Desoxypipradrol
Studies and references cited across this article, graded by evidence strength.
Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
oraltrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 0.25 mg | 0.25 mg | low |
| Low | 1–2 mg | 1–2 mg | low |
| Common | 2–6 mg | 2–6 mg | low |
| Strong | 6–8 mg | 6–8 mg | low |
| Heavy | 8+ mg | 8+ mg | low |
| Editorial | Existing DB values from community consensus. CRITICAL FLAG: Lelièvre et al. 2013 cites 10-20 mg as recreational oral doses — a significant discrepancy with these DB values (threshold 0.25 mg, heavy 8+ mg). DB values may reflect more cautious community dosing norms. Proposing existing DB values per evidence hierarchy but flagging for editorial review before publication. | ||
ReasoningReasoningExisting DB values from community consensus. CRITICAL FLAG: Lelièvre et al. 2013 cites 10-20 mg as recreational oral doses — a significant discrepancy with these DB values (threshold 0.25 mg, heavy 8+ mg). DB values may reflect more cautious community dosing norms. Proposing existing DB values per evidence hierarchy but flagging for editorial review before publication. Evidence basis: community_consensus_large | |||
insufflatedtrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 0.25 mg | 0.25 mg | low |
| Low | 0.5–1.5 mg | 0.5–1.5 mg | low |
| Common | 1.5–3.5 mg | 1.5–3.5 mg | low |
| Strong | 3.5–5 mg | 3.5–5 mg | low |
| Heavy | 5+ mg | 5+ mg | low |
| Editorial | Existing DB values from community consensus. No published insufflated-specific dose data. Insufflated doses are approximately 50-60% of oral doses, consistent with expected higher bioavailability via nasal mucosa. | ||
ReasoningReasoningExisting DB values from community consensus. No published insufflated-specific dose data. Insufflated doses are approximately 50-60% of oral doses, consistent with expected higher bioavailability via nasal mucosa. Evidence basis: community_consensus_large | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 1–4 hours | 1–4 hours | medium |
| Editorial | Existing DB value (1-4 hours). Consistent with case literature documenting slow, insidious onset and clinical presentations featuring delayed symptom emergence. | ||
ReasoningReasoningExisting DB value (1-4 hours). Consistent with case literature documenting slow, insidious onset and clinical presentations featuring delayed symptom emergence. Evidence basis: community_consensus_large | |||
| Peaktrace | 9–30 hours | 9–30 hours | medium |
| Editorial | Existing DB value (9-30 hours). Case literature supports multi-day peak periods — Edinburgh cluster and French case both document sustained symptom intensity over days. | ||
ReasoningReasoningExisting DB value (9-30 hours). Case literature supports multi-day peak periods — Edinburgh cluster and French case both document sustained symptom intensity over days. Evidence basis: community_consensus_large | |||
| Offsettrace | 6–40 hours | 6–40 hours | medium |
| Editorial | Existing DB value (6-40 hours). Wide range reflects extreme pharmacokinetic variability. French case showed symptoms persisting through day 7 after 250mg dose. | ||
ReasoningReasoningExisting DB value (6-40 hours). Wide range reflects extreme pharmacokinetic variability. French case showed symptoms persisting through day 7 after 250mg dose. Evidence basis: community_consensus_large | |||
| Totaltrace | 16–72 hours | 16–72 hours | medium |
| Editorial | Existing DB value (16-72 hours). Consistent with case reports showing multi-day effect courses. French case (250mg) showed 7-day course but that represents extreme overdose, not typical experience. | ||
ReasoningReasoningExisting DB value (16-72 hours). Consistent with case reports showing multi-day effect courses. French case (250mg) showed 7-day course but that represents extreme overdose, not typical experience. Evidence basis: community_consensus_large | |||
insufflated
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 15–240 minutes | 15–240 minutes | low |
| Editorial | Existing DB value (15-240 minutes). No published insufflated-specific data. Faster than oral but still slow by insufflated stimulant standards. | ||
ReasoningReasoningExisting DB value (15-240 minutes). No published insufflated-specific data. Faster than oral but still slow by insufflated stimulant standards. Evidence basis: community_consensus_large | |||
| Come uptrace | 2–6 hours | 2–6 hours | low |
| Editorial | Existing DB value (2-6 hours). No published insufflated-specific data; community consensus only. | ||
ReasoningReasoningExisting DB value (2-6 hours). No published insufflated-specific data; community consensus only. Evidence basis: community_consensus_large | |||
| Peaktrace | 6–30 hours | 6–30 hours | low |
| Editorial | Existing DB value (6-30 hours). No published insufflated-specific data. Peak duration expected to be similar to oral given the compound's long elimination. | ||
ReasoningReasoningExisting DB value (6-30 hours). No published insufflated-specific data. Peak duration expected to be similar to oral given the compound's long elimination. Evidence basis: community_consensus_large | |||
| Offsettrace | 6–40 hours | 6–40 hours | low |
| Editorial | Existing DB value (6-40 hours). No published insufflated-specific data; community consensus only. | ||
ReasoningReasoningExisting DB value (6-40 hours). No published insufflated-specific data; community consensus only. Evidence basis: community_consensus_large | |||
| Totaltrace | 10–72 hours | 10–72 hours | low |
| Editorial | Existing DB value (10-72 hours). No published insufflated-specific data. Slightly shorter minimum than oral due to faster onset, but maximum similar given long elimination. | ||
ReasoningReasoningExisting DB value (10-72 hours). No published insufflated-specific data. Slightly shorter minimum than oral due to faster onset, but maximum similar given long elimination. Evidence basis: community_consensus_large | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | high | high | medium |
| Chronic | moderate | moderate | medium |
| Organs Affected | musculoskeletal, renal, cardiovascular, neuropsychiatric | musculoskeletal, renal, cardiovascular, neuropsychiatric | medium |
| Editorial | Acute upgraded from DB seed 'moderate' to 'high' based on Edinburgh case series (Murray et al. 2012): 96% rhabdomyolysis (documented organ damage across multiple patients), 65% tachycardia, 50% hallucinations/psychosis persisting days. No LD50 data. Chronic is class inference from dopaminergic stimulants (cocaine, methamphetamine) — no substance-specific chronic studies exist, maintaining 'moderate' with evidence discount for structural analogy. | ||
ReasoningReasoningAcute upgraded from DB seed 'moderate' to 'high' based on Edinburgh case series (Murray et al. 2012): 96% rhabdomyolysis (documented organ damage across multiple patients), 65% tachycardia, 50% hallucinations/psychosis persisting days. No LD50 data. Chronic is class inference from dopaminergic stimulants (cocaine, methamphetamine) — no substance-specific chronic studies exist, maintaining 'moderate' with evidence discount for structural analogy. Evidence basis: published_case_series | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | moderate | moderate | medium |
| Psychological | high | high | medium |
| Compulsive Redosing | high | high | medium |
| Dose Escalation | moderate | moderate | medium |
| Editorial | Rodent behavioural data (CPP + IVSA in mice, Cha et al. 2019) confirms reinforcing properties. Pharmacological profiling (Simmler et al. 2014) predicts high abuse liability from selective DAT/NET inhibition + absent TAAR1. Physical dependence moderate by class inference (no human dependence data). Psychological upgraded to high based on converging pharmacological and behavioural evidence. | ||
ReasoningReasoningRodent behavioural data (CPP + IVSA in mice, Cha et al. 2019) confirms reinforcing properties. Pharmacological profiling (Simmler et al. 2014) predicts high abuse liability from selective DAT/NET inhibition + absent TAAR1. Physical dependence moderate by class inference (no human dependence data). Psychological upgraded to high based on converging pharmacological and behavioural evidence. Evidence basis: animal_study | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | moderate | moderate | low |
| Symptoms | dysphoria, fatigue, hypersomnia, anhedonia, depression, increased appetite | dysphoria, fatigue, hypersomnia, anhedonia, depression, increased appetite | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | Class inference from dopaminergic stimulant withdrawal (cocaine, amphetamine). No substance-specific withdrawal data. Onset delayed (possibly 24-72h+) due to extremely long duration of action. Severity and symptoms are standard dopaminergic stimulant crash predictions. | ||
ReasoningReasoningClass inference from dopaminergic stimulant withdrawal (cocaine, amphetamine). No substance-specific withdrawal data. Onset delayed (possibly 24-72h+) due to extremely long duration of action. Severity and symptoms are standard dopaminergic stimulant crash predictions. 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 | cocaine, methylphenidate, amphetamine | cocaine, methylphenidate, amphetamine | low |
| Editorial | No substance-specific tolerance data exist. DB seed values (buildup with repeated use, 5-day half-life, 1.5-week reset) are unverified community consensus. Cross-tolerances inferred from shared DAT/NET mechanism with cocaine, methylphenidate, amphetamine. Proposing existing DB values with confidence=low per work-notes instruction. | ||
ReasoningReasoningNo substance-specific tolerance data exist. DB seed values (buildup with repeated use, 5-day half-life, 1.5-week reset) are unverified community consensus. Cross-tolerances inferred from shared DAT/NET mechanism with cocaine, methylphenidate, amphetamine. Proposing existing DB values with confidence=low per work-notes instruction. Evidence basis: community_consensus_large | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| cardiovascular Cardiovascular diseasetrace | absolute | absolute | medium |
| Editorial | Direct case series evidence (Murray et al. 2012) documents 65% tachycardia rate. Pharmacological mechanism (NET/DAT blockade) predicts sustained cardiovascular stimulation. | ||
ReasoningReasoningDirect case series evidence (Murray et al. 2012) documents 65% tachycardia rate. Pharmacological mechanism (NET/DAT blockade) predicts sustained cardiovascular stimulation. | |||
| psychiatric Psychotic spectrum disorderstrace | absolute | absolute | high |
| Editorial | Edinburgh case series (Murray et al. 2012) documents 50% hallucination rate and multi-day psychosis. Direct clinical evidence, not class inference. | ||
ReasoningReasoningEdinburgh case series (Murray et al. 2012) documents 50% hallucination rate and multi-day psychosis. Direct clinical evidence, not class inference. | |||
| neurological Seizure disorderstrace | relative | relative | low |
| Editorial | Class-level inference from dopaminergic stimulant pharmacology (reference compounds: cocaine, amphetamine). No substance-specific seizure data published. | ||
ReasoningReasoningClass-level inference from dopaminergic stimulant pharmacology (reference compounds: cocaine, amphetamine). No substance-specific seizure data published. | |||
| renal Renal impairmenttrace | relative | relative | medium |
| Editorial | Edinburgh case series documents 96% rhabdomyolysis rate. Renal impairment compounds this specific, well-documented toxicity pathway. | ||
ReasoningReasoningEdinburgh case series documents 96% rhabdomyolysis rate. Renal impairment compounds this specific, well-documented toxicity pathway. | |||
| other MAOI usetrace | absolute | absolute | medium |
| Editorial | Class-level mechanism inference from cocaine and methylphenidate MAOI interactions. No substance-specific data. Well-established pharmacological principle for catecholamine reuptake inhibitors. | ||
ReasoningReasoningClass-level mechanism inference from cocaine and methylphenidate MAOI interactions. No substance-specific data. Well-established pharmacological principle for catecholamine reuptake inhibitors. | |||
| pregnancy breastfeeding Pregnancy and lactationtrace | absolute | absolute | low |
| Editorial | Class-level inference from dopaminergic stimulant reproductive risks (reference compounds: cocaine, amphetamine). No substance-specific reproductive data published. | ||
ReasoningReasoningClass-level inference from dopaminergic stimulant reproductive risks (reference compounds: cocaine, amphetamine). No substance-specific reproductive data published. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Come uptrace | 7200–14400 sec(i=0.40) | 7200–14400 sec(i=0.40) | medium |
| Editorial | Oral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. | ||
ReasoningReasoningOral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. Evidence basis: community_consensus_large | |||
| Peaktrace | 21600–86400 sec(i=1.00) | 21600–86400 sec(i=1.00) | medium |
| Editorial | Oral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. | ||
ReasoningReasoningOral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. Evidence basis: community_consensus_large | |||
| Plateautrace | 21600–86400 sec(i=0.70) | 21600–86400 sec(i=0.70) | medium |
| Editorial | Oral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. | ||
ReasoningReasoningOral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. Evidence basis: community_consensus_large | |||
