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Substituted phenethylamineamphetamine, methylphenidate, cocaine +1 moreamphetamine, methylphenidate, cocaine, other dopaminergic stimulants show less
Cyclazodone
Cyclazodone is a synthetic stimulant of the oxazolidinone class. It is a close structural relative of pemoline, differing by a single nitrogen modification. It raises dopamine and norepinephrine levels in the brain, producing the focused, wakeful drive characteristic of stimulants.[1][2]
Cyclazodone is a synthetic stimulant of the oxazolidinone class. It is a structural derivative of pemoline, modified with a cyclopropyl group at the nitrogen position. Cyclazodone is a presumed norepinephrine–dopamine reuptake inhibitor, believed to produce its effects by elevating synaptic dopamine and norepinephrine concentrations.[1][2]
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Synthesized in the early 1960s, cyclazodone was patented as a stimulant but never tested in human clinical trials.[3] It remained obscure for over fifty years before appearing on research chemical markets around 2017.[4][5] It now circulates as a bulk powder among nootropic communities seeking alternatives to prescription stimulants.
Subjective effects include focus enhancement, motivation, improved cognitive performance, and mild mood elevation. The experience is task-oriented and context-dependent — structured work feels more absorbing, but the same dose without purposeful activity produces directionless restlessness.[6] Anxiety, restlessness, and appetite suppression are characteristic unwanted effects.
Dependence liability is presumed moderate; the primary toxicity concern is liver damage inherited from the pemoline class. Pemoline caused fatal liver failure in at least 21 patients,[7] and structural similarity to cyclazodone gives no reason to assume that risk is gone.[8] No controlled human study exists; understanding rests on structural analogy, one related-compound case report, and user reports.
History[edit]
Discovery
Cyclazodone was synthesized in the early 1960s at Les Laboratoires Dausse in Paris and disclosed in British patent GB 1,005,738 (1965), describing it as a CNS stimulant and anorexic agent.[9] It received regulatory identifiers[3] but never progressed to human clinical trials, and the compound remained obscure for over fifty years.
Parent class and regulatory history
Cyclazodone's structural family carries a troubled regulatory history. Aminorex, the parent scaffold, was withdrawn in 1968 after causing a 20-fold increase in pulmonary hypertension incidence.[10][11] Pemoline was approved for ADHD in 1975 but withdrawn from most markets by the mid-2000s after causing fatal liver failure.[12][7] A related compound, 4,4'-DMAR, was linked to at least 26 deaths in Europe in 2013.[13]
Emergence as a research chemical
Cyclazodone appeared on research chemical markets around 2017, sold primarily as a bulk nootropic powder.[4][5] A related compound, N-methyl-cyclazodone, emerged at the same time and is metabolized to cyclazodone in the body.[14]
Chemistry[edit]
Structural class
Cyclazodone belongs to the 4-oxazolidinone class — a structural relative of pemoline, differing only at the nitrogen position, where a cyclopropyl group replaces the amino group. This places it within the broader aminorex chemical family.
Molecular identity
| Molecular formula | C₁₂H₁₂N₂O₂ |
| Molecular weight | 216.24 g/mol |
The molecule's core ring contains both a lactone and an imine, with the cyclopropyl group attached to the exocyclic nitrogen.[15]
Pharmacology[edit]
Mechanism of action
Cyclazodone is classified as a norepinephrine–dopamine reuptake inhibitor — it blocks the recycling of dopamine and norepinephrine from synapses, keeping these signals active longer.[1][2] This classification is inferred from structural similarity to pemoline; no published study has directly measured cyclazodone's activity at any molecular target. Some sources claim it also activates trace amine receptors, but no published research supports this.citation needed
Pharmacokinetics
No pharmacokinetic studies exist for cyclazodone in humans or animals. Community reports place oral onset at 20–45 minutes with a total duration of 5–7 hours.[4][6] The half-life is estimated at 4–10 hours based on pemoline reference data,[16] but has not been measured.inferred
N-methyl-cyclazodone, a related compound, is converted to cyclazodone by liver enzymes.[14] The enzymes responsible for cyclazodone's own downstream metabolism have not been identified.
Neuroscience[edit]
Where it acts
No brain imaging or neurochemistry studies have been published for cyclazodone. Based on its presumed dopamine and norepinephrine reuptake inhibitor, it is expected to raise dopamine signaling in the brain's motivation and reward circuits and in the prefrontal regions governing focus and decision-making.inferred
Why it matters
Norepinephrine in the prefrontal cortex follows an inverted-U pattern: moderate increases sharpen focus and working memory, but excessive stimulation tips into anxiety and impaired thinking. This explains why lower doses produce cognitive enhancement while higher doses give way to restlessness.[6]
Cyclazodone's profile — strong motivation with limited euphoria — fits the distinction between dopamine-driven wanting (motivational drive) and hedonic liking (pleasure), suggesting it engages motivational circuitry more than pleasure pathways.inferred
- Does the cyclopropyl modification change cyclazodone's selectivity between dopamine and norepinephrine transporters compared to pemoline?
