α-PHP
α-pyrrolidinohexiophenone
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α-PHP (α-pyrrolidinohexanophenone) — also known as PV-7 — is a synthetic stimulant of the pyrovalerone cathinone class. It is the direct chain-extended homolog of α-PVP, with comparable potency. α-PHP is a selective dopamine–norepinephrine reuptake inhibitor,[1] producing its effects by blocking dopamine recycling in the brain's reward and arousal circuits.[2]
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Patented in 1967 as part of a series of pyrrolidine ketones, α-PHP was never developed clinically and remained obscure for nearly five decades.[3] It appeared on illicit markets in Japan in 2014 as a replacement for α-PVP after that compound attracted intense regulatory pressure.[3] It was permanently placed in US Schedule I in June 2022[4] and UN Schedule II in December 2020.
Subjective effects include intense euphoria, physical stimulation, wakefulness, and compulsive redosing urge. The experience is overwhelmingly stimulant — a sharp, clean dopaminergic rush without empathogenic warmth, shaped heavily by route of administration. Paranoia, hallucinations, and agitated dysphoria emerge reliably with extended use or high cumulative doses.
α-PHP carries high abuse liability — animal data place its reinforcing potential equivalent to α-PVP and comparable to methamphetamine.[5] Slow dissociation from the DAT[6] drives compulsive redosing that escalates cumulative cardiovascular and psychiatric risk.[7] No controlled human studies have been conducted; the evidence base rests on animal pharmacology, forensic case series, and structural analogy with α-PVP.
History[edit]
Discovery
α-PHP belongs to a series of α-pyrrolidine ketones first described in a US patent issued in April 1967.[3] The patent covered a broad range of pyrrolidinyl phenyl ketones investigated as potential stimulant agents, but α-PHP — like most compounds in the series — was never advanced to clinical trials or marketed as a pharmaceutical. The patent expired in 1984, removing intellectual property barriers to its synthesis.
Emergence as a novel psychoactive substance
α-PHP first appeared on illicit markets in Japan in 2014,[3] entering circulation in the wake of regulatory action against its structural predecessor α-PVP.[8] The modification was minimal — a hexyl rather than pentyl side chain — but sufficient to initially circumvent scheduling controls targeting α-PVP specifically.[1] The closely related structural analog MDPHP appeared in European seizure data from approximately 2017 onward,[9] extending the same evasion logic to a ring-substituted scaffold.
Scheduling and research
International scheduling followed a well-established trajectory: the WHO Expert Committee on Drug Dependence reviewed α-PHP in December 2019[10] and recommended its placement in UN Schedule II, adopted in December 2020.[3] The US DEA permanently placed α-PHP in Schedule I effective June 2022.[4] No clinical trials have been registered; the published evidence base consists of structure–activity relationship studies,[1] animal behavioral pharmacology,[2] and forensic case series.
The name PV-7 places α-PHP seventh in the pyrovalerone series — a numbering convention reflecting increasing α-alkyl chain length across successive homologs. In online research chemical communities, α-PHP is sometimes discussed alongside α-PVP under the informal umbrella of "pyros," a shorthand for the pyrovalerone cathinone subclass. The compound's emergence exemplifies the "one atom at a time" evasion strategy that defines second-generation novel psychoactive substance markets: each new homolog preserves the pharmacological core while temporarily sidestepping substance-specific scheduling.
Chemistry[edit]
Structural class
α-PHP (α-pyrrolidinohexanophenone) is a synthetic cathinone belonging to the pyrovalerone subclass of substituted phenethylamines. The core structure consists of a phenyl ring bearing a β-keto group next to an α-carbon substituted with both an alkyl chain and a pyrrolidine nitrogen ring. α-PHP carries a six-carbon (hexyl) α-alkyl chain, making it the direct one-carbon extension of α-PVP (pentyl chain) and a two-carbon extension of pyrovalerone (butyl chain).