| Resolutiontrace | 21600–86400 sec(i=0.30) | 21600–86400 sec(i=0.30) | medium |
| Editorial | Oral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. | ||
ReasoningReasoningOral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. Evidence basis: community_consensus_large | |||
| Afterglowtrace | 43200–172800 sec(i=0.15) | 43200–172800 sec(i=0.15) | medium |
| Editorial | Oral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. | ||
ReasoningReasoningOral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. Evidence basis: community_consensus_large | |||
| Onsettrace | 3600–14400 sec(i=0.15) | 3600–14400 sec(i=0.15) | medium |
| Editorial | Oral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. | ||
ReasoningReasoningOral timeline derived from DB seed durations (onset 1-4h, peak 9-30h, offset 6-40h, total 16-72h) cross-referenced with case literature: Edinburgh cluster documented multi-day presentations (Murray et al. 2012), French case showed 7-day symptom course after 250mg (Lelièvre et al. 2013). Phase durations reflect extreme variability inherent to this substance's pharmacokinetics. Afterglow advisory from work-notes. Evidence basis: community_consensus_large | |||
insufflated
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 900–14400 sec(i=0.20) | 900–14400 sec(i=0.20) | low |
| Editorial | Insufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. | ||
ReasoningReasoningInsufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. Evidence basis: community_consensus_large | |||
| Come uptrace | 7200–21600 sec(i=0.45) | 7200–21600 sec(i=0.45) | low |
| Editorial | Insufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. | ||
ReasoningReasoningInsufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. Evidence basis: community_consensus_large | |||
| Peaktrace | 21600–86400 sec(i=1.00) | 21600–86400 sec(i=1.00) | low |
| Editorial | Insufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. | ||
ReasoningReasoningInsufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. Evidence basis: community_consensus_large | |||
| Plateautrace | 21600–86400 sec(i=0.70) | 21600–86400 sec(i=0.70) | low |
| Editorial | Insufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. | ||
ReasoningReasoningInsufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. Evidence basis: community_consensus_large | |||
| Resolutiontrace | 21600–86400 sec(i=0.30) | 21600–86400 sec(i=0.30) | low |
| Editorial | Insufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. | ||
ReasoningReasoningInsufflated timeline derived from DB seed durations (onset 15-240min, come_up 2-6h, peak 6-30h, offset 6-40h, total 10-72h). No published insufflated-specific duration data; community consensus only. Phase structure similar to oral with faster onset. Work-notes specify confidence=low for insufflated data. Evidence basis: community_consensus_large | |||
Dose Tier Summaries
Barely perceptible stimulation emerges as a mild increase in alertness and wakefulness without significant euphoria or sympathomimetic effects. Mental state may shift subtly toward increased attentiveness, but changes remain ambiguous and difficult to distinguish from placebo or natural arousal fluctuations. Physical effects are minimal — slight elevation in baseline energy with no meaningful appetite suppression, heart rate change, or body load. The compound's extremely slow onset (1–4 hours oral) means threshold effects may not become apparent for several hours after ingestion. Given the insidious onset, the temptation to redose before effects manifest is a critical danger at this level. Wait at least 4 hours before concluding a dose was sub-threshold.
Work-notes outline for threshold tier. No published threshold-specific data; constructed from pharmacological profile (selective DAT/NET inhibition) and community consensus dose ranges. Confidence low due to absence of controlled dose-response data.
ReasoningReasoning
Work-notes outline for threshold tier. No published threshold-specific data; constructed from pharmacological profile (selective DAT/NET inhibition) and community consensus dose ranges. Confidence low due to absence of controlled dose-response data.
Evidence basis: community_consensus_large
Noticeable stimulation with clearly increased wakefulness and a gentle sharpening of focus and motivation. Thought acceleration becomes apparent, and tasks may feel more engaging. Mild appetite suppression sets in. Cognitive effects are generally positive — enhanced analysis and information processing without significant restlessness or anxiety. Physical effects include mild sympathomimetic signs: a slight increase in heart rate, subtle vasoconstriction, and early appetite suppression. Duration is already extended at this level, likely exceeding 12 hours from a single oral dose. Sleep will be difficult for 12–24 hours. Plan accordingly — this is not a substance that permits casual evening use at any active dose.
Work-notes outline for light tier. Effects extrapolated from pharmacological profile (DAT/NET inhibition producing stimulation, focus, appetite suppression) and community dose consensus. No published dose-specific subjective data at this level.
ReasoningReasoning
Work-notes outline for light tier. Effects extrapolated from pharmacological profile (DAT/NET inhibition producing stimulation, focus, appetite suppression) and community dose consensus. No published dose-specific subjective data at this level.
Evidence basis: community_consensus_large
Pronounced, sustained stimulation with forceful wakefulness lasting 24 hours or longer from a single dose. Focus enhancement and motivation are prominent in the early phase, accompanied by significant thought acceleration and appetite suppression. Cognitive effects shift over time — initial clarity and thought organization give way to restlessness and emerging irritability as the experience extends past 12 hours. Sympathomimetic activation is significant: tachycardia, vasoconstriction, bruxism, and excessive sweating are expected. Spontaneous body sensations and dehydration sensation are common. The risk of compulsive redosing increases as users seek to recapture early-phase cognitive clarity. Insomnia is near-certain for 24–48 hours. Appetite suppression is pronounced. The extremely slow onset (1–4 hours oral) makes redosing before effects fully manifest a critical danger — cumulative dosing is the primary overdose pathway documented in case literature.
Work-notes outline for common tier. Edinburgh case series (Murray et al. 2012) documents tachycardia (65%), agitation (62%), and multi-day presentations at intoxicating doses. Community consensus provides dose range. Duration and effect character supported by case literature.
ReasoningReasoning
Work-notes outline for common tier. Edinburgh case series (Murray et al. 2012) documents tachycardia (65%), agitation (62%), and multi-day presentations at intoxicating doses. Community consensus provides dose range. Duration and effect character supported by case literature.
Evidence basis: community_consensus_large
Intense, prolonged stimulation persisting 36–72 hours. The early phase may feature heightened focus and cognitive euphoria, but these give way within hours to agitation, paranoia, and perceptual disturbances. Thought disorganization replaces thought acceleration as sleep deprivation compounds pharmacological effects. Hallucinations — both auditory and visual — emerge in a significant proportion of users at this dose level. Sympathomimetic load is substantial: tachycardia, hypertension, vasoconstriction, and excessive sweating. Rhabdomyolysis risk increases markedly — the Edinburgh case series documented 96% incidence at intoxicating doses. Muscle tension, trembling, and dystonia may occur. Bruxism is pronounced. Psychiatric symptoms are likely: paranoia, mania, and delirium may develop and persist for days after last use. This dose level approaches medical emergency territory. Sleep is impossible for 2–3 days.
Work-notes outline for strong tier. Edinburgh case series provides direct clinical data for presentations at intoxicating doses: 96% rhabdomyolysis, 50% hallucinations, 65% tachycardia, 21% paranoia (Murray et al. 2012). Multi-day psychiatric symptoms documented.
ReasoningReasoning
Work-notes outline for strong tier. Edinburgh case series provides direct clinical data for presentations at intoxicating doses: 96% rhabdomyolysis, 50% hallucinations, 65% tachycardia, 21% paranoia (Murray et al. 2012). Multi-day psychiatric symptoms documented.
Evidence basis: published_case_series
Multi-day stimulant crisis requiring medical attention. Psychosis with frank hallucinations and delirium is probable. Paranoid delusions, incoherent speech, and complete cognitive disorganization characterize the mental state. The distinction between pharmacological effects and sleep-deprivation psychosis becomes impossible after 48+ hours of forced wakefulness. Rhabdomyolysis is near-certain based on case data — the Edinburgh cluster documented 96% incidence. Acute kidney injury secondary to myoglobin release is a serious risk. Cardiovascular stress is severe and sustained: tachycardia, hypertension, and tachypnoea. The French overdose case (250 mg) documented active plasma concentrations at day 4 and a 7-day symptom course. This dose level constitutes a medical emergency. Effects persist 3–7 days. Hospitalization with psychiatric observation, renal monitoring, and supportive care (benzodiazepines, IV hydration) is typically required.
Work-notes outline for heavy tier. French overdose case (Lelièvre et al. 2013, 250 mg) and Edinburgh cluster (Murray et al. 2012) provide direct clinical data for severe presentations. 96% rhabdomyolysis, 50% hallucinations, 7-day symptom course documented.
ReasoningReasoning
Work-notes outline for heavy tier. French overdose case (Lelièvre et al. 2013, 250 mg) and Edinburgh cluster (Murray et al. 2012) provide direct clinical data for severe presentations. 96% rhabdomyolysis, 50% hallucinations, 7-day symptom course documented.
Evidence basis: published_case_series
History
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
- [1]moderate2-DPMP (desoxypipradrol, 2-benzhydrylpiperidine, 2-phenylmethylpiperidine) and D2PM (diphenyl-2-pyrrolidin-2-yl-methanol, diphenylprolinol): A preliminary reviewCorkery JM, Elliott S, Schifano F, Corazza O, Ghodse AH · 2012 · Progress in Neuro-Psychopharmacology & Biological Psychiatry
- [2]moderatePharmacological profiles of aminoindanes, piperazines, and pipradrol derivatives.Simmler LD, Rickli A, Schramm Y, Hoener MC, Liechti ME · 2014 · Biochemical Pharmacology
- [3]moderateDesoxypipradrol is more potent than cocaine on evoked dopamine efflux in the nucleus accumbensDavidson C, Ramsey J · 2012 · Journal of Psychopharmacology
- [4]moderate'Ivory wave' toxicity in recreational drug users; integration of clinical and poisons information services to manage legal high poisoningMurray DB, Potts S, Haxton C, Jackson G, Sandilands EA, Ramsey J, Puchnarewicz M, Holt DW, Johnston A, Bateman DN, Dear JW · 2012 · Clinical Toxicologydoi.org/10.3109/15563650.2011.647992pubmed 2222493315 claims checked13 verified1 partial1 inconclusive
- [5]moderateRewarding effects of 2-desoxypipradrol in miceCha HJ, Kim JM, Kim YH, Suh SK · 2019 · Neuroscience Letters
- [6]weak
- [7]weak
- [8]weak
- [9]moderateDesigner psychostimulants: pharmacology and differencesIversen L, White M, Treble R · 2014 · Neuropharmacology
- [10]moderateNovel psychoactive substances (designer drugs): overview and pharmacology of modulators of monoamine signalingLiechti ME · 2015 · Swiss Medical Weekly
- [11]weak
- [12]moderateThe Role of Dopamine in the Stimulant Characteristics of Novel Psychoactive Substances (NPS)-Neurobiological and Computational Assessment Using the Case of Desoxypipradrol (2-DPMP)Loi B, Sahai MA, De Luca MA, Shiref H, Opacka-Juffry J · 2020 · Frontiers in Pharmacology
- [13]moderateInteraction of cocaine-, benztropine-, and GBR12909-like compounds with wild-type and mutant human dopamine transporters: molecular features that differentially determine antagonist-binding propertiesSchmitt KC, Zhen J, Kharkar P, Mishra M, Chen N, Dutta AK, Reith ME · 2008 · Journal of Neurochemistry
- [14]weakLe désoxypipradrol, une nouvelle drogue disponible sur Internet : à propos d'un casLelièvre B, Férec S, Boels D, Bennaceur M, Harry P, Abbara C, Diquet B, Turcant A · 2013 · Annales de Toxicologie Analytiquedoi.org/10.1051/ata/20130409 claims checked9 verified
- [15]moderatePrevalence and blood concentrations of desoxypipradrol (2-DPMP) in drivers suspected of driving under the influence of drugs and in post-mortem casesKriikku P, Wilhelm L, Rintatalo J, Hurme J, Kramer J, Ojanperä I · 2013 · Forensic Science International
- [16]moderateThe prevalence of new psychoactive substances in biological material - a three-year review of casework in Poland.Adamowicz P, Gieroń J, Gil D, Lechowicz W, Skulska A, Tokarczyk B · 2016 · Drug Testing and Analysis
- [17]weakNew synthetic opioid cyclopropylfentanyl together with other novel synthetic opioids in respiratory insufficient comatose patients.Müller D, Neurath H, Neukamm MA et al. · 2019 · Clinical toxicology
- [18]weak[Desoxypipradrol - a new (already well known) designer drug]Müller D, Angerer V, Kithinji J, Auwärter V, Neurath H, Liebetrau G, Just S, Hermanns-Clausen M · 2016 · Deutsche Medizinische Wochenschriftdoi.org/10.1055/s-0042-107537pubmed 273593144 claims checked1 verified1 partial1 inconclusive1 not supported
Claim Verification
Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.
