Pentedrone
α-propyl-N-methylcathinone
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 | 5–15 mg | 5–15 mg | low |
| Common | 15–30 mg | 15–30 mg | low |
| Strong | 30–50 mg | 30–50 mg | low |
| Heavy | 50+ mg | 50+ mg | low |
| Editorial | No controlled human dose-response data exist for pentedrone. Values carried forward from existing Psychedex database (community consensus). Pentedrone is a mid-potency synthetic cathinone NDRI; dose ranges are consistent with structural analogues in the cathinone series. All values require editorial verification. | ||
ReasoningReasoningNo controlled human dose-response data exist for pentedrone. Values carried forward from existing Psychedex database (community consensus). Pentedrone is a mid-potency synthetic cathinone NDRI; dose ranges are consistent with structural analogues in the cathinone series. All values require editorial verification. Evidence basis: community_consensus_small | |||
insufflatedtrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 3 mg | 3 mg | low |
| Low | 3–10 mg | 3–10 mg | low |
| Common | 10–25 mg | 10–25 mg | low |
| Strong | 25–40 mg | 25–40 mg | low |
| Heavy | 40+ mg | 40+ mg | low |
| Editorial | No controlled human insufflated dose data for pentedrone. Values from existing database (community consensus). Insufflated doses are typically lower than oral due to faster absorption and higher bioavailability via nasal mucosa. N-ethylpentedrone human studies used 20-40 mg intranasally (Nuñez-Montero et al. 2023, 2025), providing rough calibration for the analogue. | ||
ReasoningReasoningNo controlled human insufflated dose data for pentedrone. Values from existing database (community consensus). Insufflated doses are typically lower than oral due to faster absorption and higher bioavailability via nasal mucosa. N-ethylpentedrone human studies used 20-40 mg intranasally (Nuñez-Montero et al. 2023, 2025), providing rough calibration for the analogue. Evidence basis: community_consensus_small | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 15–30 minutes | 15–30 minutes | low |
| Editorial | From existing database (community consensus). No controlled oral pentedrone onset data published. | ||
ReasoningReasoningFrom existing database (community consensus). No controlled oral pentedrone onset data published. Evidence basis: community_consensus_small | |||
| Peaktrace | 1–2 hours | 1–2 hours | low |
| Editorial | From existing database (community consensus). Consistent with short-acting cathinone NDRI profile. | ||
ReasoningReasoningFrom existing database (community consensus). Consistent with short-acting cathinone NDRI profile. Evidence basis: community_consensus_small | |||
| Offsettrace | 1–2 hours | 1–2 hours | low |
| Editorial | From existing database (community consensus). | ||
ReasoningReasoningFrom existing database (community consensus). Evidence basis: community_consensus_small | |||
| Totaltrace | 2–6 hours | 2–6 hours | low |
| Editorial | From existing database (community consensus). Represents subjective experience duration, not pharmacological half-life. | ||
ReasoningReasoningFrom existing database (community consensus). Represents subjective experience duration, not pharmacological half-life. Evidence basis: community_consensus_small | |||
| After effectstrace | 1–10 hours | 1–10 hours | low |
| Editorial | From existing database. Wide range reflects variable aftereffect duration consistent with prolonged elimination half-life suggested by N-ethylpentedrone case data (Deville et al. 2023). | ||
ReasoningReasoningFrom existing database. Wide range reflects variable aftereffect duration consistent with prolonged elimination half-life suggested by N-ethylpentedrone case data (Deville et al. 2023). Evidence basis: community_consensus_small | |||
insufflated
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 5–10 minutes | 5–10 minutes | low |
| Editorial | From existing database (community consensus). Supported by N-ethylpentedrone human data showing onset within 20 min insufflated (Nuñez-Montero et al. 2025), consistent with faster intranasal absorption. | ||
ReasoningReasoningFrom existing database (community consensus). Supported by N-ethylpentedrone human data showing onset within 20 min insufflated (Nuñez-Montero et al. 2025), consistent with faster intranasal absorption. Evidence basis: community_consensus_small | |||
