | |||
| After effectstrace | 1–2 hours | 1–2 hours | low |
| Editorial | Proposed by analogy to insufflated stimulant class norms. No published data. | ||
ReasoningReasoningProposed by analogy to insufflated stimulant class norms. No published data. Evidence basis: structural_analogy | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | moderate | moderate | medium |
| Chronic | high | high | medium |
| Organs Affected | cardiovascular, renal, gastrointestinal, neurological | cardiovascular, renal, gastrointestinal, neurological | medium |
| Editorial | Acute toxicity rated moderate based on documented organ effects in animal models and human case series (tachycardia, rhabdomyolysis) without established LD₅₀. Chronic toxicity rated high based on Foti et al. 2019 chronic mouse model showing 40% sudden death, myocardial ischemia, and renal/GI necrotic lesions, plus Nguyen et al. 2019 dopaminergic neurotoxicity cascade. Evidence primarily from animal studies with supporting human case series (White et al. 2019, 11 cases). Polydrug confounding in human data prevents definitive attribution. | ||
ReasoningReasoningAcute toxicity rated moderate based on documented organ effects in animal models and human case series (tachycardia, rhabdomyolysis) without established LD₅₀. Chronic toxicity rated high based on Foti et al. 2019 chronic mouse model showing 40% sudden death, myocardial ischemia, and renal/GI necrotic lesions, plus Nguyen et al. 2019 dopaminergic neurotoxicity cascade. Evidence primarily from animal studies with supporting human case series (White et al. 2019, 11 cases). Polydrug confounding in human data prevents definitive attribution. Evidence basis: animal_study | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | low | low | medium |
| Psychological | moderate | moderate | medium |
| Compulsive Redosing | high | high | medium |
| Dose Escalation | moderate | moderate | medium |
| Editorial | Physical dependence rated low (no physical withdrawal syndrome described in literature; psychological withdrawal only). Psychological dependence rated moderate based on locomotor sensitization in rats (Yoon et al. 2016), NAc spine remodeling (Cai et al. 2019), and user-reported compulsive redosing. WHO ECDD concluded abuse potential similar to Schedule II substances. Animal models strong but human dependence data limited to user reports. | ||
ReasoningReasoningPhysical dependence rated low (no physical withdrawal syndrome described in literature; psychological withdrawal only). Psychological dependence rated moderate based on locomotor sensitization in rats (Yoon et al. 2016), NAc spine remodeling (Cai et al. 2019), and user-reported compulsive redosing. WHO ECDD concluded abuse potential similar to Schedule II substances. Animal models strong but human dependence data limited to user reports. Evidence basis: animal_study | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | mild | mild | low |
| Symptoms | fatigue, anhedonia, low mood, irritability | fatigue, anhedonia, low mood, irritability | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | Psychological withdrawal only — no physical withdrawal syndrome described. Symptoms (fatigue, anhedonia, low mood, irritability) reported by users but not systematically studied. Duration of 1-3 days inferred from stimulant class norms; no MPA-specific data. | ||
ReasoningReasoningPsychological withdrawal only — no physical withdrawal syndrome described. Symptoms (fatigue, anhedonia, low mood, irritability) reported by users but not systematically studied. Duration of 1-3 days inferred from stimulant class norms; no MPA-specific data. Evidence basis: animal_study | |||
Tolerance Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Buildup | moderate | moderate | low |
| Half-life | 5 days | 5 days | low |
| Full Reset | 10.5 days | 10.5 days | low |
| Cross-tolerances | amphetamine, methamphetamine, methylphenidate | amphetamine, methamphetamine, methylphenidate | low |
| Editorial | Tolerance buildup rated moderate per seed data and community consensus. Half-life and reset values from community consensus only — no published human or animal tolerance study exists. Cross-tolerances inferred from shared NDRI mechanism with amphetamine, methamphetamine, and methylphenidate. | ||
ReasoningReasoningTolerance buildup rated moderate per seed data and community consensus. Half-life and reset values from community consensus only — no published human or animal tolerance study exists. Cross-tolerances inferred from shared NDRI mechanism with amphetamine, methamphetamine, and methylphenidate. Evidence basis: community_consensus_large | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| cardiovascular Pre-existing cardiovascular diseasetrace | absolute | absolute | medium |