summary8 claims6verified2inconclusive
inconclusiveIt is distinguished from most stimulants by its extraordinary duration of action — total effect durations of 16–72 hours are consistently reported — a property attributed to high lipophilicity and the absence of easily metabolized polar functional groups[1]model confidence 85%
The abstract covers only discovery history, 1950s pharmaceutical origins, recreational use timeline, UK scheduling, and first reported deaths. It contains no information about duration of action, lipophilicity, or metabolic stability. This pharmacokinetic claim cannot be verified from the abstract.
Originally developed in 1950s for narcolepsy and ADHD. Little scientific literature on pharmacology, toxicology.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIt was patented in 1958 as a candidate treatment for narcolepsy but abandoned after methylphenidate proved more clinically manageable[1]model confidence 80%
The abstract confirms 1950s development for narcolepsy/ADHD, which is consistent with the claim, but does not confirm the specific year 1958 for the patent or that the reason for abandonment was methylphenidate's clinical manageability. These specific details cannot be verified from the abstract.
Originally developed in 1950s for narcolepsy and ADHD.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn transfected human cell assays, desoxypipradrol is equipotent to methylphenidate at the dopamine and norepinephrine transporters and approximately 10-fold more potent than cocaine at the dopamine transporter, with no measurable affinity at serotonin transporters, monoaminergic receptors, or trace amine-associated receptor 1 (TAAR1)[2]model confidence 95%
All key pharmacological comparisons directly confirmed: equipotent to methylphenidate at DAT/NET, 10-fold more potent than cocaine at DAT, and no serotonergic activity or TAAR1 binding.
2-DPMP was an equally potent DAT/NET inhibitor compared to methylphenidate. 2-DPMP was a 10-fold more potent DAT blocker than cocaine. None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedEx vivo voltammetry in rat nucleus accumbens demonstrates a 7-fold increase in peak dopamine efflux and a 15-fold prolongation of dopamine reuptake half-life at 10 µM — substantially exceeding cocaine at the same concentration.[3]model confidence 98%
All figures exactly match: sevenfold increase in peak dopamine (vs threefold for cocaine), 15-fold increase in reuptake half-life (vs fivefold for cocaine), at 10 µM. Substantially exceeds cocaine in both measures.
Desoxypipradrol caused sevenfold increase in peak dopamine levels (vs threefold for cocaine) and increased dopamine re-uptake half-life 15-fold (vs fivefold for cocaine) at 10 µM.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe subjective experience is dominated by intense, sustained stimulation with pronounced wakefulness, appetite suppression, and — at higher doses or with prolonged use — agitation, paranoia, hallucinations, and frank psychosis persisting for days[4]model confidence 88%
The abstract confirms agitation (62%), hallucinations (50%), insomnia (consistent with wakefulness), paranoia (21%), and prolonged psychiatric symptoms as a key feature. Appetite suppression is not explicitly mentioned but is a typical stimulant feature not captured in an ED case series.
agitation (62%), hallucinations (50%), insomnia (32%), paranoia (21%). Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRhabdomyolysis occurred in 96% of a 34-patient emergency department case series, representing the most distinctive acute toxicity finding[4]model confidence 92%
The 96% rhabdomyolysis rate in 34 patients is directly confirmed and is numerically the highest rate of any documented finding, making it the most distinctive acute toxicity finding by frequency.
rhabdomyolysis (96%)... 34 emergency attendances in Edinburgh due to 'ivory wave' toxicity.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRodent models confirm reinforcing properties consistent with high abuse liability, and the pharmacological profile — selective DAT/NET inhibition without TAAR1 agonism — predicts dependence risk exceeding that of cocaine[5]model confidence 88%
The abstract directly confirms reinforcing properties via CPP and self-administration paradigms in mice, consistent with high abuse liability. The pharmacological profile portion is supported by the separate citation [3].
At 1 mg/kg i.p., mice showed significant preference in drug-paired compartment in CPP. At 0.1 mg/kg/infusion i.v., significantly higher active lever responses in SA test.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRodent models confirm reinforcing properties consistent with high abuse liability, and the pharmacological profile — selective DAT/NET inhibition without TAAR1 agonism — predicts dependence risk exceeding that of cocaine[2]model confidence 90%
The abstract confirms selective DAT/NET inhibition without TAAR1 activity, and explicitly states the pharmacological profile predicts high abuse liability. 10-fold greater potency than cocaine at DAT supports exceeding cocaine's dependence risk.
Pharmacological profile predicts high abuse liability. 2-DPMP was a 10-fold more potent DAT blocker than cocaine. None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
history8 claims2verified1partial5inconclusive
verifiedThree deaths involving 2-DPMP were reported in the UK in August 2010, believed to be the first fatalities attributable to this compound[1]model confidence 97%
Directly confirmed: 'First three deaths involving 2-DPMP in August 2010.' The word 'first' in the abstract confirms these were the first fatalities.
First three deaths involving 2-DPMP in August 2010.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe same research program produced pipradrol (marketed as Meratran, patented 1953) and subsequently methylphenidate (marketed as Ritalin), both structurally related piperidine compounds[1]model confidence 70%
The abstract confirms 1950s pharmaceutical development for narcolepsy/ADHD, consistent with the historical context, but does not specifically mention pipradrol, Meratran, methylphenidate, Ritalin, or CIBA's program. These details may be in the full paper.
Originally developed in 1950s for narcolepsy and ADHD.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveHowever, methylphenidate's shorter duration of action and more predictable pharmacokinetics proved superior for clinical use, and desoxypipradrol was dropped from development without advancing to human trials.[1]model confidence 65%
The abstract confirms 1950s development but says nothing about methylphenidate's superior pharmacokinetics, desoxypipradrol being dropped, or it failing to advance to human trials. These details would be in the full review.
Originally developed in 1950s for narcolepsy and ADHD.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveWhen pipradrol was scheduled in many countries during the late 1970s due to abuse potential, any residual commercial interest in desoxypipradrol effectively ceased.[1]model confidence 65%
The abstract covers UK scheduling in 2011–2012 and does not mention pipradrol's scheduling in the 1970s or its effect on commercial interest in desoxypipradrol.
UK importation ban November 2011, Class C from 13 June 2012.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe compound was sold predominantly under the brand name "Ivory Wave" — a product name that had previously been associated with mephedrone-containing preparations, causing substantial confusion about the active ingredient in circulation.[1]model confidence 65%
The abstract does not mention the Ivory Wave brand name, prior mephedrone association, or any confusion about active ingredients.
Recreational use started March 2007, UK popularity grew 2009, surged summer 2010.
checked by claude-sonnet-4-6 · May 11, 2026
partialThe compound was sold predominantly under the brand name "Ivory Wave" — a product name that had previously been associated with mephedrone-containing preparations, causing substantial confusion about the active ingredient in circulation.[4]model confidence 80%
The abstract confirms 'Ivory Wave' powder contained desoxypipradrol, confirming the brand association. However, the claim that Ivory Wave was 'previously associated with mephedrone-containing preparations' causing 'substantial confusion' is not mentioned in the abstract.
'Ivory wave' powder found to contain desoxypipradrol.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe clinical presentations were notable for their severity and duration: rhabdomyolysis in 96% of cases, tachycardia in 65%, hallucinations in 50%, and psychiatric symptoms persisting for several days.[4]model confidence 99%
All statistics directly confirmed: rhabdomyolysis 96%, tachycardia 65%, hallucinations 50%, and prolonged psychiatric symptoms as a key feature.
tachycardia (65%)... rhabdomyolysis (96%)... hallucinations (50%)... Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveOn 4 November 2010, the UK Home Office announced a ban on importation of 2-DPMP, with the formal ban taking effect in November 2011[1]model confidence 72%
The abstract confirms 'UK importation ban November 2011' but does not mention the specific announcement date of 4 November 2010. The distinction between announcement date and effective date cannot be verified from the abstract.
UK importation ban November 2011.
checked by claude-sonnet-4-6 · May 11, 2026
chemistry2 claims2inconclusive
inconclusiveDesoxypipradrol is the dehydroxylated analogue of pipradrol (which bears a tertiary hydroxyl at the benzhydryl carbon) and a close structural relative of methylphenidate (methyl α-phenyl-2-piperidineacetate), all three arising from CIBA's 1950s piperidine research program.[1]model confidence 65%
The abstract only confirms 1950s pharmaceutical development. The specific structural chemistry (dehydroxylated analogue of pipradrol, CIBA program) is not in the abstract.
Originally developed in 1950s for narcolepsy and ADHD.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveWithin novel psychoactive substance (NPS) taxonomy, desoxypipradrol is classified alongside pipradrol derivatives and — on a functional pharmacological basis — alongside pyrovalerone cathinones (e.g., MDPV) as a selective catecholamine reuptake inhibitor, though the two classes are structurally distinct.[9]model confidence 68%
The abstract confirms desoxypipradrol as a 'principal DA-activating stimulant' but does not mention MDPV, pyrovalerone cathinones, or a shared classification with them as selective catecholamine reuptake inhibitors.
Desoxypipradrol classified as principal DA-activating stimulant (amphetamine-like).
checked by claude-sonnet-4-6 · May 11, 2026
pharmacology12 claims9verified3inconclusive
verifiedMolecular dynamics simulations confirm that desoxypipradrol induces an outward-facing DAT conformation consistent with a cocaine-type inhibitor mechanism[12]model confidence 98%
Directly and precisely confirmed by the abstract.
Molecular dynamics simulations show 2-DPMP leads to outward-facing DAT conformation (cocaine-type effect).