| Peaktrace | 30–90 minutes | 30–90 minutes | low |
| Editorial | From existing database (community consensus). | ||
ReasoningReasoningFrom existing database (community consensus). Evidence basis: community_consensus_small | |||
| Offsettrace | 30–90 minutes | 30–90 minutes | low |
| Editorial | From existing database (community consensus). | ||
ReasoningReasoningFrom existing database (community consensus). Evidence basis: community_consensus_small | |||
| Totaltrace | 1–4 hours | 1–4 hours | low |
| Editorial | From existing database. N-ethylpentedrone effects returned to baseline by 3-4 hours insufflated (Nuñez-Montero et al. 2025), broadly consistent. | ||
ReasoningReasoningFrom existing database. N-ethylpentedrone effects returned to baseline by 3-4 hours insufflated (Nuñez-Montero et al. 2025), broadly consistent. Evidence basis: community_consensus_small | |||
| After effectstrace | 1–8 hours | 1–8 hours | low |
| Editorial | From existing database. Prolonged aftereffects consistent with long apparent half-life from analogue case data. | ||
ReasoningReasoningFrom existing database. Prolonged aftereffects consistent with long apparent half-life from analogue case data. Evidence basis: community_consensus_small | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | moderate | moderate | low |
| Chronic | moderate | moderate | low |
| Organs Affected | liver, cardiovascular, kidney, brain | liver, cardiovascular, kidney, brain | low |
| Editorial | Classified as moderate (acute and chronic): hepatotoxicity data is in vitro only (rat hepatocytes, HepaRG cells); severe intoxication case data derives from N-ethylpentedrone analogue, not pentedrone itself; neurotoxicity evidence is cell-line only (SH-SY5Y, PC12). Evidence discount applied — raw findings would suggest high, but all data is in vitro or analogue-extrapolated. No controlled human toxicity data exist for pentedrone. | ||
ReasoningReasoningClassified as moderate (acute and chronic): hepatotoxicity data is in vitro only (rat hepatocytes, HepaRG cells); severe intoxication case data derives from N-ethylpentedrone analogue, not pentedrone itself; neurotoxicity evidence is cell-line only (SH-SY5Y, PC12). Evidence discount applied — raw findings would suggest high, but all data is in vitro or analogue-extrapolated. No controlled human toxicity data exist for pentedrone. 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 | Conditioned place preference demonstrated for pentedrone itself (Duart-Castells et al. 2021). ΔFosB accumulation and withdrawal symptoms documented for N-ethylpentedrone analogue (Espinosa-Velasco et al. 2022). Compulsive redosing is a class-level behavioral concern for short-acting DAT blockers. Physical dependence rated low — withdrawal produces aggression and impaired social behavior in animal models but not life-threatening somatic symptoms. | ||
ReasoningReasoningConditioned place preference demonstrated for pentedrone itself (Duart-Castells et al. 2021). ΔFosB accumulation and withdrawal symptoms documented for N-ethylpentedrone analogue (Espinosa-Velasco et al. 2022). Compulsive redosing is a class-level behavioral concern for short-acting DAT blockers. Physical dependence rated low — withdrawal produces aggression and impaired social behavior in animal models but not life-threatening somatic symptoms. Evidence basis: animal_study | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | mild | mild | low |
| Symptoms | irritability, aggression, impaired social behavior, fatigue, elevated stress hormones, anhedonia, insomnia | irritability, aggression, impaired social behavior, fatigue, elevated stress hormones, anhedonia, insomnia | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | Withdrawal profile inferred from N-ethylpentedrone animal model (Espinosa-Velasco et al. 2022): increased aggression, impaired social exploration, elevated plasma corticosterone, striatal dopamine depletion. Notably, depressive-like symptoms were absent. Human withdrawal timecourse not published — values estimated from stimulant class. | ||