| Editorial | Documented in both animal chronic model (40% sudden death, myocardial ischemia) and human case series (91% tachycardia). Multiple independent sources. | ||
ReasoningReasoningDocumented in both animal chronic model (40% sudden death, myocardial ischemia) and human case series (91% tachycardia). Multiple independent sources. | |||
| other Concurrent MAOI usetrace | absolute | absolute | medium |
| Editorial | Class-level contraindication inferred from MPA's NDRI mechanism. Standard for all catecholaminergic stimulants. No MPA-specific data. | ||
ReasoningReasoningClass-level contraindication inferred from MPA's NDRI mechanism. Standard for all catecholaminergic stimulants. No MPA-specific data. | |||
| neurological Seizure disorderstrace | relative | relative | low |
| Editorial | Inferred from stimulant class mechanism. No MPA-specific seizure data. Reference compounds: methamphetamine, amphetamine. | ||
ReasoningReasoningInferred from stimulant class mechanism. No MPA-specific seizure data. Reference compounds: methamphetamine, amphetamine. | |||
| psychiatric Psychotic disorders or bipolar disordertrace | relative | relative | medium |
| Editorial | Documented acute psychosis in human case series (45% hallucinations, 64% confusion in IONA cases) and individual case report. Medium confidence due to polydrug confounding in most cases. | ||
ReasoningReasoningDocumented acute psychosis in human case series (45% hallucinations, 64% confusion in IONA cases) and individual case report. Medium confidence due to polydrug confounding in most cases. | |||
| renal Renal impairmenttrace | relative | relative | medium |
| Editorial | Supported by human case series (CK elevation in 64%) and chronic animal model (renal necrotic lesions). Polydrug confounding limits attribution certainty. | ||
ReasoningReasoningSupported by human case series (CK elevation in 64%) and chronic animal model (renal necrotic lesions). Polydrug confounding limits attribution certainty. | |||
| pregnancy breastfeeding Pregnancy and lactationtrace | relative | relative | low |
| Editorial | Class-level inference from catecholaminergic stimulant mechanism. No MPA-specific reproductive data. Reference compounds: methamphetamine, amphetamine. | ||
ReasoningReasoningClass-level inference from catecholaminergic stimulant mechanism. No MPA-specific reproductive data. Reference compounds: methamphetamine, amphetamine. | |||
| other Concurrent serotonergic medicationtrace | relative | relative | medium |
| Editorial | MPA has weak but non-zero SERT inhibition. Harm reduction organizations warn of serotonin toxicity in serotonergic combinations. No peer-reviewed case report of this specific interaction found. | ||
ReasoningReasoningMPA has weak but non-zero SERT inhibition. Harm reduction organizations warn of serotonin toxicity in serotonergic combinations. No peer-reviewed case report of this specific interaction found. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 0–3600 sec(i=0.15) | 0–3600 sec(i=0.15) | low |
| Editorial | Oral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. | ||
ReasoningReasoningOral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. Evidence basis: community_consensus_large | |||
| Come uptrace | 1800–3600 sec(i=0.40) | 1800–3600 sec(i=0.40) | low |
| Editorial | Oral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. | ||
ReasoningReasoningOral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. Evidence basis: community_consensus_large | |||
| Peaktrace | 5400–10800 sec(i=1.00) | 5400–10800 sec(i=1.00) | low |
| Editorial | Oral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. | ||
ReasoningReasoningOral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. Evidence basis: community_consensus_large | |||
| Plateautrace | 3600–7200 sec(i=0.50) | 3600–7200 sec(i=0.50) | low |
| Editorial | Oral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. | ||
ReasoningReasoningOral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. Evidence basis: community_consensus_large | |||
| Resolutiontrace | 3600–7200 sec(i=0.25) | 3600–7200 sec(i=0.25) | low |
| Editorial | Oral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. | ||
ReasoningReasoningOral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. Evidence basis: community_consensus_large | |||