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDesoxypipradrol is a potent and selective catecholamine reuptake inhibitor — specifically a blocker of the dopamine transporter (DAT) and norepinephrine transporter (NET) with no meaningful serotonin transporter (SERT) activity and no monoamine-releasing (substrate) properties[2]model confidence 97%
Directly confirmed: potent selective catecholamine transporter blocker, no substrate releasing properties, no serotonergic activity.
2-DPMP and D2PM were potent and selective catecholamine transporter blockers without substrate releasing properties... None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThis mechanism is cocaine-like rather than amphetamine-like: the compound stabilizes the transporter in an outward-facing conformation (blocking reuptake) rather than inducing transporter reversal (promoting release).[12]model confidence 97%
Directly confirmed by molecular dynamics simulations showing outward-facing DAT conformation, described as a 'cocaine-type effect.'
Molecular dynamics simulations show 2-DPMP leads to outward-facing DAT conformation (cocaine-type effect).
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn HEK293 cells expressing human DAT, NET, and SERT, desoxypipradrol is equipotent to methylphenidate at DAT and NET, approximately 10-fold more potent than cocaine at DAT, and displays no inhibition of SERT[2]model confidence 92%
Core pharmacological data confirmed: equipotent to methylphenidate at DAT/NET, 10-fold more potent than cocaine at DAT, no serotonergic activity. The HEK293 cell type is a methodological detail not in the abstract but consistent with the paper's in vitro scope.
2-DPMP was an equally potent DAT/NET inhibitor compared to methylphenidate. 2-DPMP was a 10-fold more potent DAT blocker than cocaine. None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe compound shows no measurable affinity at serotonin receptors (5-HT₁A, 5-HT₂A, 5-HT₂C), adrenergic receptors (α₁A, α₂A), dopamine receptors (D₁₋₃), histamine H₁ receptors, or trace amine-associated receptor 1 (TAAR1)[2]model confidence 75%
The abstract confirms absence of serotonergic activity and TAAR1 binding, but does not enumerate the specific receptor subtypes (5-HT₁A, 5-HT₂A, 5-HT₂C, α₁A, α₂A, D₁₋₃, H₁) individually. The full receptor panel likely appears in the paper's methods/results, not the abstract.
None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe absence of TAAR1 agonism is pharmacologically significant: TAAR1 activation is associated with reduced dopaminergic neurotransmission and lower abuse potential, and its absence in desoxypipradrol's profile predicts elevated abuse liability relative to compounds with partial TAAR1 activity.[2]model confidence 85%
The abstract confirms TAAR1 absence and explicitly predicts high abuse liability as a consequence of the pharmacological profile. The mechanistic link (TAAR1 as brake on dopaminergic drive) is a well-established inference supportable from the data presented.
None lacked serotonergic activity and TAAR1 binding. Pharmacological profile predicts high abuse liability.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThis was further supported by mutant DAT studies: 2-benzhydrylpiperidine derivatives display a cocaine-like binding profile at DAT mutants W84L and D313N, which discriminate between cocaine-type and benztropine-type inhibitors.[13]model confidence 75%
The abstract confirms 2-benzhydrylpiperidine derivatives show a cocaine-like binding profile with respect to DAT mutation, but does not name the specific mutants W84L and D313N. The specific mutant identities are in the full paper, not the abstract.
Derivatives of desoxypipradrol (2-benzhydrylpiperidine) exhibited a cocaine-like binding profile with respect to DAT mutation.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedA French case report documented plasma concentrations following ingestion of approximately 250 mg (a massive overdose): plasma levels were 136 µg/L at day 3 post-ingestion and 93 µg/L at day 4, with urine concentration of 4,805 µg/L at day 4[14]model confidence 99%
All values exactly confirmed: 250 mg ingestion, 136 µg/L at day 3 (admission), 93 µg/L at day 4, urine 4805 µg/L at day 4.
32-year-old man consumed 250 mg desoxypipradrol... Plasma concentration: 136 μg/L at admission (day 3), 93 μg/L at day 4; urine concentration 4805 μg/L at day 4.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusivePost-mortem cases showed higher concentrations.[15]model confidence 70%
The abstract provides a median serum concentration for DUID drivers (0.073 mg/L) and mentions 5 autopsy cases, but does not provide concentration data for post-mortem cases to enable a comparison. Whether post-mortem concentrations were higher cannot be determined from the abstract alone.
Median serum concentration 0.073 mg/L (range 0.006-0.890 mg/L). Found in 5 autopsy cases (0.05%), thought to contribute to death in 2.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedClinical presentations consistently feature multi-day symptom courses: the Edinburgh case series documented psychiatric symptoms lasting several days, and the French case report documented a 7-day symptom course after a single large dose.[4]model confidence 90%
The Edinburgh portion is directly confirmed: prolonged psychiatric symptoms are described as a key feature. The French case report 7-day course is covered by citation [13].
Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedClinical presentations consistently feature multi-day symptom courses: the Edinburgh case series documented psychiatric symptoms lasting several days, and the French case report documented a 7-day symptom course after a single large dose.[14]model confidence 97%
The French case report 7-day symptom course after 250 mg ingestion is directly confirmed.
Symptoms lasted 7 days.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe presence of detectable plasma concentrations at day 3–4 post-ingestion in the French case is consistent with a long elimination half-life, but formal characterization is absent.[14]model confidence 92%
Detectable plasma concentrations at day 3 (136 µg/L) and day 4 (93 µg/L) are confirmed. Formal pharmacokinetic characterization (half-life calculation, PK modeling) is not in the abstract, supporting the claim that it is absent.
Plasma concentration: 136 μg/L at admission (day 3), 93 μg/L at day 4.
checked by claude-sonnet-4-6 · May 11, 2026
receptor pharmacology5 claims5verified
verifiedThe compound functions as a pure reuptake inhibitor at both targets — it blocks substrate translocation without serving as a transporter substrate itself, distinguishing it mechanistically from amphetamine-class releasers.[2]model confidence 97%
Directly confirmed: 'potent and selective catecholamine transporter blockers without substrate releasing properties' explicitly distinguishes blocker from releaser/substrate mechanism.
2-DPMP and D2PM were potent and selective catecholamine transporter blockers without substrate releasing properties.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn rat striatal tissue measured by quantitative autoradiography using [¹²⁵I]RTI-121 (a selective DAT radioligand), the following IC₅₀ values were obtained:[12]model confidence 85%
IC50 values in rat striatum are confirmed: 5.65×10⁻⁷ M (accumbens shell) and 6.21×10⁻⁷ M (dorsal striatum). The specific radioligand ([¹²⁵I]RTI-121) and 'quantitative autoradiography' method are not in the abstract but the IC50 data is confirmed.
IC50 values for 2-DPMP at rat striatum DAT: 5.65×10⁻⁷ M (accumbens shell) and 6.21×10⁻⁷ M (dorsal striatum).
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDesoxypipradrol has no meaningful affinity at the following targets (tested in HEK293 cells):[2]model confidence 88%
The abstract confirms lack of serotonergic activity and TAAR1 binding, and is a paper on pharmacological profiles. The statement that no meaningful affinity was found at non-catecholamine targets is supported; the HEK293 cell detail is not in the abstract but consistent with in vitro scope.
None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedTAAR1 agonism normally provides a brake on dopaminergic neurotransmission; its absence removes this regulatory mechanism.[2]model confidence 82%
The abstract confirms absence of TAAR1 binding and links the pharmacological profile (including TAAR1 absence) to high abuse liability prediction. The mechanistic inference about TAAR1 as a brake is a standard pharmacological inference supported by the data.
None lacked serotonergic activity and TAAR1 binding. Pharmacological profile predicts high abuse liability.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDesoxypipradrol derivatives display a cocaine-type (not benztropine-type) binding profile.[13]model confidence 97%
Directly confirmed: '2-benzhydrylpiperidine derivatives exhibited a cocaine-like binding profile with respect to DAT mutation.'
Derivatives of desoxypipradrol (2-benzhydrylpiperidine) exhibited a cocaine-like binding profile with respect to DAT mutation.
checked by claude-sonnet-4-6 · May 11, 2026
neuroscience5 claims5verified
verifiedIn vivo microdialysis in freely moving rats confirms dose-dependent increases in extracellular dopamine in both nucleus accumbens shell and dorsal striatum following intravenous desoxypipradrol administration[12]model confidence 90%
In vivo dose-dependent extracellular dopamine increases in accumbens shell and dorsal striatum confirmed. Microdialysis method and IV route are not stated in the abstract but are consistent with the in vivo component of the study.
Dose-dependent increases in extracellular dopamine in accumbens-shell and striatum in vivo.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedEx vivo voltammetry in nucleus accumbens core slices demonstrates that desoxypipradrol produces a 7-fold increase in peak dopamine efflux — more than double cocaine's effect at the same concentration — and a 15-fold prolongation of dopamine reuptake half-life.[3]model confidence 98%
Exactly confirmed: 7-fold vs 3-fold (cocaine) peak dopamine increase, 15-fold vs 5-fold reuptake half-life at 10 µM. The 7-fold is more than double cocaine's 3-fold.
Desoxypipradrol caused sevenfold increase in peak dopamine levels (vs threefold for cocaine) and increased dopamine re-uptake half-life 15-fold (vs fivefold for cocaine) at 10 µM.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThis magnitude and duration of dopamine accumulation in the nucleus accumbens provides the neurobiological substrate for the compound's reinforcing properties, confirmed behaviourally by conditioned place preference and intravenous self-administration in mice.[5]model confidence 92%
CPP and i.v. self-administration in mice are directly confirmed, validating the reinforcing properties claim.
At 1 mg/kg i.p., mice showed significant preference in drug-paired compartment in CPP. At 0.1 mg/kg/infusion i.v., significantly higher active lever responses in SA test.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDAT inhibition in the dorsal striatum (IC₅₀ = 621 nM) would be expected to modulate motor function and habit-related circuits[12]model confidence 90%
IC50 of 6.21×10⁻⁷ M = 621 nM in dorsal striatum directly confirmed. The functional inference about motor and habit circuits is standard neuroscience knowledge about dorsal striatum function.
IC50 values for 2-DPMP at rat striatum DAT: 6.21×10⁻⁷ M (dorsal striatum).
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe extremely prolonged duration of transporter occupancy means these circuits remain potentiated for days rather than hours, distinguishing desoxypipradrol's neural impact from shorter-acting stimulants and potentially explaining the multi-day psychosis, sustained insomnia, and persistent agitation documented in clinical case series.[4]model confidence 88%
Multi-day psychosis (prolonged psychiatric symptoms key feature), sustained insomnia (32%), and persistent agitation (62%) are all confirmed in the Edinburgh case series. The mechanistic explanation about transporter occupancy is a reasonable synthesis.
agitation (62%)... insomnia (32%)... hallucinations (50%)... Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
pharmacokinetic detail1 claim1inconclusive
inconclusiveConfirmation requires liquid chromatography–tandem mass spectrometry (LC-MS/MS) or gas chromatography–mass spectrometry (GC-MS)[15]model confidence 70%
The abstract reports confirmed desoxypipradrol detection and concentration data from Finnish DUID and forensic cases, but does not mention the analytical methods (LC-MS/MS or GC-MS) used for confirmation.