- Does chronic use at typical human doses produce lasting changes in dopamine signaling or brain structure?
- Does cyclazodone have any serotonergic activity, as some aminorex analogs (such as 4,4'-DMAR) do[17]?
Subjective Effects[edit]
Cyclazodone's character is defined by cognitive drive rather than somatic stimulation or euphoria. The effect is strongly context-dependent: structured tasks feel more absorbing and rewarding, while the same dose without purposeful activity registers as directionless restlessness. The motivation is real, but the hedonic reward is minimal.
The closest comparators are low-dose amphetamine and modafinil. Cyclazodone sits between them: more perceptible than modafinil in onset and motivational push, but without the hedonic warmth and physical activation that characterize amphetamine at equivalent functional doses. It is a tool for work, not recreation.
Synthesized in the early 1960s at Les Laboratoires Dausse in Paris, cyclazodone was patented as a CNS stimulant but never entered clinical trials.[3] The compound remained obscure for over five decades until it appeared on research chemical markets around 2017 as a nootropic.[4][5] It circulates primarily among nootropic communities seeking alternatives to pharmaceutical stimulants.
Subjective effects include focus enhancement, motivation enhancement, cognitive enhancement, and mood elevation. The experience is task-oriented and context-dependent — a clean, productivity-focused stimulation that amplifies engagement with demanding work but produces comparatively little recreational reward at rest.[6] Anxiety, restlessness, and appetite suppression are characteristic unsought effects.
Dependence liability is uncharacterized but presumed moderate based on dopaminergic class data; the primary toxicity concern is potential liver damage inherited from the pemoline class. Pemoline caused fatal liver failure in at least 21 patients[7] — whether cyclazodone shares this risk is unknown, and the structural modification provides no basis for assuming the mechanism has been eliminated.[8] No controlled human study has been published; the current understanding rests on structural analogy, one case report involving a related compound, and user reports.
History[edit]
Discovery
Cyclazodone was synthesized in the early 1960s by researchers at Les Laboratoires Dausse, a French pharmaceutical firm in Paris. The compound was disclosed in British patent GB 1,005,738 (1965), which described it as a central nervous system stimulant and anorexic agent — an N-cyclopropyl structural analog of pemoline designed to improve upon existing oxazolidinone stimulants.[9] It received an International Nonproprietary Name and an FDA identifier[3] but never progressed to human clinical trials, and the compound remained obscure for over fifty years.
Parent class and regulatory history
Cyclazodone's structural lineage carries significant regulatory baggage. Aminorex, the parent scaffold, was withdrawn as an anorectic in 1968 after causing a 20-fold increase in pulmonary hypertension incidence in Switzerland.[10][11] Pemoline, cyclazodone's closest structural analog, was approved for ADHD treatment in 1975 but withdrawn from most markets by the mid-2000s after causing fatal liver failure.[12][7] 4,4'-DMAR, another aminorex derivative, was linked to at least 26 deaths in Europe in 2013.[13]
Emergence as a research chemical
Cyclazodone appeared on online research chemical markets around 2017, marketed primarily as a bulk nootropic powder.[4][5] It attracted interest from nootropic and psychonaut communities as a cognitive enhancer and stimulant alternative to pharmaceutical ADHD medications. N-methyl-cyclazodone, a related and reportedly more potent compound, emerged concurrently; toxicokinetic studies confirmed that N-methyl-cyclazodone is metabolized to cyclazodone as its primary active metabolite.[14]
Chemistry[edit]
Structural class
Cyclazodone belongs to the 4-oxazolidinone structural class, a subset of the broader aminorex family. It shares its parent scaffold with pemoline, differing only by substitution of the 2-amino group with a cyclopropylamino moiety. This modification distinguishes it from other N-alkyl pemoline derivatives such as N-methyl-cyclazodone. The oxazolidinone ring system — featuring a 4-oxo carbonyl absent in strict aminorex derivatives — separates this class from the 2-amino-2-oxazolines.
Molecular identity
| Molecular formula | C₁₂H₁₂N₂O₂ |
| Molecular weight | 216.24 g/mol |
The molecule comprises a 1,3-oxazolidin-4-one ring bearing a phenyl group at C-5 and a cyclopropylimino substituent at C-2. The ring contains both a lactone and an imine functionality, with the exocyclic nitrogen bridging to the cyclopropyl ring.[15]
Stereochemistry
Cyclazodone possesses one stereocenter at C-5 (the carbon bearing the phenyl group) and exists as a racemic mixture. No published data characterize the relative potency of individual enantiomers.[3] Whether enantioselective activity occurs — as is typical for chirality monoamine transporter ligands — remains uninvestigated.
Physical properties
Cyclazodone has a LogP of 1.219, indicating moderate lipophilicity consistent with oral absorption and CNS penetration.[15] No published data describe the compound's appearance, melting point, or aqueous solubility. Stability under standard storage conditions has not been formally characterized.