ReasoningReasoningWithdrawal profile inferred from N-ethylpentedrone animal model (Espinosa-Velasco et al. 2022): increased aggression, impaired social exploration, elevated plasma corticosterone, striatal dopamine depletion. Notably, depressive-like symptoms were absent. Human withdrawal timecourse not published — values estimated from stimulant class. 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 days | 10 days | low |
| Cross-tolerances | cocaine, amphetamine, methamphetamine, methylphenidate, other synthetic cathinones | cocaine, amphetamine, methamphetamine, methylphenidate, other synthetic cathinones | low |
| Editorial | Tolerance timecourse values from existing database (community consensus). Mechanism inferred from DAT-selective pharmacology. No published pentedrone-specific tolerance studies exist. Cross-tolerance list based on shared DAT blockade mechanism. | ||
ReasoningReasoningTolerance timecourse values from existing database (community consensus). Mechanism inferred from DAT-selective pharmacology. No published pentedrone-specific tolerance studies exist. Cross-tolerance list based on shared DAT blockade mechanism. Evidence basis: community_consensus_small | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| psychiatric bipolar disordertrace | relative | relative | medium |
| Editorial | Standard contraindication for dopaminergic stimulants. | ||
ReasoningReasoningStandard contraindication for dopaminergic stimulants. | |||
| neurological epilepsytrace | absolute | absolute | medium |
| Editorial | Class-level contraindication for CNS stimulants. | ||
ReasoningReasoningClass-level contraindication for CNS stimulants. | |||
| pregnancy breastfeeding pregnancy and breastfeedingtrace | absolute | absolute | high |
| Editorial | Standard absolute contraindication for all stimulants in pregnancy. | ||
ReasoningReasoningStandard absolute contraindication for all stimulants in pregnancy. | |||
| other MAOI usetrace | absolute | absolute | high |
| Editorial | Standard absolute contraindication for all monoamine reuptake inhibitors combined with MAOIs. | ||
ReasoningReasoningStandard absolute contraindication for all monoamine reuptake inhibitors combined with MAOIs. | |||
| psychiatric psychotic disorderstrace | relative | relative | medium |
| Editorial | Class-level contraindication for dopaminergic stimulants. Paranoid ideation documented in cathinone surveys and persecution delusions in N-ethylpentedrone case. | ||
ReasoningReasoningClass-level contraindication for dopaminergic stimulants. Paranoid ideation documented in cathinone surveys and persecution delusions in N-ethylpentedrone case. | |||
| cardiovascular hypertensiontrace | absolute | absolute | medium |
| Editorial | Class-level sympathomimetic mechanism. N-ethylpentedrone human studies documented blood pressure increases (Nuñez-Montero et al. 2025). Severe intoxication case showed tachycardia (Deville et al. 2023). | ||
ReasoningReasoningClass-level sympathomimetic mechanism. N-ethylpentedrone human studies documented blood pressure increases (Nuñez-Montero et al. 2025). Severe intoxication case showed tachycardia (Deville et al. 2023). | |||
| cardiovascular coronary artery diseasetrace | absolute | absolute | medium |
| Editorial | Standard contraindication for all sympathomimetic stimulants. | ||
ReasoningReasoningStandard contraindication for all sympathomimetic stimulants. | |||
| cardiovascular cardiac arrhythmiastrace | absolute | absolute | medium |
| Editorial | Class-level inference from stimulant pharmacology. | ||
ReasoningReasoningClass-level inference from stimulant pharmacology. | |||
| hepatic hepatic impairmenttrace | relative | relative | medium |
| Editorial | Direct pentedrone in vitro hepatotoxicity data from Valente et al. 2016. | ||
ReasoningReasoningDirect pentedrone in vitro hepatotoxicity data from Valente et al. 2016. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 900–1800 sec(i=0.05) | 900–1800 sec(i=0.05) | low |
| Editorial | Oral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | ||
ReasoningReasoningOral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | |||
| Come uptrace | 900–1800 sec(i=0.35) | 900–1800 sec(i=0.35) | low |
| Editorial | Oral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | ||
ReasoningReasoningOral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | |||
| Peaktrace | 3600–7200 sec(i=1.00) | 3600–7200 sec(i=1.00) | low |
| Editorial | Oral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | ||