106 positive desoxypipradrol samples from apprehended DUID drivers in Finland... Median serum concentration 0.073 mg/L.
checked by claude-sonnet-4-6 · May 11, 2026
safety27 claims20verified1partial5inconclusive1not supported
verifiedTachycardia was documented in 65% of Edinburgh cases and tachypnoea in 76%[4]model confidence 99%
Exact percentages directly confirmed in the abstract.
tachycardia (65%), tachypnoea (76%)
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRhabdomyolysis is the most consistently documented severe adverse effect, occurring in 96% of the 34-patient Edinburgh case series[4]model confidence 96%
96% rhabdomyolysis rate in 34 patients directly confirmed. At 96%, it is the highest-frequency finding in the case series.
rhabdomyolysis (96%)... 34 emergency attendances in Edinburgh due to 'ivory wave' toxicity.
checked by claude-sonnet-4-6 · May 11, 2026
not supportedDesoxypipradrol use can produce "states of psychosis, mania and addiction at a significantly higher rate than other stimulants"[18]model confidence 90%
cited source's abstract does not support this claim — flagged for editorial review
The abstract of citation [10] covers rhabdomyolysis cases and serotonin syndrome risk via 5-HT2A/1A receptor stimulation. It contains no information about rates of psychosis, mania, or addiction compared to other stimulants. This claim is not about the topic this paper covers.
Reports cases of rhabdomyolysis in patients after consumption of desoxypipradrol in combination with other NPS. Synergistic serotonergic effects may cause serotonergic syndrome via 5-HT2A/1A receptor stimulation.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedPsychosis may persist for days after last use.[4]model confidence 92%
Supported by 'prolonged psychiatric symptoms key feature' — in the context of an ED case series involving hallucinations (50%) and paranoia (21%), prolonged psychiatric symptoms is consistent with psychosis persisting for days.
Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedPsychosis may persist for days after last use.[14]model confidence 95%
The French case confirms auditory/visual hallucinations and incoherent speech lasting 7 days, supporting psychosis persisting for days.
auditory and visual hallucinations, incoherent speech... Symptoms lasted 7 days.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThree deaths involving desoxypipradrol were reported in the UK in August 2010[1]model confidence 97%
Directly confirmed: 'First three deaths involving 2-DPMP in August 2010.'
First three deaths involving 2-DPMP in August 2010.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedFinnish forensic data identified 2-DPMP in 5 autopsy cases, with the compound thought to contribute to death in 2; polydrug co-ingestion was present in the majority[15]model confidence 98%
All key facts confirmed: 5 autopsy cases, contributing to death in 2, most cases had amphetamine and/or benzodiazepines.
Found in 5 autopsy cases (0.05%), thought to contribute to death in 2. Most cases also had amphetamine and/or benzodiazepines.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedGerman forensic data co-detected 2-DPMP with synthetic opioids in respiratory-insufficient comatose patients[17]model confidence 95%
Confirmed: desoxypipradrol co-detected alongside opioids in 2 of 3 severe cyclopropylfentanyl (synthetic opioid) intoxication cases with respiratory insufficiency.
3 severe cyclopropylfentanyl intoxication cases. In 2 cases, desoxypipradrol was co-detected alongside opioids in blood/urine toxicology.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIn published post-mortem data, desoxypipradrol is rarely the sole cause of death — polydrug use is consistently present.[1]model confidence 70%
The abstract mentions three deaths but provides no information about polydrug co-involvement. The scope covers first reported deaths but not polydrug analysis.
First three deaths involving 2-DPMP in August 2010.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn published post-mortem data, desoxypipradrol is rarely the sole cause of death — polydrug use is consistently present.[15]model confidence 92%
The Finnish data confirms polydrug use: 'Most cases also had amphetamine and/or benzodiazepines,' and desoxypipradrol was only 'thought to contribute to death in 2' of 5 autopsy cases, not definitively the sole cause.
Found in 5 autopsy cases, thought to contribute to death in 2. Most cases also had amphetamine and/or benzodiazepines.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedHallucinations (auditory and visual) occurred in 50% of Edinburgh cluster cases, paranoia in 21%[4]model confidence 98%
Exact percentages directly confirmed: hallucinations 50%, paranoia 21%.
hallucinations (50%)... paranoia (21%)
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe French case report documented hallucinations and incoherent speech persisting for days.[14]model confidence 98%
Directly confirmed: auditory and visual hallucinations and incoherent speech, with symptoms lasting 7 days.
auditory and visual hallucinations, incoherent speech... Symptoms lasted 7 days.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveUnlike cocaine or amphetamine psychosis, which typically resolves within hours to a day of cessation, desoxypipradrol-associated psychosis can persist for 3–7 days[4]model confidence 72%
The abstract confirms prolonged psychiatric symptoms as a key feature but does not specify the duration as 3–7 days, nor does it make a comparison to cocaine or amphetamine psychosis resolution time. The specific range and comparative framing are not in the abstract.
Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedUnlike cocaine or amphetamine psychosis, which typically resolves within hours to a day of cessation, desoxypipradrol-associated psychosis can persist for 3–7 days[14]model confidence 88%
The 7-day symptom course confirmed in this case is consistent with and directly supports the '3–7 days' range claim. The comparison to cocaine/amphetamine is a clinical inference not explicitly in the abstract, but the 7-day duration data supports the claim.
Symptoms lasted 7 days.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveDelirium and mania are noted in the clinical literature as features of severe intoxication[10]model confidence 68%
The abstract mentions acute toxicity including agitation and psychosis, but does not specifically enumerate delirium or mania. These may appear in the full review text.
acute toxicity includes prolonged stimulation, insomnia, agitation, psychosis.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRodent models confirm reinforcing properties: conditioned place preference was established at 1 mg/kg i.p. in mice, and intravenous self-administration was maintained at 0.1 mg/kg/infusion[5]model confidence 98%
Exactly confirmed: CPP at 1 mg/kg i.p. and significant lever responses in SA at 0.1 mg/kg/infusion i.v.
At 1 mg/kg i.p., mice showed significant preference in drug-paired compartment in CPP. At 0.1 mg/kg/infusion i.v., significantly higher active lever responses in SA test.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDopamine release in synaptosomes increased in a dose-dependent manner.[5]model confidence 99%
Directly confirmed: 'Dopamine increased in dose-dependent manner in synaptosomes.'
Dopamine increased in dose-dependent manner in synaptosomes.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe pharmacological profile predicts high abuse liability based on multiple converging indicators: (1) highly selective DAT/NET inhibition — a cocaine-like rather than MDMA-like profile; (2) absence of TAAR1 agonism, removing a natural brake on dopaminergic drive; (3) 10-fold greater potency than cocaine at DAT; (4) greater magnitude and duration of dopamine efflux enhancement compared to cocaine[2]model confidence 90%
Points 1–3 are directly confirmed: selective DAT/NET inhibition, no TAAR1, 10-fold greater potency than cocaine at DAT, and explicit statement that pharmacological profile predicts high abuse liability. Point 4 (efflux magnitude and duration) is from citation [9] but this citation supports the overall conclusion.
Potent and selective catecholamine transporter blockers without substrate releasing properties. 2-DPMP was a 10-fold more potent DAT blocker than cocaine. None lacked serotonergic activity and TAAR1 binding. Pharmacological profile predicts high abuse liability.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe pharmacological profile predicts high abuse liability based on multiple converging indicators: (1) highly selective DAT/NET inhibition — a cocaine-like rather than MDMA-like profile; (2) absence of TAAR1 agonism, removing a natural brake on dopaminergic drive; (3) 10-fold greater potency than cocaine at DAT; (4) greater magnitude and duration of dopamine efflux enhancement compared to cocaine[3]model confidence 90%
Point 4 (greater magnitude and duration of dopamine efflux compared to cocaine) is directly confirmed: sevenfold vs threefold peak dopamine, 15-fold vs fivefold reuptake half-life at the same concentration.
Desoxypipradrol caused sevenfold increase in peak dopamine levels (vs threefold for cocaine) and increased dopamine re-uptake half-life 15-fold (vs fivefold for cocaine) at 10 µM.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveDesoxypipradrol is classified among the "principal DA-activating stimulants" with the highest addiction potential, alongside MDPV and naphyrone.[9]model confidence 70%
The abstract confirms desoxypipradrol is classified as a 'principal DA-activating stimulant' but does not specify 'highest addiction potential' or list MDPV and naphyrone as companions in that classification. These details may be in the full review.
Desoxypipradrol classified as principal DA-activating stimulant (amphetamine-like).
checked by claude-sonnet-4-6 · May 11, 2026
partialHowever, when combined with serotonergic substances (MDMA, mephedrone, other serotonin-releasing NPS), the interaction can produce serotonin syndrome through a compound mechanism: the co-ingestant releases serotonin while desoxypipradrol's NET blockade reduces norepinephrine-mediated serotonin clearance in certain brain regions[18]model confidence 82%
The abstract confirms that serotonin syndrome can result from desoxypipradrol combined with serotonergic NPS. However, the mechanism described in the claim (NET blockade reducing NE-mediated serotonin clearance) differs from the abstract's mechanism (synergistic 5-HT2A/1A receptor stimulation). The general serotonin syndrome risk is confirmed but the specific mechanistic pathway is not.
Synergistic serotonergic effects may cause serotonergic syndrome via 5-HT2A/1A receptor stimulation.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRhabdomyolysis cases involving 2-DPMP co-ingested with serotonergic NPS have been attributed to synergistic 5-HT₂A/5-HT₁A receptor stimulation.[18]model confidence 97%
Directly confirmed: rhabdomyolysis cases with desoxypipradrol + NPS co-ingestion, mechanism attributed to synergistic serotonergic effects via 5-HT2A/1A receptor stimulation.
Reports cases of rhabdomyolysis in patients after consumption of desoxypipradrol in combination with other NPS. Synergistic serotonergic effects may cause serotonergic syndrome via 5-HT2A/1A receptor stimulation.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThis severity classification is mechanistically well-supported.[18]model confidence 60%
This is a meta-claim about whether a severity classification is well-supported. The abstract provides some mechanistic detail (5-HT2A/1A receptor stimulation) but 'this severity classification' refers to context outside this abstract. Cannot verify without knowing what severity classification is referenced.
Synergistic serotonergic effects may cause serotonergic syndrome via 5-HT2A/1A receptor stimulation.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDesoxypipradrol was co-detected with synthetic opioids (including cyclopropylfentanyl) in respiratory-insufficient comatose patients in German forensic data[17]model confidence 95%
Directly confirmed: co-detection of desoxypipradrol with cyclopropylfentanyl (a synthetic opioid) in severe intoxication cases with respiratory insufficiency.
3 severe cyclopropylfentanyl intoxication cases. In 2 cases, desoxypipradrol was co-detected alongside opioids in blood/urine toxicology.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedCo-detection of desoxypipradrol with amphetamine was documented in Finnish DUID cases[15]model confidence 97%
Directly confirmed: most DUID cases also had amphetamine and/or benzodiazepines.
Most cases also had amphetamine and/or benzodiazepines.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDesoxypipradrol produces psychosis in 50% of the documented clinical population at intoxicating doses; sustained dopaminergic stimulation lasting days represents an extreme precipitant in predisposed individuals.[4]model confidence 88%
Hallucinations in 50% confirmed (hallucinations are a core feature of psychosis). Prolonged psychiatric symptoms as a key feature supports the claim about sustained stimulation lasting days. The 'predisposed individuals' framing is a reasonable clinical inference.
hallucinations (50%)... Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedRenal impairment: Relative contraindication given the 96% rhabdomyolysis rate documented in clinical cases[4]model confidence 88%
The 96% rhabdomyolysis rate is directly confirmed. The clinical inference that this constitutes a relative contraindication for renal impairment (rhabdomyolysis causes myoglobinuria and acute kidney injury) is a standard clinical inference well-supported by the data.
rhabdomyolysis (96%)
checked by claude-sonnet-4-6 · May 11, 2026
clinical evidence8 claims7verified1inconclusive
verifiedA single individual consumed approximately 250 mg of desoxypipradrol purchased online — a dose substantially exceeding the reported recreational range of 10–20 mg[14]model confidence 99%
Directly confirmed: 250 mg consumed, and recreational doses noted as 10–20 mg.
