Cyclazodone
2-(cyclopropylamino)-5-phenyl-1 · 3-oxazol-4-one · cyclopropyl-pemoline
Last updated
At a glance
Overview
Why Cyclazodone#
Cyclazodone is an oxazolinone stimulant — a cyclopropyl analog of pemoline, sitting in the same chemical family as thozalinone and aminorex. The community runs it for one reason: it produces clean, long-acting dopaminergic stimulation with strong anorectic effects, at oral doses around 10–15mg, without the jittery sympathetic load of an amphetamine. Nootropic-focused users reach for it on deep-work days; physique-focused users use it situationally as an appetite suppressant on a cut.
The compound was patented in the 1960s by Laboratoires Dausse as an "excitant" with anti-fatigue, locomotor-stimulating, and appetite-suppressing properties. It never reached clinical development, so all dose-finding lives in the research-chemical community and in the structural analogy to pemoline.
"Compounds in the aminorex–oxazolinone family — including pemoline analogs — act as weak dopamine and noradrenaline releasers characterized by prominent CNS-stimulant effects and relatively low cardiovascular toxicity compared to amphetamines." — Docherty, Br J Pharmacol 2008
The appeal is the profile: ~6–10h of focused stimulation from a single oral dose, reliable appetite suppression, and a subjective "cleanness" that experienced users describe as closer to methylphenidate than to amphetamine. The catch is the parent compound — pemoline was withdrawn from the market for fulminant hepatic failure, and cyclazodone shares the same oxazolinone backbone. That single fact governs how the community runs it: low dose, low frequency, with LFT monitoring.
The sections below cover documented cyclazodone dosage tiers, the N-methyl-cyclazodone (NMC) prodrug variant, stacking with racetams and cholinergics, the anorectic protocol on a cut, the hepatic and cardiovascular side-effect profile, and the frequency discipline that separates sustainable use from the toxicology case reports.
How Cyclazodone works
Cyclazodone is a centrally acting oxazolinone stimulant in the aminorex / pemoline family. Its pharmacology has never been formally mapped in a binding-panel or microdialysis study — what is known is extrapolated from the well-characterised parent compound pemoline and the structurally adjacent thozalinone, plus the original American Cyanamid and Laboratoires Dausse patent pharmacology from the 1960s. The mechanism is best understood as weak monoamine release plus reuptake inhibition, biased toward dopamine and noradrenaline, with minimal serotonergic action.
Dopamine and Noradrenaline Release#
The oxazolinone scaffold acts on the dopamine and noradrenaline transporters as a weak releaser, raising extracellular DA and NA in the prefrontal cortex and striatum. Unlike amphetamines, the chemotype has limited affinity for the serotonin transporter, which explains the cleaner cognitive-stimulant profile (focus, motor activation, anti-fatigue) reported in subjective accounts and the relative absence of euphoria or hallucinatory effects.
"Compounds in the aminorex–oxazolinone family — including pemoline analogs — act as weak dopamine and noradrenaline releasers characterized by prominent CNS-stimulant effects and relatively low cardiovascular toxicity compared to amphetamines." — Docherty JR, British Journal of Pharmacology, 2008
The practical correlate for the reader: cognitive output is the lead effect. Elevated prefrontal DA/NA tone drives the working-memory, sustained-attention, and motivational lift that defines the dose window. Locomotor and sympathomimetic effects scale with dose but lag behind the cognitive signal at 5–15 mg.
Locomotor Activation and Anti-Fatigue Signalling#
The original patent pharmacology characterised cyclazodone as an "excitant" with sustained locomotor and anti-fatigue effects in rodents, with a long duration consistent with the 6–10 h subjective window users describe.
"Cyclazodone was an 'excitant' with anti-fatigue, anorectic, and locomotor-stimulating effects at 10 mg/kg in mice, persisting for more than 6 hours and peaking at 120–180 minutes." — De Marne V et al., GB Patent 1,005,738 (Laboratoires Dausse), 1965
The 120–180 min peak in the rodent data maps cleanly onto the ~2.5 h Tmax reported in community accounts. This is also why dosing twice in a day stacks badly — the second dose lands on a still-rising or only partially cleared first exposure, with predictable consequences for sleep that night and baseline mood the day after.
Hypothalamic Anorectic Action#
Anorexia is the single most reliable subjective effect at low dose and was the original patented application of the molecule. Mechanistically this is the same lateral-hypothalamic NA/DA-mediated suppression of feeding behaviour seen with pemoline and the broader aminorex family — not a peripheral lipolytic action, not a leptin-axis effect, just central appetite suppression. For physique-focused users running a cut, this is the practical hook: 5–10 mg in the morning blunts hunger for the working day without the cardiovascular load of clenbuterol or the jitter of high-dose ephedrine.