ReasoningReasoningOral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | |||
| Resolutiontrace | 3600–7200 sec(i=0.30) | 3600–7200 sec(i=0.30) | low |
| Editorial | Oral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | ||
ReasoningReasoningOral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | |||
| Afterglowtrace | 3600–36000 sec(i=0.05) | 3600–36000 sec(i=0.05) | low |
| Editorial | Oral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | ||
ReasoningReasoningOral duration data derived from community consensus in the research brief (onset 15-30 min, peak 1-2 h, offset 1-2 h, aftereffects 1-10 h, total 2-6 h). No controlled human oral dosing studies for pentedrone exist. Values are plausible given the DAT/NET reuptake inhibitor mechanism and short-acting cathinone class profile. | |||
insufflated
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 300–600 sec(i=0.05) | 300–600 sec(i=0.05) | low |
| Editorial | Insufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | ||
ReasoningReasoningInsufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | |||
| Come uptrace | 300–900 sec(i=0.40) | 300–900 sec(i=0.40) | low |
| Editorial | Insufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | ||
ReasoningReasoningInsufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | |||
| Peaktrace | 1800–5400 sec(i=1.00) | 1800–5400 sec(i=1.00) | low |
| Editorial | Insufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | ||
ReasoningReasoningInsufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | |||
| Resolutiontrace | 1800–5400 sec(i=0.25) | 1800–5400 sec(i=0.25) | low |
| Editorial | Insufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | ||
ReasoningReasoningInsufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | |||
| Afterglowtrace | 3600–28800 sec(i=0.05) | 3600–28800 sec(i=0.05) | low |
| Editorial | Insufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | ||
ReasoningReasoningInsufflated duration data from community consensus in the research brief (onset 5-10 min, peak 30-90 min, offset 30-90 min, aftereffects 1-8 h, total 1-4 h). Supported by N-ethylpentedrone human observational data: onset within 20 minutes insufflated, return to baseline by 3-4 hours (Nuñez-Montero et al. 2025). No controlled pentedrone insufflated dosing studies exist. | |||
Dose Tier Summaries
At threshold doses, pentedrone produces barely perceptible stimulation — a mild lift in alertness and mood that could be mistaken for caffeine. Slight motivation enhancement and faint appetite suppression may be noticed. Effects are sub-euphoric and easily overlooked. Physically, minor increases in heart rate and very slight pupil dilation may occur. Sleep disruption is unlikely at this level, and functional impairment is negligible.
No controlled human dose data exist for pentedrone. Threshold estimated from community consensus for synthetic cathinone stimulants of similar potency class. All values require editorial verification.
ReasoningReasoning
No controlled human dose data exist for pentedrone. Threshold estimated from community consensus for synthetic cathinone stimulants of similar potency class. All values require editorial verification.
Evidence basis: community_consensus_small
At light doses, pentedrone produces noticeable stimulation with mild cognitive euphoria — a sense of increased mental clarity, thought acceleration, and motivation enhancement. Wakefulness is clearly elevated. Appetite suppression becomes apparent. Social effects may include increased talkativeness and confidence. Physically, heart rate increase becomes perceptible, along with slight vasoconstriction and mild jaw tension. Temperature may rise slightly. Sleep is difficult for several hours after dosing. The urge to redose may begin to emerge at this level.
Inferred from community cathinone reports and the DAT-selective NDRI mechanism profile. No controlled pentedrone dosing studies exist. Subjective character based on pharmacological analogy with cocaine/methylphenidate-class compounds.
ReasoningReasoning
Inferred from community cathinone reports and the DAT-selective NDRI mechanism profile. No controlled pentedrone dosing studies exist. Subjective character based on pharmacological analogy with cocaine/methylphenidate-class compounds.