| Afterglowtrace | 3600–7200 sec(i=0.10) | 3600–7200 sec(i=0.10) | low |
| Editorial | Oral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. | ||
ReasoningReasoningOral timeline derived from existing DB / community consensus duration data (onset 30-60 min, peak 2-4 h, offset 2-3 h, total 6-10 h, aftereffects 1-2 h). No published controlled study. Come_up phase interpolated from onset-to-peak transition. Plateau phase inferred from the 6-10 h total duration minus onset/peak/offset phases. Intensity weights from work-notes. Evidence basis: community_consensus_large | |||
insufflated
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 0–900 sec(i=0.30) | 0–900 sec(i=0.30) | low |
| Editorial | Insufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. | ||
ReasoningReasoningInsufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. Evidence basis: structural_analogy | |||
| Come uptrace | 300–1800 sec(i=0.60) | 300–1800 sec(i=0.60) | low |
| Editorial | Insufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. | ||
ReasoningReasoningInsufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. Evidence basis: structural_analogy | |||
| Peaktrace | 1800–7200 sec(i=1.00) | 1800–7200 sec(i=1.00) | low |
| Editorial | Insufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. | ||
ReasoningReasoningInsufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. Evidence basis: structural_analogy | |||
| Resolutiontrace | 3600–7200 sec(i=0.35) | 3600–7200 sec(i=0.35) | low |
| Editorial | Insufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. | ||
ReasoningReasoningInsufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. Evidence basis: structural_analogy | |||
| Afterglowtrace | 3600–7200 sec(i=0.15) | 3600–7200 sec(i=0.15) | low |
| Editorial | Insufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. | ||
ReasoningReasoningInsufflated timeline entirely inferred from structural analogy to insufflated methamphetamine and stimulant class norms, adjusted for MPA's lower potency. No published insufflated duration data for MPA. Onset 5-15 min, peak 1-2 h, total 3-6 h per work-notes. Intensity weights from work-notes. Evidence basis: structural_analogy | |||
Dose Tier Summaries
Minimal perceptible stimulation emerges as a slight increase in alertness and wakefulness without overt euphoria or noticeable mood elevation. Cognitive effects are subtle — a faint sense of thought acceleration and marginally improved focus that may be difficult to distinguish from placebo. Physical effects are negligible at this tier. Heart rate may increase slightly but remains within normal resting range. Appetite suppression is absent or barely perceptible. No significant temperature dysregulation, sweating, or bruxism expected. Oral onset may take 30–60 minutes, making premature redosing a risk. Duration commitment is modest. Sleep disruption is unlikely unless taken late in the day.
Based on community consensus dose ranges (oral threshold ~10 mg). No controlled human study at threshold. Effects extrapolated from the substance's NDRI mechanism and user reports describing MPA as mild/caffeine-like at low doses.
ReasoningReasoning
Based on community consensus dose ranges (oral threshold ~10 mg). No controlled human study at threshold. Effects extrapolated from the substance's NDRI mechanism and user reports describing MPA as mild/caffeine-like at low doses.
Evidence basis: community_consensus_large
Noticeable wakefulness and mild focus enhancement become apparent. Thought acceleration is gentle — a sense of mental alertness comparable to moderate caffeine. Cognitive euphoria is minimal or absent. Motivation enhancement may be subtly present, manifesting as increased willingness to engage with routine tasks. Appetite suppression emerges at a low level. Heart rate may be slightly elevated, and some users notice increased heart rate perception. Stimulation is functional rather than forceful — body high is largely absent. Spontaneous body sensations are minimal. Functional impairment is unlikely at this tier. Oral duration extends to 6–8 hours. The mild character of effects at this range may encourage dose escalation — note that MPA has a steep dose-response curve.
Based on community consensus dose ranges (oral 20-30 mg, insufflated 5-20 mg). User reports consistently describe MPA as methylphenidate-like at lower doses (DrugWise). No controlled study.
ReasoningReasoning
Based on community consensus dose ranges (oral 20-30 mg, insufflated 5-20 mg). User reports consistently describe MPA as methylphenidate-like at lower doses (DrugWise). No controlled study.