This progressive chain elongation has been systematically studied for its effects on DAT inhibition potency.[1] Extension from the pentyl to hexyl chain enhances both dopamine and NET inhibition within the pyrovalerone series.[2]
Molecular properties
| Molecular formula | C₁₆H₂₃NO |
| Molecular weight | 245.36 g/mol |
The molecule consists of a phenyl ring bonded to a carbonyl group (the β-keto moiety characteristic of all cathinones), an α-carbon bearing the pyrrolidine ring, and a linear hexyl chain extending from the α-carbon. The pyrrolidine nitrogen is tertiary — a structural motif that distinguishes pyrovalerone cathinones from simpler cathinones and contributes to the class's enhanced dopamine transporter inhibition potency.
Stereochemistry
α-PHP has a single chirality center at the α-carbon, producing R and S mirror-image forms (enantiomers). The compound is typically encountered as a racemic mixture on unregulated markets. Within the related pyrovalerone series, S-enantiomers of α-PVP and MDPV demonstrate markedly slower dissociation from the dopamine transporter than R-enantiomers — a property that directly predicts longer-lasting stimulant effects.[6] Whether this same pattern applies to α-PHP is presumed on structural grounds but remains unconfirmed experimentally.
Physical properties
| Melting point | 108.90 °C |
| Boiling point | 339.06 °C |
| Water solubility (25 °C) | 39.83 mg/L |
| Appearance | Transparent to whitish/yellowish crystals; beige to brownish powder |
Physical property data are from computational and analytical characterization.[3] The low water solubility reflects the lipophilic hexyl chain. α-PHP circulates on unregulated markets as either the free base or a hydrochloride salt; salt-specific physical properties have not been separately published.
Pharmacology[edit]
Mechanism of action
α-PHP works by blocking the proteins that recycle dopamine and norepinephrine back into nerve cells — the DAT (DAT) and NET (NET). This blockade increases the concentration of both neurotransmitters in the spaces between neurons, amplifying reward signaling and physical arousal. α-PHP does not force neurotransmitter release the way amphetamines do — it is strictly a reuptake blocker, placing it in the same mechanistic category as cocaine and methylphenidate.[2]
α-PHP inhibits dopamine reuptake with potency at least equivalent to α-PVP and shows strong selectivity for dopamine over serotonin.[1] It has no meaningful activity at serotonin receptors,[2] which explains the absence of empathogenic or psychedelic qualities in the experience.
A key feature of the pyrovalerone class is that the active form of the molecule (the S-enantiomer) clings to the dopamine transporter longer than cocaine or methylphenidate does.[6] This slow release directly predicts the prolonged and compulsive stimulant effects observed in practice. Substance-specific binding kinetic data have not been published for α-PHP itself, but the pattern is established across the pyrovalerone series.
Pharmacokinetics
No controlled pharmacokinetic study has been conducted for α-PHP in humans. Available data derive from forensic case analyses, laboratory metabolism studies, and review literature.
Routes of administration include oral, nasal (insufflation), sublingual, rectal, intravenous, and inhalation (vaporization).[3]
Half-life: A value of approximately 37 hours has been cited in review literature, with a corresponding total elimination time of approximately 150 hours.[3] This figure likely derives from community estimates rather than a controlled study; no peer-reviewed primary pharmacokinetic study measuring α-PHP half-life in humans has been published. safety citation needed
Metabolism: α-PHP undergoes extensive processing in the liver. Across all published studies, 19 Phase I and 9 Phase II metabolites have been identified.[3] In a 29-case forensic series, the most abundant urinary markers were dihydroxy-pyrrolidinyl-α-PHP and dihydro-α-PHP.[7] No specific liver enzymes have been identified as primarily responsible for α-PHP metabolism, though CYP2C19 and CYP3A4 are candidate enzymes based on related cathinones.[3] inferred
Neuroscience[edit]
Where it acts
α-PHP's primary neural target is the mesolimbic pathway — the brain's core reward circuit. By blocking dopamine recycling in the nucleus accumbens, α-PHP floods this region with dopamine, activating the neurons that encode reward and motivation. Concurrent norepinephrine blockade in the prefrontal cortex and brainstem projections produces the arousal, heightened vigilance, and cardiovascular activation that accompany the stimulant experience.