Evidence basis: community_consensus_small
At common doses, pentedrone's full stimulant profile manifests: pronounced cognitive euphoria, strong motivation enhancement, thought acceleration, and marked wakefulness. Focus intensification can produce a driven, task-oriented state. Appetite suppression is strong. Entactogenic effects are notably absent — the experience is primarily dopaminergic rather than serotonergic. Cardiovascular effects become significant: elevated heart rate, increased blood pressure, and vasoconstriction. Jaw tension (bruxism), sweating, and mydriasis are typical. Body temperature rises modestly. The compulsive redosing urge is prominent at this range due to the short peak duration. Sleep is impossible for 2–4 hours after the last dose. Aftereffects include residual stimulation, irritability, and potential low mood as dopaminergic effects wane.
Based on community cathinone consensus, user survey data (Ashrafioun et al. 2016 — increased energy, rapid heartbeat, racing thoughts, insomnia, euphoria, decreased appetite), and the DAT/NET-selective NDRI mechanism. No controlled human dose-response data for pentedrone.
ReasoningReasoning
Based on community cathinone consensus, user survey data (Ashrafioun et al. 2016 — increased energy, rapid heartbeat, racing thoughts, insomnia, euphoria, decreased appetite), and the DAT/NET-selective NDRI mechanism. No controlled human dose-response data for pentedrone.
Evidence basis: community_consensus_small
At strong doses, stimulation becomes intense and potentially uncomfortable. Cognitive euphoria may transition to anxious overstimulation with racing thoughts, restlessness, and difficulty focusing. Paranoid ideation may begin to emerge. The compulsive redosing urge intensifies significantly. Cardiovascular strain is substantial: pronounced tachycardia, hypertension, and vasoconstriction. Bruxism, sweating, tremor, and mydriasis are prominent. Hyperthermia risk increases, particularly during physical activity or in warm environments. Appetite is completely suppressed. Sleep is impossible for 4–6 hours post-dose. The comedown is marked by irritability, dysphoria, and fatigue as dopamine depletion takes effect. Psychological distress risk escalates with repeated dosing at this level.
Inferred from cathinone class reports, user surveys, and pharmacological mechanism. Paranoid ideation at higher doses is documented in cathinone literature. Cardiovascular effects scaled from analogue and class data.
ReasoningReasoning
Inferred from cathinone class reports, user surveys, and pharmacological mechanism. Paranoid ideation at higher doses is documented in cathinone literature. Cardiovascular effects scaled from analogue and class data.
Evidence basis: community_consensus_small
At heavy doses, pentedrone produces severe sympathomimetic toxicity risk. Stimulation is extreme and dysphoric — anxiety, paranoia, agitation, and possible psychotic symptoms dominate the experience. Thought acceleration becomes uncontrollable racing thoughts. The compulsive redosing urge is overwhelming. Cardiovascular emergency risk is significant: severe tachycardia, dangerous hypertension, and hyperthermia. Rhabdomyolysis, metabolic acidosis, and renal failure have been documented in severe cathinone intoxications. Seizure threshold is lowered. The N-ethylpentedrone case report documents blood concentrations exceeding 2,000 ng/mL producing coma, organ failure, and near-fatal outcome requiring ICU admission. Sleep deprivation compounds toxicity across all organ systems. This dose range carries acute life-threatening risk.
Extrapolated from cathinone class toxicity data and the N-ethylpentedrone severe intoxication case (Deville et al. 2023). No controlled data define pentedrone's heavy dose threshold specifically. Safety-critical content — all values require editorial review.
ReasoningReasoning
Extrapolated from cathinone class toxicity data and the N-ethylpentedrone severe intoxication case (Deville et al. 2023). No controlled data define pentedrone's heavy dose threshold specifically. Safety-critical content — all values require editorial review.
Evidence basis: community_consensus_small
History
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.
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