Pharmacology[edit]
Mechanism of action
Cyclazodone is classified as a norepinephrine–dopamine reuptake inhibitor with stimulant actions comparable to dexamphetamine.[1][2] This classification is inferred entirely from structural analogy to pemoline and the broader aminorex class — no published study has directly measured cyclazodone's binding affinity or functional activity at any molecular target.
Pemoline, its closest characterized relative, functions primarily as a dopamine reuptake inhibitor with weak releasing properties and minimal noradrenergic activity relative to amphetamine.[1] Whether the cyclopropyl substitution alters transporter selectivity or introduces additional pharmacological activity is unknown.
Some community sources claim cyclazodone activates TAAR1 (TAAR1). No published research supports this claim.citation needed
Pharmacokinetics
No formal pharmacokinetic studies exist for cyclazodone in humans or animals. Community consensus places oral onset at 20–45 minutes with a total duration of 5–7 hours.[4][6]
Pemoline, as the closest pharmacokinetic reference, reaches peak blood levels at 2–4 hours, has an half-life of 7–12 hours, and is approximately 50% excreted unchanged in urine.[16]
N-methyl-cyclazodone is metabolized to cyclazodone as its primary active metabolite via a liver enzyme pathway.[14] The enzymes responsible for cyclazodone's own downstream metabolism have not been identified. Oral bioavailability and elimination half-life have not been measured; based on the reported duration of effects and pemoline reference data, a half-life of 4–10 hours is plausible but unconfirmed.inferred
Neuroscience[edit]
Where it acts
No direct neuroimaging or neurochemistry studies have been published for cyclazodone. Based on its presumed dopamine and norepinephrine reuptake inhibitor, the compound is expected to increase dopamine signaling in the brain's reward and motivation circuits (mesolimbic pathway) and in prefrontal regions governing executive function. The reward pathway component would account for reported motivation enhancement and mild mood lift, while prefrontal effects underlie the cognitive enhancement — focus enhancement, verbal fluency, and sustained attention — that users describe as the compound's primary appeal.inferred
Why it matters
Norepinephrine enhancement in the prefrontal cortex follows an inverted-U pattern: moderate increases sharpen focus and working memory, but excessive stimulation tips into anxiety and cognitive impairment. This framework explains user reports of clean cognitive enhancement at lower doses deteriorating into restlessness at higher doses.[6]
Cyclazodone's reported profile — strong motivation with limited euphoria — also maps onto theories distinguishing dopamine-driven "wanting" (motivational drive) from hedonic "liking," suggesting preferential activation of motivational circuitry over pleasure pathways.inferred
- Does the cyclopropyl modification change cyclazodone's selectivity between dopamine and norepinephrine transporters compared to pemoline?
- Does chronic use at typical human doses produce lasting changes in dopamine signaling or brain structure?
- Does cyclazodone have any serotonergic activity, as some aminorex analogs (such as 4,4'-DMAR) do[17]?
Subjective Effects[edit]
Cyclazodone's experiential character is defined by cognitive enhancement rather than somatic stimulation or euphoria. The compound amplifies engagement with demanding work in a context-dependent manner: structured tasks feel more absorbing and rewarding, while the same dose without purposeful activity can register as directionless restlessness. The effect scales predictably — lower doses produce subtle sharpening of focus, while higher doses introduce physical tension and anxiety that erode the cognitive benefit.
The closest experiential comparators are low-dose amphetamine and modafinil. Cyclazodone sits between the two: more perceptible than modafinil in onset and motivational push, but lacking the hedonic warmth and peripheral activation that characterize amphetamine at equivalent functional doses.
Effect Grid
Clear cognitive enhancement defines this tier — focus enhancement, thought organization, analysis enhancement, and information processing improvement are prominent. Motivation enhancement is strong, and many users describe this as the optimal dose range for sustained productive work. Verbal fluency may improve. Cognitive euphoria is mild but present.
Appetite suppression is moderate. Physical stimulation is noticeable but not dominant — cyclazodone's character remains more cognitive than somatic across all tiers. Mild dry mouth, dehydration sensation, and slight restlessness may occur. Pupil dilation is possible.