The slow dissociation from the DAT demonstrated for S-enantiomers of the pyrovalerone class[6] means dopamine stays elevated in the reward circuit longer than equilibrium binding alone would predict — providing a neurochemical explanation for the intense and prolonged reward signaling associated with α-PHP.
Why it matters
The Robinson and Berridge incentive salience model offers the most relevant framework. Sustained dopamine transporter blockade in the mesolimbic pathway is predicted to disproportionately enhance wanting (the motivational drive to redose) relative to liking (actual pleasure).[11] The slow-off kinetics of the pyrovalerone class[6] may amplify this dissociation — driving compulsive redosing even as subjective euphoria diminishes with repeated doses.
Animal brain-reward studies support this picture: α-PHP dose-dependently facilitated brain reward at 5–10 mg/kg in rats, with a magnitude equivalent to α-PVP and comparable to methamphetamine.[5][12]
- Does α-PHP produce the same slow-off dopamine transporter kinetics as α-PVP and MDPV? Structural continuity suggests it should, but direct measurement is lacking.[6]
- Does repeated α-PHP exposure produce lasting changes to dopamine signaling or brain damage? No repeated-dose animal studies have been published — a critical gap given the compound's potency.
- Are sex differences in α-PHP response observed in mice[13] reproduced in humans? If so, this has direct harm reduction implications.
Subjective Effects[edit]
Route of administration decisively shapes the α-PHP experience. Inhalation and intravenous use deliver a rapid, intense onset dominated by euphoric rush and a powerful compulsive redosing urge — the pyrovalerone class's slow release from the DAT[6] sustains reward-circuit activation beyond what the brief peak might suggest. Oral dosing produces a slower, more plateau-like stimulation. Across all routes, the character is overwhelmingly dopaminergic: pronounced physical energy, wakefulness, and sympathomimetic arousal with no empathogenic warmth or perceptual distortion at typical doses. Extended sessions reliably shift the experience toward paranoia, hallucinations, and agitated dysphoria.
Relative to α-PVP, α-PHP produces comparable stimulation intensity and compulsive redosing potential, consistent with their near-identical pharmacology and equivalent brain-reward facilitation in animal models.[5] Compared to cocaine, α-PHP delivers longer-lasting effects per dose — predicted by slower dopamine transporter dissociation[6] — but lacks cocaine's serotonergic component, yielding a "cleaner" stimulant character without empathogenic overtones.
Effect Grid
Pronounced euphoria and strong stimulation dominate the experience. Cognitive euphoria is vivid, thought acceleration is marked, and wakefulness is sustained. The compulsive redosing urge becomes a prominent feature — the slow dissociation of α-PHP from the dopamine transporter sustains incentive motivation even as peak euphoria begins to plateau.
Heart rate and blood pressure are clearly elevated. Appetite suppression is strong, excessive sweating is common, and restlessness may become difficult to manage. Temperature dysregulation and trembling may appear.