Evidence basis: community_consensus_large
Clear stimulant effects establish themselves: sustained wakefulness, focus enhancement, and mild cognitive euphoria. Thought acceleration and thought organization improve task engagement. Analysis enhancement is noticeable. Motivation enhancement supports sustained productivity. Music enhancement may be subtly present. Appetite suppression is moderate and reliable. Stimulation is clearly perceptible — increased energy and physical alertness without the intensity of amphetamine. Heart rate elevation is common. Spontaneous body sensations and mild temperature dysregulation may emerge. Bruxism and excessive sweating are possible but typically mild. Compulsive redosing urge may emerge at this tier — users frequently describe wanting to sustain the functional stimulation. Oral duration is 6–10 hours. Insomnia is likely if taken in the afternoon or evening. Comedown involves mild fatigue, irritability, and low mood.
Based on community consensus dose ranges (oral 30-50 mg, insufflated 20-40 mg). Effects profile drawn from user reports (DrugWise) and work-notes effects data. Compulsive redosing emphasized per work-notes.
ReasoningReasoning
Based on community consensus dose ranges (oral 30-50 mg, insufflated 20-40 mg). Effects profile drawn from user reports (DrugWise) and work-notes effects data. Compulsive redosing emphasized per work-notes.
Evidence basis: community_consensus_large
Pronounced stimulation dominates the experience. Wakefulness is intense and persistent. Focus enhancement may shift from productive to scattered as overstimulation narrows cognitive flexibility. Thought acceleration intensifies. Cognitive euphoria is more apparent but still moderate compared to classical stimulants. Irritability and anxiety may emerge alongside stimulation. Cardiovascular effects become significant: tachycardia, vasoconstriction, and abnormal heartbeat are likely. Bruxism intensifies. Excessive sweating and temperature dysregulation are common. Appetite suppression is strong. Restlessness replaces productive stimulation. Pupil dilation is probable. Compulsive redosing urge intensifies markedly at this tier. The steep dose-response curve means the transition from common to strong effects may feel abrupt. Sleep is impossible for an extended period. Comedown is more pronounced — depression, cognitive fatigue, and motivation suppression are expected.
Based on community consensus dose ranges (oral 50-60 mg, insufflated 40-60 mg). Cardiovascular effects supported by animal models showing steep dose-response curve (Tuv et al. 2021) and human case series (91% tachycardia at intoxicating doses, White et al. 2019).
ReasoningReasoning
Based on community consensus dose ranges (oral 50-60 mg, insufflated 40-60 mg). Cardiovascular effects supported by animal models showing steep dose-response curve (Tuv et al. 2021) and human case series (91% tachycardia at intoxicating doses, White et al. 2019).
Evidence basis: community_consensus_large
Risk of cardiovascular toxicity is significantly elevated at this tier. The narrow margin between strong and heavy doses — a steep dose-response curve documented in rodent models — means effects may escalate rapidly. Tachycardia, vasoconstriction, and abnormal heartbeat are expected. Rhabdomyolysis (muscle breakdown) is a documented risk at intoxicating doses. Psychological effects may become destabilizing: confusion, agitation, hallucinations, and paranoid delusions are documented in clinical cases at high doses. Cognitive impairment replaces cognitive enhancement. Delirium is possible. Aggressive behavior has been demonstrated at higher doses in animal models. Sleep is impossible for an extended period. Compulsive redosing urge remains high. Comedown is severe — prolonged fatigue, depression, irritability, and cognitive fatigue. Seek emergency medical attention if chest pain, severe confusion, or hallucinations develop.
Based on community consensus dose ranges (oral 60+ mg, insufflated 60+ mg). Cardiovascular and psychological toxicity documented in IONA case series (White et al. 2019) — 91% tachycardia, 64% confusion, 45% hallucinations. Animal model steep dose-response curve (Tuv et al. 2021).
ReasoningReasoning
Based on community consensus dose ranges (oral 60+ mg, insufflated 60+ mg). Cardiovascular and psychological toxicity documented in IONA case series (White et al. 2019) — 91% tachycardia, 64% confusion, 45% hallucinations. Animal model steep dose-response curve (Tuv et al. 2021).
Evidence basis: community_consensus_large
History
+ Methiopropamine (MPA) - DrugWise (2020)
− Methiopropamine - MPA - DrugWise harm reduction information (2023)
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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