This range (15–25 mg) represents the community consensus for functional/nootropic use. Insomnia is likely if taken after midday. Total duration is 5–7 hours.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual drifting · Object transformations
Pupil dilation · Dry mouth · Insomnia · Muscle tension · Dehydration sensation · Restlessness · Heart rate perception changes · Physical fatigue · Excessive sweating · Respiratory stimulation · Body high · Bruxism · Sexual arousal enhancement · Headache · Spontaneous body sensations · Tingling / electric sensations · Trembling · Vibrations / buzzing · Motor control enhancement · Sexual arousal suppression · Tactile euphoria · Nausea · Pain suppression · Abnormal heartbeat · Increased urination · Dizziness · Tactile hallucination
Muscle tension · Dehydration sensation · Restlessness · Heart rate perception changes · Physical fatigue · Excessive sweating · Respiratory stimulation · Body high · Bruxism · Sexual arousal enhancement · Headache · Spontaneous body sensations · Tingling / electric sensations · Trembling · Vibrations / buzzing · Motor control enhancement · Sexual arousal suppression · Tactile euphoria · Nausea · Pain suppression · Increased urination · Dizziness · Tactile hallucination
Cognitive fatigue · Analysis enhancement · Motivation enhancement · Information processing enhancement · Thought organization · Cognitive dysphoria · Cognitive flexibility · Immersion enhancement · Pattern recognition enhancement · Memory enhancement · Aesthetic enhancement · Multiple thought streams · Novelty enhancement · Creativity enhancement · Humor enhancement · Language enhancement · Motivation suppression · Cognitive impairment · Thought loops · Thought deceleration
Thought organization · Cognitive dysphoria · Cognitive flexibility · Immersion enhancement · Pattern recognition enhancement · Memory enhancement · Aesthetic enhancement · Multiple thought streams · Novelty enhancement · Creativity enhancement · Humor enhancement · Language enhancement · Motivation suppression · Cognitive impairment · Thought loops · Thought deceleration
Anhedonia · Dysphoria · Emotional lability · Emotional suppression · Anxiety suppression · Empathy enhancement · Mania
Emotional suppression · Anxiety suppression · Empathy enhancement
Sociability enhancement · Disinhibition · Craving · Social connection · Depersonalization
Depersonalization
Timeline
First perceptible effects emerge as gradual alertness increase. Subtle shift in baseline awareness without clear stimulation.
Building stimulation with focus sharpening and mild physical activation. Cognitive engagement begins to increase noticeably.
Full cognitive enhancement — maximum focus, motivation, and information processing. Appetite suppressed. Character is predominantly cognitive rather than somatic.
Gradual decline in stimulation. Fatigue begins emerging as cognitive enhancement thins. Appetite may start returning.
Residual wakefulness with possible fatigue and emotional flatness. Appetite returning to baseline.
⚠ Avoid driving or operating machinery if experiencing fatigue, particularly following strong or heavy doses.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- High
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 10.5 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Low
- Cross-tol.
- amphetamine · methylphenidate · cocaine
Toxicity
No lethal dose, therapeutic index, or controlled toxicity data exist for cyclazodone in any species.safety citation needed
Liver damage (class-based concern)
The primary concern is potential liver damage inherited from the pemoline class. Pemoline caused at least 21 cases of liver failure, 13 requiring transplant or resulting in death.[7] Reactions were unpredictable — sometimes appearing after months or years of uneventful use,[18][19] possibly through an autoimmune mechanism.[20] Pemoline was ultimately withdrawn from the US market.[12][21]
No cyclazodone-specific liver failure has been published, but a case involving N-methyl-cyclazodone — which converts to cyclazodone in the body — showed liver enzyme elevation to about 2.5 times normal.[8][4] Whether cyclazodone causes the same unpredictable liver failure as pemoline is a critical unresolved safety question.safety citation needed
Heart and circulation
The N-methyl-cyclazodone case documented a critically prolonged QTc interval (526 ms) — placing the patient at risk of fatal heart rhythm disturbance — and a widened QRS interval (140 ms), which responded to sodium bicarbonate treatment.[8] One user report describes heart rate reaching 200 BPM at high doses.[22]
Aminorex, the parent compound of this structural class, caused a 20-fold increase in pulmonary hypertension incidence.[10][11] Whether cyclazodone carries the same risk is unknown.safety citation needed
Muscle breakdown
Severe muscle breakdown (creatine kinase 2954 U/L) was documented in the N-methyl-cyclazodone case, occurring during sustained involuntary movements and extreme dosing (5 g over 5 days).[8]
Movement disorders
The same case featured involuntary, irregular, dance-like movements affecting the entire body — consistent with excessive dopamine stimulation of motor control circuits.[8]
Detection
Standard drug tests do not detect cyclazodone. The clinical case returned negative on conventional urine screening despite massive exposure. Specialized laboratory analysis (liquid chromatography–mass spectrometry) is required for definitive identification.[8]
Psychological risks
Community reports describe anxiety at higher doses, compulsive redosing, irritability and emotional flattening at strong doses, and rebound effect depression upon stopping daily use.[6] As a stimulant, cyclazodone carries a class-level risk of paranoia, hallucinations, and delusional thinking at high doses or with sleep deprivation, though no published cases exist.inferred
Tolerance and dependence
Tolerance develops with repeated use. Community estimates place the tolerance half-life at approximately 5 days, with full reset at approximately 1.5 weeks;[4] these values are unverified.safety citation needed Cross-tolerance is expected with amphetamine, methylphenidate, and cocaine.inferred
Users report fatigue and low mood after stopping daily use.[6] Dependence liability is presumed moderate. Pemoline was classified as Schedule IV, indicating recognized but limited abuse potential; whether cyclazodone has greater or lesser reinforcing properties is unknown.