Insomnia is virtually guaranteed for many hours after dosing. Extended sessions at this tier reliably escalate toward anxiety and paranoid ideation. Functional impairment is significant.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Shadow people
Insomnia · Pupil dilation · Body high · Dry mouth · Heart rate perception changes · Restlessness · Dehydration sensation · Excessive sweating · Muscle tension · Respiratory stimulation · Tactile euphoria · Bruxism · Spontaneous body sensations · Tingling / electric sensations · Vibrations / buzzing · Headache · Nausea · Sexual arousal enhancement · Trembling · Dizziness · Involuntary body movements
Heart rate perception changes · Restlessness · Dehydration sensation · Excessive sweating · Muscle tension · Respiratory stimulation · Tactile euphoria · Bruxism · Spontaneous body sensations · Tingling / electric sensations · Vibrations / buzzing · Headache · Nausea · Sexual arousal enhancement · Trembling · Dizziness · Involuntary body movements
Multiple thought streams · Thought loops · Cognitive dysphoria · Focus enhancement · Information processing enhancement · Cognitive impairment · Confusion · Thought disorganization · Delusions
Focus enhancement · Information processing enhancement · Cognitive impairment · Confusion · Thought disorganization
Dysphoria
Sociability enhancement · Social connection · Flow state · Ego inflation · Derealization
Derealization
Timeline
Gradual emergence of stimulation and mild mood lift. A subtle increase in wakefulness and alertness develops.
Rising euphoria with increasing heart rate. Appetite fades and focus sharpens noticeably.
Full stimulation and cognitive euphoria. Wakefulness is strong, compulsive redosing urge is at its maximum, and cardiovascular activation is pronounced.
Stimulation fading with residual wakefulness. Emerging dysphoria and restlessness if not redosed.
Lingering wakefulness and mild fatigue with possible low mood. Residual appetite suppression may persist.
⚠ Avoid driving during afterglow — residual stimulation and fatigue may impair reaction time and judgment.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 14 days
- Physical
- Low
- Psychological
- High
- Compulsive redosing
- High
- Dose escalation
- Moderate
- Cross-tol.
- cocaine · methylphenidate · α-PVP
Toxicity
No lethal dose has been established for α-PHP in any species. No therapeutic index exists. All human toxicity data derive from uncontrolled forensic and clinical cases involving multiple substances simultaneously.
Acute toxicity
The acute toxicity pattern resembles other powerful stimulants: agitation, tremors, rapid heart rate, high blood pressure, dangerously elevated body temperature, and in severe cases muscle breakdown.[13] A 29-case forensic series found blood concentrations ranging from 1–83 ng/mL, but near-universal polydrug use (opioids in 60%, benzodiazepines in 35%) prevents attribution of specific toxicity thresholds to α-PHP alone.[7]
Hyperthermia
Dangerously elevated body temperature represents a particularly serious acute risk across stimulant cathinones.[14] The mechanism involves both direct heat generation from stimulant activity and agitation-driven muscular heat production. When combined with enclosed spaces, physical exertion, or co-administration of other stimulants or serotonergic drugs, life-threatening core temperature elevation can develop rapidly.
Reproductive toxicity
A case report documented fetal death associated with maternal use of both MDPHP and α-PHP.[15] Polydrug context prevents definitive attribution, but the case constitutes a serious reproductive safety signal. Two additional cases of neonatal α-PHP exposure were confirmed via meconium analysis.[7] safety citation needed
Genotoxicity
Laboratory testing in human cell lines found that α-PHP itself was not directly mutagenic.[16] However, when processed through simulated liver metabolism, its metabolites demonstrated mutagenic potential. Cell toxicity was observed at concentrations of 35–100 µM. These findings suggest that the genotoxic risk may come from metabolites rather than the parent compound — relevant to chronic exposure scenarios where metabolite accumulation is sustained.
Neurotoxicity
Synthetic cathinones as a class produce neurological harm including brain swelling, seizures, seizure threshold reduction, and excited delirium.[14] α-PHP's minimal serotonin activity reduces its serotonin syndrome risk relative to serotonergic cathinones, but the dopaminergic toxicity profile — including seizure threshold reduction and excited delirium — applies based on mechanism. inferred No direct neurotoxicity studies have been published for α-PHP.
Psychological risks
No controlled studies have characterized the psychological risk profile of α-PHP.
Agitation and aggression were documented in forensic and clinical cases.[7][13] The combination of dopamine activation and norepinephrine arousal produces a high-energy agitated state that can escalate to violent behavior.