32-year-old man consumed 250 mg desoxypipradrol purchased online... Article notes recreational doses reported as 10-20 mg.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThree deaths involving 2-DPMP were reported in the UK in August 2010, believed to be the first fatalities attributable to this compound[1]model confidence 97%
Directly confirmed: 'First three deaths involving 2-DPMP in August 2010.'
First three deaths involving 2-DPMP in August 2010.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe only published reference to recreational dose ranges describes oral doses of approximately 10–20 mg[14]model confidence 90%
The 10–20 mg recreational dose range is directly confirmed in the abstract. Whether this is the 'only' published reference cannot be verified from the abstract alone, but the dose data is confirmed.
Article notes recreational doses reported as 10-20 mg.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe largest clinical case series documented 34 emergency department attendances in Edinburgh, Scotland, during summer 2010, associated with "Ivory Wave" products confirmed to contain desoxypipradrol[4]model confidence 99%
Directly confirmed: 34 Edinburgh ED attendances, Ivory Wave toxicity in Jul-Aug 2010, powder confirmed to contain desoxypipradrol.
34 emergency attendances in Edinburgh due to 'ivory wave' toxicity Jul-Aug 2010. 'Ivory wave' powder found to contain desoxypipradrol.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedProlonged psychiatric symptoms were described as a key feature, persisting for several days beyond initial presentation[4]model confidence 97%
Directly confirmed as stated in the abstract.
Prolonged psychiatric symptoms key feature.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedActive plasma concentrations persisted through day 4; the full symptom course resolved over 7 days.[14]model confidence 98%
Directly confirmed: plasma concentrations at day 3 (136 µg/L) and day 4 (93 µg/L), and symptoms lasting 7 days.
Plasma concentration: 136 μg/L at admission (day 3), 93 μg/L at day 4... Symptoms lasted 7 days.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedGerman forensic studies detected 2-DPMP alongside synthetic opioids in co-intoxication cases[17]model confidence 95%
Confirmed: desoxypipradrol co-detected with synthetic opioids (cyclopropylfentanyl) in 2 of 3 severe intoxication cases.
In 2 cases, desoxypipradrol was co-detected alongside opioids in blood/urine toxicology.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIn the published post-mortem literature, desoxypipradrol is rarely the sole identified substance — polydrug use is consistently present.[1]model confidence 65%
The abstract mentions three deaths but provides no information about polydrug involvement in those cases.
First three deaths involving 2-DPMP in August 2010.
checked by claude-sonnet-4-6 · May 11, 2026
comparative pharmacology6 claims4verified2inconclusive
verifiedHowever, desoxypipradrol is approximately 10-fold more potent than cocaine at the dopamine transporter in transfected human cell assays.[2]model confidence 97%
Directly confirmed: '2-DPMP was a 10-fold more potent DAT blocker than cocaine.'
2-DPMP was a 10-fold more potent DAT blocker than cocaine.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn transfected cell assays, the two compounds are equipotent at DAT and NET[2]model confidence 97%
Directly confirmed: '2-DPMP was an equally potent DAT/NET inhibitor compared to methylphenidate.'
2-DPMP was an equally potent DAT/NET inhibitor compared to methylphenidate.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveFunctionally, MDPV has a shorter duration of action than desoxypipradrol, and its compulsive redosing profile differs — MDPV use tends toward high-frequency repeated dosing within a session, while desoxypipradrol's extreme duration makes redosing particularly hazardous because initial effects may not manifest before cumulative toxicity develops.[10]model confidence 70%
The abstract classifies pipradrols/piperidines as selective catecholamine uptake inhibitors with prolonged stimulation, but does not specifically compare MDPV's shorter duration, MDPV's high-frequency redosing profile, or the specific hazard of cumulative toxicity from desoxypipradrol redosing. These specific comparative claims may be in the full review text.
Comprehensive review classifying pipradrols/piperidines as selective catecholamine uptake inhibitors. Dopaminergic drugs highly addictive; acute toxicity includes prolonged stimulation, insomnia, agitation, psychosis.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDesoxypipradrol and cocaine share a cocaine-type DAT binding mechanism — both stabilize the transporter in an outward-facing conformation and function as pure reuptake inhibitors without substrate-releasing properties[12]model confidence 93%
Confirmed: molecular dynamics simulations show 2-DPMP leads to outward-facing DAT conformation, described as 'cocaine-type effect,' implying cocaine shares this mechanism.
Molecular dynamics simulations show 2-DPMP leads to outward-facing DAT conformation (cocaine-type effect).
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThis single structural difference (ester vs. no ester) accounts for much of the difference in clinical manageability that led CIBA to pursue methylphenidate over desoxypipradrol for therapeutic development.[1]model confidence 65%
The abstract does not discuss structural differences between desoxypipradrol and methylphenidate or CIBA's development decisions. This mechanistic-historical claim cannot be verified from the abstract.
Originally developed in 1950s for narcolepsy and ADHD.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedNeither compound has serotonergic activity or TAAR1 binding.[2]model confidence 96%
Directly confirmed: 'None lacked serotonergic activity and TAAR1 binding' — i.e., all compounds tested, including 2-DPMP, had no serotonergic activity and no TAAR1 binding.
None lacked serotonergic activity and TAAR1 binding.
checked by claude-sonnet-4-6 · May 11, 2026
Coverage & Gaps
Research Trail
substance-article pipeline-v5 May 11, 2026
| Step | Source | Query | Results |
|---|---|---|---|
| 1database lookup | PubChem | desoxypipradrol | 1 result, 1 selected |
selection rationaleselection rationaleConfirmed chemical identity data for brief verification | |||
| 2literature search | PubMed | desoxypipradrol pharmacology | 15 results, 10 selected |
selection rationaleselection rationaleCore pharmacology, toxicology, and clinical literature for the substance | |||
| 3literature search | PubMed | 2-benzhydrylpiperidine stimulant dopamine | 1 result, 1 selected |
selection rationaleselection rationaleDAT binding profile characterization | |||
| 4clinical trial search | ClinicalTrials.gov | desoxypipradrol | 0 results |
selection rationaleselection rationaleConfirmed no registered trials | |||
| 5literature search | OpenAlex | desoxypipradrol 2-DPMP dopamine transporter inhibitor | 10 results, 5 selected |
selection rationaleselection rationaleBroader landscape context and additional case report | |||
| 6literature search | PubMed | desoxypipradrol 2-DPMP serum blood concentration driving | 1 result, 0 selected |
selection rationaleselection rationaleAlready captured | |||
| 7literature search | OpenAlex | desoxypipradrol ivory wave legal high toxicity UK | 10 results, 1 selected |
selection rationaleselection rationaleMurray 2012 confirmed for clinical toxidrome data | |||
| 8web search | WebSearch | desoxypipradrol 2-DPMP legal status scheduling US DEA Australia Canada | 10 results, 2 selected |
selection rationaleselection rationaleLegal status not available in academic databases | |||
| 9web search | WebSearch | pipradrol Ciba pharmaceutical 1950s synthesis narcolepsy ADHD history methylphenidate | 10 results, 1 selected |
selection rationaleselection rationaleHistorical context not available via PubMed | |||
| 10web search | WebSearch | desoxypipradrol 2-DPMP stereochemistry R S isomer active enantiomer chirality | 10 results, 1 selected |
selection rationaleselection rationaleStereochemistry data not available in PubMed | |||
| 11web search | WebSearch | desoxypipradrol 2-DPMP legal status scheduling US DEA Australia Canada | 10 results, 2 selected |
selection rationaleselection rationaleLegal status not in academic databases | |||
| 12web search | WebSearch | desoxypipradrol CAS 519-74-4 melting point solubility physical properties | 10 results, 1 selected |
selection rationaleselection rationalePhysical properties not available in academic databases | |||
| 13web search | WebSearch | desoxypipradrol 2-DPMP stereochemistry R S isomer active enantiomer chirality | 10 results, 1 selected |
selection rationaleselection rationaleStereochemistry data on enantiomers | |||
| 14database lookup | Crossref/DOI | DOI verification batch 1 | 4 results, 1 selected |
selection rationaleselection rationaleVerification of key citations | |||
| 15web search | WebSearch | desoxypipradrol EMCDDA early warning system 2010 2011 report Europe | 10 results, 1 selected |
selection rationaleselection rationaleRegulatory history context | |||
| 16literature search | PubMed | research chemicals legal highs pipradrol derivatives case review 2012 | 1 result, 1 selected |
selection rationaleselection rationaleKey review paper summarizing pipradrol class pharmacology and toxicology | |||
| 17literature search | OpenAlex | MDPV desoxypipradrol cathinone DAT selectivity abuse potential comparison | 7 results, 1 selected |
selection rationaleselection rationaleAddictive neuropharmacology context | |||
Research document (raw, unedited pipeline output)
# Research Output: Desoxypipradrol
## Chemical Identity
**Molecular Formula:** C₁₈H₂₁N
**Molecular Weight:** 251.4 g/mol
**IUPAC Name:** 2-benzhydrylpiperidine
**Systematic name:** (RS)-2-benzhydrylpiperidine (racemate); also written as 2-diphenylmethylpiperidine
**CAS Number:** 519-74-4 (racemate); hydrochloride salt CAS: 5807-81-8
**PubChem CID:** 160506
**InChIKey:** RWTNXJXZVGHMGI-UHFFFAOYSA-N
**Molecular SMILES:** Not retrieved directly from PubChem tool response, but derivable from 2-benzhydrylpiperidine structure
**Verified via PubChem CID 160506:** Formula C₁₈H₂₁N, MW 251.4, IUPAC 2-benzhydrylpiperidine, InChIKey RWTNXJXZVGHMGI-UHFFFAOYSA-N [Ref 22].
**Physical Properties (web-retrieved, not primary literature):**
- Melting point: 59–61°C
- Boiling point: 366.3°C at 760 mmHg
- Density: 1.027 g/cm³
- Appearance: Pale brown solid
- Solubility: Soluble in chloroform and methanol [Ref 24]
**Stereochemistry:** Desoxypipradrol possesses a single chiral center at C-2 of the piperidine ring. The commercially available form is a racemate (RS). The (R)-(−) enantiomer is more pharmacologically active than the (S)-(+) enantiomer as an inhibitor of the dopamine transporter ("phenethylamine pump"). The more active enantiomers of pipradrol and desoxypipradrol are stereochemically superimposable on each other but are NOT superimposable on the more active (S)-(+)-enantiomer of amphetamine, indicating a distinct binding geometry at the transporter [Ref 27]. No published controlled studies characterizing enantiomer-specific Ki values in humans were found; this data derives from older pharmacological literature cited via web sources.
**Brief seed data discrepancies:** The brief lists no SMILES, molecular formula, or PubChem CID. All three have now been confirmed via PubChem API: formula C₁₈H₂₁N, MW 251.4, CID 160506. The brief's systematic name "2-benzhydrylpiperidine" is correct.
---
## Pharmacology
### Mechanism of Action
Desoxypipradrol (2-DPMP) is a potent and selective **catecholamine reuptake inhibitor** — specifically a dopamine transporter (DAT) and norepinephrine transporter (NET) blocker with no meaningful serotonin transporter (SERT) activity and no monoamine-releasing ("substrate") properties. This distinguishes it mechanistically from amphetamine-class drugs [Ref 3].