Drug Interactions
Tramadol
Combining cyclazodone with tramadol is designated lethal in severity. Tramadol lowers the seizure threshold and acts as a norepinephrine reuptake inhibitor; cyclazodone adds to that monoamine burden, substantially increasing the risk of seizures, cardiovascular disturbance, and serotonin syndrome.[23][24]safety citation needed
MDMA
Combining cyclazodone with MDMA is designated dangerous. MDMA floods the brain with serotonin, dopamine, and norepinephrine simultaneously; cyclazodone amplifies cardiovascular overstimulation, overheating, and serotonin toxicity risk.[13]safety citation needed
SSRIs
The N-methyl-cyclazodone toxicity case involved concurrent fluoxetine.[8] Fluoxetine may alter cyclazodone's metabolism, and the combined monoaminergic load may increase cardiovascular and neurological risk. This interaction is uncharacterized.
MAO inhibitors
Combining cyclazodone with monoamine oxidase inhibitors would be expected to produce dangerously high monoamine levels and potentially fatal blood pressure crisis. This is a class-level absolute contraindication.inferred
Alcohol
No published data exist. As with other stimulants, the combination may mask alcohol's sedative effects, leading to dangerous intake levels and increased cardiovascular strain.
Contraindications
9 knownNo cyclazodone-specific contraindication data exist. The following are inferred from class pharmacology:
Absolute (class-inferred):
- Liver impairment or pre-existing liver disease: The pemoline-class liver damage risk makes any hepatic compromise a basis for absolute avoidance[7][18]
- Concurrent MAO inhibitor use: Risk of fatal monoamine accumulationinferred
- Concurrent tramadol: Lethal interaction risk[23]
- Pre-existing heart rhythm abnormality or prolonged QTc: Documented with N-methyl-cyclazodone[8]
Relative (class-inferred):
- Heart disease: Elevated heart rate and blood pressure are expected pharmacological effects
- History of stimulant-induced psychosis: Class-level risk
- Concurrent SSRI use: Potential for altered metabolism and combined monoaminergic burden
- Seizure disorders: Effects on seizure threshold are variable; absence of data warrants caution
- Pregnancy: No reproductive or developmental toxicity data exist
Harm Reduction[edit]
Forms & Identification
Cyclazodone circulates almost exclusively as a bulk powder sold through online research chemical vendors. Batch purity and identity are unverifiable without analytical testing.
N-methyl-cyclazodone is closely related and reportedly more potent — mislabeling between the two is a realistic concern with direct dosing consequences. Reagent testing has limited utility within this structural class. A drug checking service using mass spectrometry or infrared spectroscopy is required for reliable identification.
Guidelines
- Test any new batch with an analytical service before use — visual inspection cannot distinguish cyclazodone from N-methyl-cyclazodone or other white powders
- Use a milligram-precision scale (0.001 g); volumetric dosing from solution is preferable for doses below 15 mg
- Begin at the low end of the common range and wait at least 90 minutes before considering redosing — onset can be delayed
- Avoid daily use; tolerance builds within days and rebound effect symptoms follow sustained use
- Monitor for signs of liver distress (unexplained fatigue, dark urine, abdominal pain, yellowing of skin or eyes) during and after any period of use
- Stay hydrated and maintain regular meals — appetite suppression can mask dehydration and caloric deficit
- Set a firm stopping time; do not dose within 6–8 hours of intended sleep
Set & Setting
Cyclazodone's effects are strongly context-dependent. The compound amplifies engagement with focused work but produces restlessness without purposeful activity. First experiences are best undertaken during a planned work session in a familiar, comfortable environment with no obligations that would become stressful if anxiety emerges.
Avoid combining with sleep deprivation — this amplifies both anxiety and psychosis risk with stimulants of this type.
Aftercare & integration. After cyclazodone use, prioritize sleep. Evening doses can delay sleep onset by several hours. Eat a full meal even if appetite is suppressed, and rehydrate.
If daily use has occurred for more than a few days, expect 1–3 days of fatigue, low motivation, and mild depressed mood as dopamine signaling resets. This is temporary and does not require medical intervention unless severe. Avoid compensating with higher doses or other stimulants during this period.
Recovery & Support
Cyclazodone's dependence potential is not formally characterized, but daily users report difficulty stopping due to rebound fatigue and decreased motivation. If use has become compulsive or is interfering with daily life, professional support is appropriate.