Hallucinations and paranoia — both visual and auditory hallucinations, along with paranoid thinking and disorientation — are reported in clinical cases.[7][13] These effects are consistent with excessive dopamine stimulation and are characteristic of high-dose or prolonged stimulant use.
Excited delirium represents the severe end of the spectrum — extreme agitation, altered consciousness, dangerously elevated body temperature, and risk of sudden death. This syndrome is documented across the cathinone class[14] and is particularly associated with high-dose or prolonged stimulant binges. inferred
Compulsive redosing is driven by the pharmacological profile: potent DAT blockade with slow receptor dissociation sustains activation of the brain's wanting circuitry.[6][11] This pattern increases cumulative exposure, raising the probability of cardiovascular, hyperthermic, and psychiatric adverse effects.
Psychiatric effects of synthetic cathinones reviewed systematically include anxiety, depression, and psychotic symptoms persisting beyond acute intoxication in some cases.[17] Whether α-PHP specifically produces persistent psychiatric consequences has not been studied.
Tolerance and dependence
No controlled tolerance or dependence studies have been published for α-PHP.
Abuse liability: Animal brain-reward data provide the strongest signal. α-PHP facilitates brain reward at doses of 5–10 mg/kg in rats, with a magnitude equivalent to α-PVP and comparable to methamphetamine.[5][12] The slow dopamine transporter dissociation of pyrovalerone S-enantiomers[6] may produce more sustained reward signaling than cocaine at equivalent doses, potentially elevating addiction risk beyond what standard potency comparisons would suggest.
Tolerance: No substance-specific data exist. Based on other dopamine-blocking stimulants, acute tolerance to euphoria with preserved cardiovascular stimulation is expected with repeated dosing. Chronic tolerance mechanisms have not been characterized. inferred
Cross-tolerance: Expected with other dopamine/norepinephrine reuptake inhibitors (cocaine, methylphenidate, other pyrovalerone cathinones) based on shared mechanism. No published data specific to α-PHP. inferred
Physical dependence and withdrawal: No clinical withdrawal characterization exists. By analogy with cocaine and methamphetamine, a withdrawal syndrome featuring dysphoria, anhedonia, fatigue, and hypersomnia is expected following heavy or prolonged use.[14] inferred
Compulsive use: The combination of potent dopamine transporter blockade and slow receptor dissociation strongly promotes compulsive redosing.[11] In the forensic case series, co-use of opioids and benzodiazepines in 60% and 35% of cases respectively[7] likely reflects concurrent dependence across multiple substance classes.
Drug interactions
No published drug interaction studies exist for α-PHP. The following interactions are inferred from its mechanism and class-level evidence.
Monoamine oxidase inhibitors (MAOIs): Co-administration with MAOIs (phenelzine, tranylcypromine, moclobemide) presents a risk of life-threatening crisis. Dopamine/NET blockade combined with impaired monoamine breakdown results in dangerous catecholamine accumulation.[14] safety citation needed
Other stimulants: Co-administration with cocaine, amphetamines, or other cathinones produces additive cardiovascular and nervous system stimulation. Cocaine co-use was found in 20% of forensic cases.[7]
Opioids: The pairing of stimulants and opioids was the most common polydrug pattern in forensic data (60% opioid co-use).[7] This combination presents dual risks: the opioid's respiratory depression may be masked by α-PHP stimulation, and the stimulant's cardiovascular effects compound hemodynamic instability.
Serotonergic agents: α-PHP itself has minimal SERT activity,[1] but serotonin syndrome has been reported across the cathinone class.[14] Caution is warranted with SSRIs, SNRIs, triptans, tramadol, and linezolid. safety citation needed
Lithium: lithium may lower seizure threshold, and combination with a stimulant that independently reduces seizure threshold[14] could produce additive risk. No direct data. safety citation needed
Contraindications
No substance-specific contraindication data have been published. The following are inferred from α-PHP's mechanism and class-level evidence.