Prodrug Activation of N-Methyl-Cyclazodone#
The N-methyl analog (NMC) circulating on the research-chemical market is best understood as a prodrug. CYP-mediated N-demethylation in the liver generates cyclazodone as the primary active metabolite, which then carries most of the pharmacological signal.
"N-demethylation to cyclazodone represents the primary metabolic pathway for N-methyl-cyclazodone, confirming cyclazodone as the main active metabolite." — Gampfer TM et al., Metabolites, 2025
The practical consequence is a slower come-up and a slightly less anxious peak on NMC versus equimolar cyclazodone, because the active species accumulates gradually as the parent is demethylated rather than arriving as a bolus. The two compounds are otherwise interchangeable in stacking, frequency discipline, and side-effect liability — anything said about cyclazodone applies to NMC once first-pass metabolism has run.
Hepatic Liability — Why the Mechanism Matters Off-Target#
The oxazolinone core is the same backbone that gave pemoline its black-box hepatotoxicity and eventually pulled it from the US market. The mechanism is not fully resolved but is thought to involve reactive metabolite formation during oxidative metabolism of the oxazolinone ring. Until a clean human PK and hepatotoxicity dataset exists for cyclazodone specifically, the prudent assumption is that the parent and the NMC prodrug both carry the same liability. This is the mechanistic reason the community standard caps frequency at ≤2 days per week and excludes the compound entirely from cycles running 17-aa orals — two hepatotoxic insults sharing the same phase-I pathway is a stacking error, not a synergy.
Cardiovascular and QT Effects at High Exposure#
At community doses the sympathomimetic load is modest — mild tachycardia, mild BP elevation, cold peripheries — consistent with the weak-releaser profile. At supratherapeutic exposure the picture changes sharply. The single published toxicology case (≈1 g/day NMC × 5 days) documented QRS widening, QTc prolongation, and rhabdomyolysis alongside choreoathetoid movements, indicating direct effects on cardiac conduction and striatal dopaminergic tone at high dose.
"The individual developed generalized choreiform motions, QRS and QTc prolongation, elevated transaminases, and rhabdomyolysis following repeated high-dose N-methyl-cyclazodone exposure." — Basile J et al., American Academy of Clinical Toxicology (CFSRE abstract), 2022
The window between functional cognitive dose (10–20 mg) and the case-report toxic exposure (1,000 mg/day) is wide on paper, but the dose–response is logarithmic on benefit and roughly linear on cardiovascular load — pushing past ~30 mg trades very little additional cognitive lift for disproportionate sympathetic and hepatic strain.
Protocol
| Level | Dose | Frequency | Notes |
|---|---|---|---|
| Low | 5–10 mg | As needed | Documented entry-level range |
| Mid | 10–20 mg | As needed | Most commonly studied range |
| High | 20–30 mg | As needed | Acute / situational use only. Community standard is ≤2 days per week with ≥48h between exposures. Daily dosing builds tolerance fast, wrecks sleep through the long elimination tail, and stacks hepatic risk. |
Cycle length & outcomes
Cycle Length & Frequency Framework#
Cyclazodone is not cycled in the traditional sense — it is an acute, situational stimulant with a long elimination tail and a hepatic-risk profile inherited from its parent compound pemoline. There is no loading phase, no taper, and no continuous "run." The variable that matters is frequency, not duration.
| Use Case | Protocol Length | Per-Dose Range | Frequency Cap |
|---|---|---|---|
| Acute deep-work / cognitive sprint | Situational, single doses | 10–15 mg oral | ≤2 days/week, ≥48h between exposures |
| Anorectic adjunct on a cut | Up to 4 weeks situational | 5–10 mg oral, AM | 2–3 days/week, never daily |
| Beginner dose-finding | Single exposures × 2–3 occasions | 5–10 mg oral | One exposure per week until tolerability established |
| Advanced ceiling | Single doses only | 20–30 mg oral | 1 day/week, hard ceiling |
| N-methyl-cyclazodone (NMC) prodrug variant | Substituted 1:1 in any of the above | 10–20 mg oral | Same frequency rules apply |
The maxEfficacyWeeks figure of 4 reflects the practical window before tolerance, sleep disruption, and accumulated hepatic load erode the risk/reward — not a continuous-dosing schedule. After four weeks of intermittent use, the community standard is a minimum two-week washout.