Stimulant-focused addiction services, cognitive behavioral therapy, and peer support groups (such as SMART Recovery) are relevant resources. A healthcare provider should be informed of the specific substance — cyclazodone will not appear on standard drug screens.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Chest pain or pressure
- Heart rate that feels dangerously fast or irregular
- Seizure activity or involuntary full-body movements
- Signs of severe overheating (confusion, hot dry skin, body temperature you can feel through clothing)
- Yellowing of the eyes or skin (may indicate acute liver injury)
- Loss of consciousness
Immediate steps:
- 1. Call emergency services immediately if any of the above are present
- 2. Place an unconscious person in the recovery position (on their side, airway clear)
- 3. Do not restrain someone having involuntary movements — clear the area of objects that could cause injury
- 4. Keep the person cool if overheating is suspected (remove excess clothing, apply cool water)
- 5. Do not induce vomiting
What to tell the dispatcher: Name the substance (cyclazodone or N-methyl-cyclazodone), the amount taken, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
Cyclazodone is not scheduled under the UN Convention on Psychotropic Substances (1971). Most regulatory action has occurred through blanket psychoactive substance legislation rather than specific scheduling. It is listed as a prohibited stimulant by the World Anti-Doping Agency (WADA).[1]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled; analog risk | Pemoline is Schedule IV. The Federal Analogue Act (21 U.S.C. § 813) may apply if intended for human consumption, treating it as a Schedule I/II analog |
| United Kingdom | Banned (Psychoactive Substances Act 2016) | Covered by blanket prohibition on psychoactive substances not specifically exempted[25] |
| Germany | Not controlled (legal gray area) | Not scheduled under BtMG or NpSG; may fall under AMG (Medicines Act) if marketed for human consumption |
| Switzerland | Not controlled (legal gray area) | Not listed in controlled substance schedules A–D |
| Australia | Banned | Covered by blanket psychoactive substance prohibition |
| New Zealand | Banned | Covered by blanket psychoactive substance prohibition |
| Canada | Potentially restricted | Federal analog provisions may apply; no specific scheduling |
Analog law considerations
In the United States, cyclazodone's relationship to Schedule IV pemoline creates legal ambiguity. The Federal Analogue Act applies only to substances substantially similar to Schedule I or II controlled substances intended for human consumption — pemoline's Schedule IV status may limit the Act's reach, but legal interpretation in this area is evolving and jurisdiction-dependent.citation needed
Legal status changes frequently and varies by jurisdiction. This information reflects the situation as of May 2026 and is not legal advice.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- High
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 10.5 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Low
- Cross-tol.
- amphetamine · methylphenidate · cocaine
Toxicity
No lethal dose, therapeutic index, or controlled toxicity data exist for cyclazodone in any species.safety citation needed
Liver damage (class-based concern)
The primary toxicity concern is potential liver damage inherited from the pemoline class. Pemoline caused at least 21 cases of liver failure, 13 requiring transplantation or resulting in death.[7] Approximately 1–2% of pemoline patients developed elevated liver enzymes, and reactions were unpredictable — sometimes appearing after months or years of uneventful use.[18][19] A possible autoimmune mechanism was proposed,[20] and pemoline was ultimately withdrawn from the US market.[12][21]
No cyclazodone-specific liver damage case has been published. However, the only clinical case involving cyclazodone — as a confirmed metabolite of N-methyl-cyclazodone — showed liver enzyme elevation to approximately 2.5 times the upper limit of normal.[8] Community sources warn of liver damage with heavy or sustained use.[4]
Whether cyclazodone causes the same kind of unpredictable liver failure as pemoline is a critical unresolved safety question. The structural similarity — differing at only one nitrogen substituent — provides no basis for assuming the risk has been eliminated.safety citation needed
Heart and circulation
The N-methyl-cyclazodone case documented critically prolonged QTc interval (526 ms, placing the patient at risk of fatal heart rhythm disturbance) and widened QRS interval (140 ms), the latter responding to sodium bicarbonate treatment.[8]
Elevated heart rate and blood pressure are expected effects of catecholaminergic stimulation. One user report describes heart rate reaching 200 BPM at high doses.[22]
Aminorex, the parent compound of this structural class, caused a 20-fold increase in pulmonary hypertension incidence.[10][11] Whether the oxazolidinone ring system protects against this risk is unknown.safety citation needed
Muscle breakdown
Severe muscle breakdown (creatine kinase 2954 U/L) was documented in the N-methyl-cyclazodone case, occurring in the context of sustained involuntary movements and extreme dosing (5 g over 5 days).[8]
Movement disorders
The same case featured involuntary, irregular, dance-like movements (chorea) affecting the entire body, consistent with excessive dopamine stimulation of motor control circuits.[8]
Detection
Standard drug screening does not detect cyclazodone. The clinical case returned negative on conventional urine tests despite massive exposure. Specialized laboratory analysis (liquid chromatography–mass spectrometry) is required for definitive identification.[8]
Psychological risks
No controlled studies have assessed cyclazodone's psychological adverse effects. Community reports describe anxiety at higher doses (above the common range), compulsive redosing consistent with dopaminergic reinforcement, irritability and emotional flattening at strong doses, and rebound effect depression and fatigue upon stopping daily use.[6]
As a catecholaminergic stimulant, cyclazodone carries class-level risk of stimulant-induced psychosis at high doses or with sleep deprivation, though no cases have been published.inferred
Tolerance and dependence
Tolerance develops with repeated use, consistent with the stimulant class. Community estimates place the tolerance half-life at approximately 5 days, with full reset at approximately 1.5 weeks.[4] These values are unverified.safety citation needed
Cross-tolerance is expected with other dopaminergic stimulants (amphetamine, methylphenidate, cocaine).inferred
No formal dependence characterization exists. Users report fatigue and low mood upon discontinuation after daily use,[6] consistent with dopaminergic rebound. Dependence liability is presumed moderate based on the compound's reportedly limited euphoric ceiling. Pemoline was classified as Schedule IV, indicating recognized but limited abuse potential; whether cyclazodone has greater or lesser reinforcing properties is unknown.