Absolute contraindications:
- Concurrent MAOI use: Risk of fatal hypertensive crisis.[14] safety citation needed
- Pregnancy: Fetal death associated with α-PHP exposure (polydrug context);[15] neonatal exposure confirmed via meconium.[7] Potent stimulant activity poses inherent risk to fetal blood flow regardless of whether α-PHP is the sole cause.
- Severe heart conditions: Pre-existing conditions including uncontrolled high blood pressure, coronary artery disease, heart failure, and irregular heart rhythm are absolute contraindications given the documented rapid heart rate, high blood pressure, and chest pain in clinical cases.[13] inferred
Relative contraindications:
- Seizure disorders: Synthetic cathinones as a class reduce seizure threshold.[14] inferred
- Psychiatric conditions: Documented hallucinations, paranoia, and delirium[7] suggest that pre-existing psychotic disorders, bipolar disorder, and severe anxiety disorders increase risk.
- Liver impairment: α-PHP undergoes extensive liver metabolism.[3] Impaired liver function could alter metabolite profiles and exposure levels unpredictably. inferred
- Kidney impairment: Impaired kidney function may prolong metabolite exposure. inferred
Harm Reduction[edit]
Forms & Identification
Reagent testing is particularly important for α-PHP because pyrovalerone cathinones are visually indistinguishable from one another — and from many unrelated substances sold as white or off-white powders. The free base and hydrochloride salt forms differ in appearance and vaporization behavior, which affects both testing and dosing decisions. Because α-PHP has never been pharmaceutical-grade, purity varies dramatically between batches; even material from the same source can differ in potency. This variability makes accurate dosing impossible without confirming substance identity and estimating purity first.
Guidelines
- Test every batch with reagent kits before use. Confirm substance identity and check for common adulterants.
- Pre-measure all doses before a session begins. Set a maximum total dose and a hard stop time.
- Have a sober, trusted person present — particularly with inhalation or intravenous routes, which carry the highest compulsive redosing risk.
- Stay hydrated with small, regular sips of water or electrolyte solution. Do not overhydrate.
- Monitor body temperature. If skin feels hot to the touch, move to a cool environment, remove excess clothing, and apply cool water.
- Do not use in enclosed, overheated spaces. Ambient heat compounds stimulant-driven hyperthermia.
- Avoid redosing when euphoria fades — this is the pharmacological profile working as expected, not a signal that more is needed.
- Eat a meal before use. Stimulants suppress appetite, and caloric depletion worsens comedown severity.
Set & Setting
α-PHP's pharmacological profile — potent DAT blockade with slow dissociation — creates a powerful compulsive redosing urge that intensifies as a session continues. Setting matters enormously: using alone removes the external check that another person provides against compulsive redosing, and enclosed, hot environments compound hyperthermia risk. Physical exhaustion, sleep deprivation, and pre-existing anxiety or paranoid tendencies all lower the threshold for the agitated, paranoid states that emerge with escalating cumulative dose.
Deciding on a firm endpoint before beginning — and having a trusted person present who can enforce it — materially reduces the probability of a session escalating into a multi-dose binge.
Aftercare & integration. The comedown from α-PHP follows the standard stimulant pattern: as dopamine levels normalize, dysphoria, fatigue, irritability, and strong sleep drive set in. This is expected, not dangerous — but the temptation to redose to avoid the comedown is the single most common pathway into extended binges.
Sleep is the highest priority. Stimulant use disrupts sleep architecture; allow extended rest without alarm clocks. Darkness and quiet accelerate recovery.
Nutrition follows sleep. Eat calorie-dense, easy-to-digest food as soon as appetite returns. Stimulant-driven appetite suppression means the body is often in caloric deficit.
Hydration — continue regular fluid intake through the comedown period. Electrolyte replacement is useful after extended sessions.
Avoid making significant decisions during the 24–48 hours following use. Cognitive and emotional baseline takes time to restore. If low mood, anhedonia, or anxiety persist beyond 72 hours, consider consulting a healthcare provider.