**Key in vitro pharmacology (Simmler et al. 2014 [Ref 3]):**
- 2-DPMP was characterized using HEK293 cells expressing human DAT, NET, and SERT
- Equipotent DAT/NET inhibitor compared to methylphenidate in that assay system
- Approximately **10-fold more potent** at DAT than cocaine
- No serotonin transporter inhibition
- No monoamine-releasing properties (pure reuptake inhibitor, not a substrate releaser)
- No TAAR1 binding
- No meaningful affinity at monoaminergic receptors (including serotonin 5-HT₁A, 5-HT₂A, 5-HT₂C, α₁A/₂A-adrenergic, dopamine D₁₋₃, histamine H₁)
**DAT binding IC₅₀ values in rat striatum (Loi et al. 2020 [Ref 1]):**
- Accumbens shell: IC₅₀ = 5.65 × 10⁻⁷ M (565 nM)
- Dorsal striatum: IC₅₀ = 6.21 × 10⁻⁷ M (621 nM)
- Measured by quantitative autoradiography using [¹²⁵I]RTI-121, a selective DAT radioligand
**In vivo dopamine release (Loi et al. 2020 [Ref 1]; Davidson & Ramsey 2012 [Ref 9]):**
- Intravenous 2-DPMP produced dose-dependent increases in extracellular dopamine in nucleus accumbens shell and dorsal striatum in freely moving rats
- In rat nucleus accumbens core slices with fast cyclic voltammetry (Davidson & Ramsey 2012 [Ref 9]):
- 2-DPMP at 10 µM caused a **7-fold** increase in peak dopamine efflux (vs. 3-fold for cocaine at same concentration)
- 2-DPMP increased dopamine re-uptake half-life **15-fold** (vs. 5-fold for cocaine)
- 2-DPMP is substantially **more potent than cocaine** at dopamine terminals in this ex vivo preparation
**DAT conformational dynamics (Loi et al. 2020 [Ref 1]):**
- Molecular dynamics simulations show 2-DPMP induces outward-facing DAT conformation — consistent with a **cocaine-type** (inhibitor) mechanism, not an amphetamine-type (inward-facing/releasor) mechanism
- This was confirmed by mutant DAT studies (Schmitt et al. 2008 [Ref 12]): 2-benzhydrylpiperidine derivatives display a cocaine-like binding profile at DAT mutants W84L and D313N
**Classification within NPS pharmacology:**
- 2-DPMP belongs to the pipradrol/piperidine subclass of NPS stimulants — a group defined by selective catecholamine reuptake inhibition analogous to methylphenidate and MDPV (pyrovalerone cathinone), but with greater duration of action (Liechti 2015 [Ref 15]; Iversen et al. 2014 [Ref 4])
- Unlike MDMA-like NPS, 2-DPMP has no serotonergic activity, meaning its toxicity profile differs markedly (no serotonin syndrome as a primary risk from the drug itself; see Interactions section)
### Pharmacokinetics
No published **human pharmacokinetic studies** were identified. All available human data derives from case reports and forensic toxicology.
**Observed plasma concentrations in clinical cases:**
- French case report (Lelièvre et al. 2013 [Ref 13]): after consumption of 250 mg 2-DPMP purchased online, plasma concentration was 136 µg/L at day 3 post-ingestion and 93 µg/L at day 4; urine concentration was 4,805 µg/L at day 4
- Finnish DUID study (Kriikku et al. 2013 [Ref 5]): median serum concentration 0.073 mg/L (range 0.006–0.890 mg/L) in 106 confirmed DUID-positive drivers; concentrations in post-mortem cases ranged higher
**Duration of effects:** Extremely prolonged. Total duration has been reported as 16–72 hours in user reports; clinical presentations in emergency departments consistently feature multi-day symptoms [Ref 8, 13]. The French case report documented a 7-day symptom course after a single large dose [Ref 13]. The Ivory Wave Edinburgh cluster described psychiatric symptoms lasting several days [Ref 8].
**Lipophilicity and metabolism:** No published metabolic studies or CYP enzyme data were identified. The compound is highly lipophilic with no easily metabolized polar functional groups, which is believed to account for its exceptional duration of action relative to other stimulants (web sources [Ref 22]). Metabolic pathway is not characterized in the published literature.
**Half-life:** Not formally determined in human pharmacokinetic studies. Web-sourced estimates of 16–20 hours (potentially 1.5–2 days for the effective half-life given its lipophilicity) are not supported by published human PK data. The DB seed value of 5 days half-life appears to derive from user-report/community consensus rather than published pharmacokinetic studies. ⚠️ **FLAG: No published human PK study. Half-life value is unverified.**
---
## History
**Synthesis and pharmaceutical origins:**
- Desoxypipradrol was developed by **CIBA** (now Novartis) in the **1950s** as part of research on cyclic amine derivatives. It was patented in **1958** as a potential psychomotor stimulant and treatment for narcolepsy [Ref 22, 7].
- CIBA also developed the closely related compound **pipradrol** (marketed as Meratran, patented 1953), and subsequently **methylphenidate** (Ritalin), both from the same research program.
- Desoxypipradrol was dropped from clinical development after methylphenidate proved superior for ADHD due to its shorter duration of action and more predictable pharmacokinetics [Ref 7, 22].
- Pipradrol was eventually scheduled in many countries in the late 1970s due to abuse potential, which effectively also curtailed any commercial interest in desoxypipradrol.
**Emergence as a novel psychoactive substance:**
- Recreational use of 2-DPMP appears to have started in approximately **March 2007**, initially developing slowly [Ref 7].
- Popularity grew in the **UK in 2009** and surged rapidly in **summer 2010**, primarily sold under the brand name **"Ivory Wave"** — a product name shared with mephedrone-containing products, causing confusion about its active ingredient [Ref 7, 8].
- In summer 2010, a cluster of 34 emergency department attendances was documented in Edinburgh associated with "Ivory Wave" use; analysis of a powder sample confirmed desoxypipradrol as the active ingredient [Ref 8].
- **First reported deaths:** Three deaths involving 2-DPMP were reported in August 2010 in the UK, believed to be the first fatalities from this compound [Ref 7].
- The EMCDDA Early Warning System issued alerts on 2-DPMP in 2010 [Ref 28].
**Regulatory response (chronological):**
- **4 November 2010:** UK Home Office announced a ban on importation of 2-DPMP following ACMD recommendation [Ref 7, 23, 28]
- **November 2011:** Formal UK importation ban imposed [Ref 7]
- **13 June 2012:** 2-DPMP became a **Class B drug** in the UK (initially entered as Class C; reclassified upward), placed in Schedule 1 (no medicinal use) [Ref 7]
- **2012:** Controlled in **Finland** and **Sweden** [Ref 22]
- **13 December 2014:** Controlled in **Germany** under Anlage II BtMG (Narcotics Act, Schedule II) [Ref 22]
- **October 2015:** Controlled in **China** [Ref 22]
- **26 May 2016:** UK Psychoactive Substances Act 2016 came into force, making production and supply of all psychoactive substances (except specific exemptions) illegal in the UK — this supersedes the Class B scheduling for most practical purposes
---
## Subjective Effects
No controlled human studies of desoxypipradrol have been published. Subjective effect data derives entirely from case reports, forensic toxicology, and online user reports.
**Effects documented in clinical case reports and emergency presentations:**
*Stimulant/sympathomimetic effects:*
- Pronounced stimulation and wakefulness (multi-day insomnia documented) [Ref 8, 13]
- Tachycardia (reported in 65% of Edinburgh cluster cases) [Ref 8]
- Tachypnoea (reported in 76% of Edinburgh cluster cases) [Ref 8]
- Agitation (62% of Edinburgh cluster cases) [Ref 8]
- Rhabdomyolysis (96% of Edinburgh cluster cases) [Ref 8] — particularly notable frequency
- Leucocytosis (57% of Edinburgh cluster cases) [Ref 8]
*Psychiatric/perceptual effects:*
- Hallucinations — both auditory and visual (50% Edinburgh cluster; confirmed in French case report) [Ref 8, 13]
- Paranoia (21% Edinburgh cluster) [Ref 8]
- Psychosis (described as a key feature of prolonged toxicity) [Ref 8, 15]
- Incoherent speech [Ref 13]
- Delirium and mania (noted in clinical literature) [Ref 15]
*Physical effects:*
- Anorexia/appetite suppression [Ref 13]
- Mild mydriasis (pupil dilation) [Ref 13]
- Dystonia (18% Edinburgh cluster) [Ref 8]
**Duration of subjective effects:** Extremely prolonged compared to most psychostimulants. A single ingestion can produce effects lasting 3–7 days based on case reports. The French case documented active plasma concentrations and symptoms at day 3 post-ingestion, with full resolution by day 7 [Ref 13]. The Edinburgh cluster featured "prolonged psychiatric symptoms as a key feature" [Ref 8].
**Dose information (published case reports):**
- Recreational oral doses reported as approximately **10–20 mg** in case report literature (Lelièvre et al. 2013 [Ref 13])
- The individual in the French case consumed **250 mg** — this represents an extreme overdose substantially above any reported recreational dose
- The brief's DB dose ranges (oral: threshold 0.25 mg → heavy 8+ mg; insufflated: threshold 0.25 mg → heavy 5+ mg) appear notably lower than the 10–20 mg recreational dose range described in case report literature. ⚠️ **FLAG: DB dose ranges appear low relative to the only published human dose reference. Editorial review recommended.**
---
## Safety & Toxicity
### Acute Toxicity
**Rhabdomyolysis** is the most consistently documented severe adverse effect, occurring in 96% of the Edinburgh case series (34 patients) [Ref 8]. The mechanism is not established but is presumed to relate to the combination of extreme stimulant activity, hyperthermia, and dystonia. Rhabdomyolysis can lead to acute renal failure.
**Cardiovascular:** Tachycardia was documented in 65% of clinical presentations; hypertension is expected from the sympathomimetic mechanism but not specifically quantified in the reviewed literature. Vasoconstriction is a pharmacologically predicted effect of NET/DAT inhibition.
**Psychiatric toxicity:** Prolonged psychosis, hallucinations, paranoia, and delirium are the defining features of severe toxicity, distinguishing 2-DPMP from shorter-acting stimulants. Müller et al. 2016 [Ref 10] explicitly warns that 2-DPMP use can lead to "states of psychosis, mania and addiction at a significantly higher rate than other stimulants." Psychosis may persist for days after last use [Ref 8, 13].
**Serotonergic syndrome risk with polydrug use:** Müller et al. 2016 [Ref 10] reports rhabdomyolysis cases where 2-DPMP was combined with other NPS that had serotonergic activity, with synergistic stimulation of 5-HT₂A/5-HT₁A receptors proposed as a contributing mechanism. Note: 2-DPMP itself has no serotonergic activity; the risk arises from polydrug combinations with serotonergic co-ingestion [Ref 10].
**Fatalities:**
- First three deaths attributed to 2-DPMP were reported in the UK in August 2010 (Corkery et al. 2012 [Ref 7])
- Finnish forensic data (Kriikku et al. 2013 [Ref 5]): 2-DPMP was detected in 5 autopsy cases and thought to contribute to death in 2 of these; however, the majority of cases also had co-ingested other psychoactive drugs (amphetamine, benzodiazepines, alcohol)
- 2-DPMP was detected alongside opioids (including synthetic opioids) in co-intoxication cases in Germany (Müller et al. 2019 [Ref 21])
- In published post-mortem data, 2-DPMP is rarely the sole cause of death; polydrug use is consistently present [Ref 5, 7]
**No LD50 data in humans or standard laboratory animals was identified in the published literature.** Acute toxicity is described as "moderate" in the DB seed; this characterization is inferred from pharmacological class and case reports, not from formal toxicological dose-response studies. ⚠️ **FLAG: No published LD50 data found.**
### Chronic Toxicity
No formal chronic toxicity studies in humans or animals were identified. The general profile of prolonged high-potency dopaminergic stimulation suggests risks comparable to or exceeding those of cocaine and methamphetamine for cardiovascular, psychiatric, and renal sequelae with repeated use. This is a class inference, not substance-specific data.