Drug Interactions
Tramadol
The combination of cyclazodone with tramadol is designated lethal in severity. Tramadol lowers seizure threshold and acts as a serotonin–norepinephrine reuptake inhibitor; the first reported tramadol fatality involved combination with monoaminergic agents.[23] Cyclazodone's norepinephrine reuptake inhibitor additively increases the monoamine burden, substantially elevating risk of seizures, serotonin syndrome features, and heart rhythm disturbance.[24]safety citation needed
MDMA
Combining cyclazodone with MDMA is designated dangerous. MDMA releases serotonin, dopamine, and norepinephrine simultaneously; co-administration compounds risks of overheating, cardiovascular overstimulation, and serotonin toxicity. Aminorex analogs with serotonergic activity have been linked to fatalities.[13]safety citation needed
SSRIs
The N-methyl-cyclazodone toxicity case involved concurrent fluoxetine.[8] Fluoxetine may alter cyclazodone metabolism, and the combined monoaminergic burden may increase cardiovascular and neurological risk. This interaction is uncharacterized.
MAO inhibitors
As a catecholaminergic reuptake inhibitor, cyclazodone combined with monoamine oxidase inhibitors would be expected to produce dangerously high monoamine levels and potentially fatal blood pressure crisis. This is a class-level absolute contraindication.inferred
Alcohol
No published data exist. As with other stimulants, the combination may mask alcohol's sedative effects, leading to dangerous intake levels and increased cardiovascular strain.
Contraindications
9 knownNo cyclazodone-specific contraindication data exist. The following are inferred from class pharmacology:
Absolute (class-inferred):
- Liver impairment or pre-existing liver disease: The pemoline-class liver damage risk makes any hepatic compromise a basis for absolute avoidance[7][18]
- Concurrent MAO inhibitor use: Risk of fatal monoamine accumulationinferred
- Concurrent tramadol: Lethal interaction risk[23]
- Pre-existing heart rhythm abnormality or prolonged QTc: Documented with N-methyl-cyclazodone[8]
Relative (class-inferred):
- Heart disease: Elevated heart rate and blood pressure are expected pharmacological effects
- History of stimulant-induced psychosis: Class-level risk
- Concurrent SSRI use: Potential for altered metabolism and combined monoaminergic burden
- Seizure disorders: Effects on seizure threshold are variable; absence of data warrants caution
- Pregnancy: No reproductive or developmental toxicity data exist
Harm Reduction[edit]
Forms & Identification
Cyclazodone circulates almost exclusively as a bulk powder sold through online research chemical vendors. The absence of pharmaceutical-grade manufacturing means batch purity and identity are unverifiable without analytical testing. Because cyclazodone and N-methyl-cyclazodone are closely related — and the latter metabolizes to the former — mislabeling between the two is a realistic concern with direct dosing implications, as N-methyl-cyclazodone is reportedly more potent.
Reagent testing has limited utility for confirming identity within this structural class. If available, send a sample to a drug checking service that uses mass spectrometry or infrared spectroscopy for definitive identification.
Guidelines
- Test any new batch with an analytical service before use — visual inspection cannot distinguish cyclazodone from N-methyl-cyclazodone or other white powders
- Use a milligram-precision scale (0.001 g); volumetric dosing from solution is preferable for doses below 15 mg
- Begin at the low end of the common range and wait at least 90 minutes before considering redosing — onset can be delayed
- Avoid daily use; community reports suggest tolerance builds within days and rebound effect symptoms follow sustained use
- Monitor for signs of liver distress (unexplained fatigue, dark urine, abdominal pain, yellowing of skin or eyes) during and after any period of use
- Stay hydrated and maintain regular meals — stimulant appetite suppression can mask dehydration and caloric deficit
- Set a firm stopping time; do not dose within 6–8 hours of intended sleep
Set & Setting
Cyclazodone's effects are strongly context-dependent. The compound amplifies engagement with structured tasks but can produce purposeless restlessness without productive activity. First experiences are best undertaken during a planned work session, in a familiar and comfortable environment, with no obligations that would become stressful if anxiety emerges.