Recovery & Support
α-PHP's pharmacological profile — potent dopamine reward activation with slow transporter dissociation — produces a compulsive use pattern that can escalate quickly from occasional use to regular bingeing. Recognizing the pattern early is critical: increasing session frequency, rising cumulative dose per session, and difficulty stopping mid-session are warning signs.
Professional support options include addiction medicine physicians, cognitive behavioral therapy (CBT) programs — which have the strongest evidence base for stimulant use disorders — and peer support groups such as SMART Recovery or Narcotics Anonymous. No medication is specifically approved for pyrovalerone cathinone dependence, but treatment approaches developed for cocaine and methamphetamine use disorders are considered applicable.
If compulsive use has developed, abrupt cessation is not physically dangerous (unlike alcohol or benzodiazepine withdrawal), but the psychological withdrawal — dysphoria, anhedonia, fatigue, and strong cravings — benefits from structured support.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
The following signs indicate a medical emergency, not just discomfort:
- Chest pain or pressure
- Seizure or uncontrollable muscle twitching
- Body temperature so high it can be felt through clothing
- Loss of consciousness or inability to respond
- Extreme confusion with violent agitation (excited delirium)
- Breathing difficulties
Immediate steps
- 1. Call emergency services immediately if any of the above signs are present.
- 2. Move the person to a cool, quiet environment. Remove excess clothing.
- 3. If unconscious but breathing, place in the recovery position (on their side, airway clear).
- 4. Apply cool (not ice-cold) water to the neck, armpits, and groin to reduce body temperature.
- 5. Do NOT restrain a severely agitated person unless they are in immediate danger of harming themselves or others — restraint can worsen hyperthermia.
- 6. Do NOT induce vomiting.
- 7. Stay with the person until help arrives. Monitor breathing and consciousness.
What to tell the dispatcher
State the substance name (α-PHP or "a synthetic cathinone stimulant"), the approximate amount used, the time of last dose, the route of administration, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
α-PHP is internationally controlled under Schedule II of the 1971 United Nations Convention on Psychotropic Substances, following the WHO Expert Committee on Drug Dependence critical review in December 2019[10] and formal placement in December 2020.[3] The compound is also independently scheduled in numerous national jurisdictions under both substance-specific and generic novel psychoactive substance legislation.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Temporarily scheduled July 18, 2019; extended July 2021; permanently placed June 1, 2022[4] |
| United Nations | Schedule II (Convention on Psychotropic Substances 1971) | Recommended by WHO ECDD December 2019; placed December 2020[3] |
| United Kingdom | Class B (Misuse of Drugs Act 1971) | Controlled under generic cathinone provisionscitation needed |
| Netherlands | Banned | Controlled under 1971 Vienna Convention implementation; effective October 29, 2021[3] |
| Portugal | Controlled | Law 25/2021, effective May 2021[3] |
| China | Controlled | Under NPS legislation[3] |
| Sweden | Controlled | Under NPS legislation[3] |
| Poland | Controlled | Under NPS legislation[3] |
| Italy | Controlled | Under NPS legislation[3] |
| Canada | Potentially controlled | CDSA analogue provisions may apply; case-by-case determination via structural similaritycitation needed |
| Australia | Potentially controlled | Federal and state analogue laws apply structural similarity testscitation needed |
α-PHP's permanent Schedule I placement in the United States renders the Federal Analogue Act moot for domestic enforcement — the compound is directly scheduled rather than relying on analogue provisions. In jurisdictions without substance-specific scheduling, generic cathinone bans or structural analog laws may apply, though enforcement depends on the specificity of the relevant legislation.
references
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- [4]
- [5] ^abcdTaffe MA, Nguyen JD, Vandewater SA, Grant Y, Dickerson TJ (2021) Effects of α-pyrrolidino-phenone cathinone stimulants on locomotor behavior in female rats. — Drug and Alcohol Dependence doi:10.1016/j.drugalcdep.2021.108910
- [6]