---
## Harm Reduction
### Interaction Warnings
**Tramadol (listed as lethal in seed data):**
The specific mechanism for a "lethal" classification of tramadol + desoxypipradrol was not confirmed in any identified primary publication. General mechanism: tramadol lowers the seizure threshold and has serotonergic activity (weak SNRI + µ-opioid agonist). Combined with a potent stimulant, risks include: (1) seizure threshold reduction from both stimulant-induced hyperexcitability and tramadol's seizure-lowering effects; (2) cardiovascular strain from combined stimulant and tramadol-mediated catecholamine effects; (3) hyperthermia. The "lethal" severity rating in the DB seed is plausible but **not confirmed against any specific published report of a 2-DPMP + tramadol death.** ⚠️ **FLAG: Interaction severity requires editorial verification against a primary source.**
**MDMA (listed as "dangerous" in seed data):**
MDMA releases serotonin and dopamine; 2-DPMP blocks dopamine/norepinephrine reuptake. Combined use creates risk of: (1) serotonin syndrome (MDMA serotonin release + blocked NET can increase synaptic serotonin); (2) hyperthermia (both drugs individually elevate body temperature); (3) cardiovascular toxicity (additive sympathomimetic effects). The "dangerous" rating is mechanistically well-supported. Müller et al. 2016 [Ref 10] specifically warns about synergistic serotonergic effects when 2-DPMP is combined with serotonergic NPS.
**Alcohol (listed as "unknown" in seed data):**
No published data found on the specific combination.
### Other Harm Reduction Considerations
1. **Dose titration is extremely difficult:** The extraordinarily long duration (up to 72 hours) means users cannot easily titrate based on effects, as peak effects may be delayed significantly from administration [Ref 8]
2. **Redosing danger:** Compulsive redosing at sub-threshold dose perception can lead to massive cumulative doses before significant effects manifest; the French case (250 mg consumed) illustrates this risk [Ref 13]
3. **Product adulteration:** "Ivory Wave" products were inconsistently formulated; different batches contained different active ingredients, making historical self-reported dose data unreliable [Ref 8, 22]
4. **Standard drug screening:** 2-DPMP is not detected by routine immunoassay drug panels; detection requires LC-MS/MS or GC-MS [Ref 5, 17]
5. **Emergency management:** Treatment is supportive. Benzodiazepines for agitation/dystonia; monitoring for rhabdomyolysis with appropriate renal protection (hydration); psychiatric observation for several days due to prolonged symptom course [Ref 8]
---
## Tolerance & Dependence
### Rodent Dependence Models (Cha et al. 2019 [Ref 2])
The only published substance-specific dependence study found:
- **Conditioned Place Preference (CPP):** At 1 mg/kg i.p., mice showed significant preference for the drug-paired compartment
- **Intravenous Self-Administration (SA):** At 0.1 mg/kg/infusion i.v., mice showed significantly elevated active lever responding — confirming reinforcing properties
- Dopamine increased in a dose-dependent manner in synaptosomes
- Conclusion: 2-DPMP has rewarding and reinforcing effects confirming dependence liability
### Pharmacological Basis for Abuse Liability
Simmler et al. 2014 [Ref 3] explicitly states: "The pharmacological profiles of D2PM and 2-DPMP likely predict a high abuse liability." This is based on:
1. Highly selective DAT/NET inhibition with no SERT involvement (cocaine-like > MDMA-like profile)
2. Absence of TAAR1 activation (TAAR1 agonism is associated with reduced abuse potential)
3. 10-fold greater DAT potency than cocaine [Ref 3]
4. Greater dopamine efflux and prolonged reuptake inhibition compared to cocaine [Ref 9]
Iversen et al. 2014 [Ref 4] places 2-DPMP in the category of "principal DA-activating stimulants" with high addiction potential, alongside MDPV and naphyrone.
### Tolerance
No published tolerance studies specific to 2-DPMP were identified. The DB seed value of 5-day half-life for tolerance "cross-tolerance: dopamine, stimulant" is a class inference consistent with stimulant pharmacology but not directly sourced. ⚠️ **FLAG: Tolerance build-up rate not substantiated by substance-specific published data.**
### Withdrawal
No published withdrawal characterization studies for 2-DPMP were found. Withdrawal from dopaminergic stimulants generally involves dysphoria, fatigue, hypersomnia, anhedonia, and depression — these are class-level predictions. The prolonged half-life suggests a potentially prolonged "crash" period but this has not been studied.
---
## Interactions
### Summary of Known/Suspected Interactions
| Agent | DB Severity | Mechanism | Evidence Level |
|---|---|---|---|
| Tramadol | Lethal | Seizure threshold lowering (tramadol) + stimulant hyperexcitability; possibly serotonergic | Class inference; no identified primary 2-DPMP+tramadol report |
| MDMA | Dangerous | Serotonin syndrome risk (MDMA serotonin release + 2-DPMP NET blockade); hyperthermia; cardiovascular | Mechanistically supported; Müller 2016 [Ref 10] documents serotonergic risk in NPS co-use |
| Alcohol | Unknown | CNS effects may mask stimulant toxicity; cardiovascular strain | No published data |
| Opioids | — | Not in DB; co-detected in fatal cases [Ref 21]; general respiratory depression + stimulant interaction | Case series [Ref 21] |
| Amphetamines | — | Not in DB; co-detected in Finnish DUID cases [Ref 5]; additive dopaminergic toxicity expected | Forensic co-detection data only |
| Benzodiazepines | — | Not in DB; co-detected in Finnish DUID cases [Ref 5] | Forensic data only |
| Other serotonergic NPS | — | Serotonin syndrome via synergistic 5-HT₂A stimulation [Ref 10] | Case reports (rhabdomyolysis) |
**⚠️ FLAG: The tramadol "lethal" interaction severity was not confirmed against a specific published report. Mechanism is plausible (seizure threshold) but the lethal classification specifically should be editorially verified.**
---
## Legal Status
All legal status data is web-retrieved [Ref 22, 23]; no primary legal documents were accessible in full text.
| Jurisdiction | Status | Details | Date |
|---|---|---|---|
| **United Kingdom** | Class B, Schedule 1 | Controlled under Misuse of Drugs Act. UK importation ban announced Nov 2010; formal ban Nov 2011; Class C then reclassified to Class B from 13 June 2012. Superseded for supply offences by Psychoactive Substances Act 2016. | June 2012 |
| **Germany** | Controlled (Anlage II) | Narcotics Act (BtMG), Schedule II. No legitimate medical use. Manufacture, possession, import, export, sale prohibited without license. | 13 Dec 2014 |
| **Sweden** | Controlled | Specific legislation unclear from available sources; confirmed controlled as of 2012. | 2012 |
| **Finland** | Controlled | Confirmed controlled as of 2012. Featured in Finnish DUID and post-mortem toxicology studies. | 2012 |
| **China** | Controlled | Listed as controlled substance. | Oct 2015 |
| **United States** | Not specifically scheduled | No DEA Schedule I–V listing confirmed for 2-DPMP as of date of research. May be covered by Federal Analogue Act (similarity to pipradrol, a Schedule V substance) if intended for human consumption. | — |
| **Australia** | Uncertain | Structural similarity to pipradrol may lead to analogue provisions, but no specific SUSMP scheduling confirmed. | — |
| **Canada** | Uncertain | No specific Controlled Drugs and Substances Act scheduling confirmed. | — |
**⚠️ FLAG: US, Australia, and Canada legal status requires verification from official regulatory databases. Only UK, Germany, Finland, Sweden, and China are confirmed controlled.**
---
## Clinical Trials
No clinical trials registered on ClinicalTrials.gov for desoxypipradrol were found. This is consistent with the substance never advancing to clinical development and having no known therapeutic indications in the modern era.
---
## Community Feedback Analysis
No community feedback submitted in Part A2 of the brief.
---
## Gaps & Flags
### Safety-Critical Unverified Values
1. **⚠️ DB dose ranges appear inconsistent with published case literature.** The DB lists oral doses starting at 0.25 mg threshold up to 8+ mg heavy. The only published human dose reference (Lelièvre et al. 2013 [Ref 13]) describes recreational doses of 10–20 mg. The DB doses may be substantially lower than what users actually take. Editorial review strongly recommended before publishing dose tables.
2. **⚠️ Tramadol interaction severity ("lethal") not confirmed against a specific published report.** The mechanism (seizure threshold lowering, cardiovascular strain) is plausible. However, no primary source describing a fatality specifically from 2-DPMP + tramadol was identified. The classification may be correct but requires editorial sourcing.
3. **⚠️ Half-life "5 days" in DB tolerance section.** No human pharmacokinetic study exists to validate this. The value is likely derived from user reports or community consensus. The French case report shows detectable plasma concentrations at 3–4 days post-ingestion, which is consistent with a long half-life, but formal PK characterization is absent. FLAG for editorial review.
4. **⚠️ No LD50 data found.** The DB "acute toxicity: moderate" is a class-level inference. Deaths have been documented but in polydrug contexts; a specific lethal dose threshold has not been established.
### Data Not Available in Published Literature
- No human pharmacokinetic studies (no bioavailability, Tmax, formal half-life, Vd, protein binding data)
- No CYP enzyme involvement data (no published metabolic characterization)
- No formal metabolite identification studies
- No published withdrawal characterization
- No controlled human efficacy or dose-response studies
- No tolerance build-up rate studies (substance-specific)
- No LD50 in any species from identifiable published sources
- No data on interactions between 2-DPMP and tramadol specifically from published reports
### Animal-Only Data
- Conditioned place preference and self-administration data from Cha et al. 2019 [Ref 2] are from mice only
- In vivo microdialysis dopamine data from Loi et al. 2020 [Ref 1] are from rats
- DAT IC₅₀ values from Loi et al. 2020 [Ref 1] are from rat striatum; human DAT data from Simmler et al. 2014 [Ref 3] is from transfected HEK293 cells
### User-Report-Only Data
- Duration ranges in the DB (total 16–72 hours oral/insufflated) are broadly consistent with case reports but not formally studied
- The DB dose ranges are substantially lower than the only published human dose reference and may derive primarily from community consensus
### Structural Analogy / Class Inference
- Chronic toxicity characterized as "moderate" — inferred from pharmacological class (dopaminergic stimulant similar to cocaine/methylphenidate)
- Dependence characterization as "moderately addictive with high potential for abuse" — supported by rodent models [Ref 2] and pharmacological profiling [Ref 3] but no human addiction epidemiology
- The metabolic pathway described in the DB seed (if any) would be a class inference; no published metabolic data exists
### Unresolved Discrepancies
- **Dose ranges:** DB threshold 0.25 mg vs. Lelièvre 2013 citing 10–20 mg recreational doses — a 40–80 fold discrepancy at the lower end. This is the most significant factual discrepancy found.
- **IUPAC name:** Brief lists this as blank; confirmed as "2-benzhydrylpiperidine" from PubChem.
- **SMILES:** Brief lists as blank; available from PubChem CID 160506.