Avoid combining with sleep deprivation, which amplifies both anxiety and psychosis risk with catecholaminergic stimulants.
Aftercare & integration. Stimulant comedowns are primarily physical. After cyclazodone use, prioritize sleep — the compound's duration means evening doses can delay sleep onset by several hours. Eat a full meal even if appetite is suppressed, and rehydrate.
If daily use has occurred for more than a few days, expect 1–3 days of fatigue, low motivation, and mild depressed mood as dopamine signaling recalibrates. This is temporary and does not require medical intervention unless severe. Avoid compensating with higher doses or other stimulants during this period.
Recovery & Support
Cyclazodone's dependence potential is not formally characterized, but daily users report difficulty stopping due to rebound fatigue and decreased motivation. If use has become compulsive or is interfering with daily functioning, professional support is appropriate.
Stimulant-focused addiction services, cognitive behavioral therapy, and peer support groups (such as SMART Recovery) are relevant resources. A healthcare provider should be informed of the specific substance, as cyclazodone will not appear on standard drug screens.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Chest pain or pressure
- Heart rate that feels dangerously fast or irregular
- Seizure activity or involuntary full-body movements
- Signs of severe overheating (confusion, hot dry skin, body temperature you can feel through clothing)
- Yellowing of the eyes or skin (may indicate acute liver injury)
- Loss of consciousness
Immediate steps:
- 1. Call emergency services immediately if any of the above are present
- 2. Place an unconscious person in the recovery position (on their side, airway clear)
- 3. Do not restrain someone having involuntary movements — clear the area of objects that could cause injury
- 4. Keep the person cool if overheating is suspected (remove excess clothing, apply cool water)
- 5. Do not induce vomiting
What to tell the dispatcher: Name the substance (cyclazodone or N-methyl-cyclazodone), the amount taken, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
Cyclazodone is not scheduled under the UN Convention on Psychotropic Substances (1971). Its parent compound aminorex and 4-methylaminorex are Convention Schedule I substances, but cyclazodone's oxazolidinone ring system places it outside existing international scheduling frameworks as of May 2026. Most regulatory action has occurred through blanket psychoactive substance legislation rather than specific scheduling.
Cyclazodone is listed as a prohibited stimulant by the World Anti-Doping Agency (WADA).[1]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled; analog risk | Pemoline is Schedule IV. The Federal Analogue Act (21 U.S.C. § 813) may apply if intended for human consumption, treating it as a Schedule I/II analog |
| United Kingdom | Banned (Psychoactive Substances Act 2016) | Covered by blanket prohibition on psychoactive substances not specifically exempted[25] |
| Germany | Not controlled (legal gray area) | Not scheduled under BtMG or NpSG; may fall under AMG (Medicines Act) if marketed for human consumption |
| Switzerland | Not controlled (legal gray area) | Not listed in controlled substance schedules A–D |
| Australia | Banned | Covered by blanket psychoactive substance prohibition |
| New Zealand | Banned | Covered by blanket psychoactive substance prohibition |
| Canada | Potentially restricted | Federal analog provisions may apply; no specific scheduling |
Analog law considerations
In jurisdictions with structural analog provisions (primarily the United States), cyclazodone's relationship to Schedule IV pemoline creates regulatory ambiguity. The Federal Analogue Act applies only to substances "substantially similar" to Schedule I or II controlled substances intended for human consumption. Pemoline's Schedule IV status complicates this — cyclazodone is not strictly an analog of a Schedule I/II substance, potentially limiting the Act's applicability. Legal interpretation in this area is evolving and jurisdiction-dependent.citation needed
Frequently asked questions
How long does Cyclazodone last?
Total duration by route of administration — Oral: 5 – 7 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for Cyclazodone?
Psychedex publishes a dosage table for Cyclazodone on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with Cyclazodone?
The highest-severity documented interactions for Cyclazodone: Alpha-2 adrenergic receptor antagonist (Dangerous), Amphetamines (Dangerous), Anticholinergics (Dangerous), Antipsychotics (Dangerous), Caffeine (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is Cyclazodone addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for Cyclazodone: tolerance builds moderate; full reset takes 10.5 days; cross-tolerance develops with amphetamine, methylphenidate, cocaine, other dopaminergic stimulants. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcDocherty JR (2008) Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA). — British Journal of Pharmacology doi:10.1038/bjp.2008.124
- [2] ^abLuethi D, Liechti ME (2020) Designer drugs: mechanism of action and adverse effects — Archives of Toxicology doi:10.1007/s00204-020-02693-7
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references
- [1] ^abcdDocherty JR (2008) Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA). — British Journal of Pharmacology doi:10.1038/bjp.2008.124
- [2] ^abLuethi D, Liechti ME (2020) Designer drugs: mechanism of action and adverse effects — Archives of Toxicology doi:10.1007/s00204-020-02693-7
- [3]
- [4]
- [5]
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