Onset, Peak, and the Long Tail#
Subjective onset is 30–60 minutes orally on an empty stomach. Peak effects land at roughly 2–3 hours, mirroring the 120–180 minute motor-activity peak documented in the original rodent patent work:
"Cyclazodone was an 'excitant' with anti-fatigue, anorectic, and locomotor-stimulating effects at 10 mg/kg in mice, persisting for more than 6 hours and peaking at 120–180 minutes." — De Marne et al., GB Patent 1,005,738 (1965)
Active stimulation runs 6–10 hours. Residual insomnia and appetite suppression frequently bleed into a second day. Because of this tail, morning dosing is non-negotiable — anything past noon compromises that night's sleep, and re-dosing within the same day stacks onto residual drug rather than producing a clean second peak.
No Loading, No Taper#
Cyclazodone is non-hormonal, has no documented endocrine activity, and produces no HPTA suppression. There is no PCT requirement, no taper, no front-load. The compound is either dosed on a given day or it isn't.
What the protocol does require is frequency discipline. The most common failure mode in community reports is daily-use creep — the drug feels productive enough that users escalate, lose the acute effect to tolerance within a week, and end up with insomnia, anhedonia, and a flat baseline. Holding ≤2 exposures per week is the single most important protocol variable.
NMC Prodrug Considerations#
N-methyl-cyclazodone is interchangeable with cyclazodone in any of the above tiers, with a slower come-up and slightly less anxious peak because the active parent must be generated hepatically:
"N-demethylation to cyclazodone represents the primary metabolic pathway for N-methyl-cyclazodone, confirming cyclazodone as the main active metabolite." — Gampfer et al., Metabolites (2025)
This means NMC carries the same hepatic load through a CYP-mediated step before the pharmacology even begins — frequency caps are identical, and stacking NMC with hepatotoxic orals is the same bad idea as stacking cyclazodone with them.
Bloodwork Cadence#
Given the pemoline lineage, LFT monitoring is the community-prudent standard even though the dosing pattern is intermittent:
| Timepoint | Panel |
|---|---|
| Baseline (prior to first exposure) | ALT, AST, ALP, GGT, bilirubin |
| After 4 weeks of intermittent use | ALT, AST, ALP, GGT, bilirubin |
| If frequency exceeds 2 days/week or doses exceed 20 mg | Add CK, basic metabolic panel |
| Any subjective hepatic warning sign (RUQ discomfort, dark urine, jaundice, fatigue) | Full LFT immediately; protocol halted |
Protocol is discontinued on any transaminase elevation above ~2× ULN. Cyclazodone is not stacked with 17α-alkylated orals (anavar, tbol, superdrol, anadrol), high-dose paracetamol, or isotretinoin — the hepatic risk is additive and the published toxicology case demonstrates that the chemotype can produce hepatocellular injury at high exposure.
Onset of Subjective Effects#
Unlike peptides or hormonal compounds with delayed pharmacodynamics, cyclazodone's effects are felt on the same dose. Dose-finding is therefore fast — a single 5–10 mg morning exposure tells the user almost everything they need to know about tolerability, anorectic response, and sleep impact within 24 hours. The community pattern is to start at 5 mg, wait a week, then titrate by 5 mg increments across subsequent single exposures until the working dose is identified. Above 20 mg the cardiovascular and anxiogenic curve steepens sharply, and 30 mg is the practical ceiling — not a target.
Used inside these frequency and bloodwork constraints, cyclazodone occupies a defensible niche as an occasional cognitive and anorectic tool. Used daily, it is the same compound that got pemoline pulled from the market.
Risks & mistakes
Common (most users)#
At the 5–20 mg range community users land on, the side-effect profile is the predictable sympathomimetic / dopaminergic package. Most are managed with dose, timing, and frequency discipline rather than ancillaries.
- Insomnia — the 6–10h elimination tail means a 10 a.m. dose can still push sleep onset past midnight. Mitigation: dose before 10 a.m., cap at one exposure per day, and never re-dose. Magnesium glycinate and a strict no-caffeine-after-noon rule on dosing days help.
- Anorexia — frequently desired on a cut, occasionally a problem on a recomp or bulk. The patent literature flagged the anorectic effect as a primary action at 10 mg/kg in mice, so it is not avoidable above threshold doses. Mitigation: protein-forward liquid meals (shakes, kefir) on dosing days to hit macros without appetite.
- Jaw tension and mild bruxism — classic dopaminergic stimulant sign. Mitigation: stay hydrated, magnesium, and back the dose down 5 mg if it becomes painful.
- Anxiety / overstimulation — most often at the upper end of a tier or in caffeine-naïve users who stack 200+ mg caffeine on top. Mitigation: drop concurrent caffeine to ≤100 mg, add 200 mg L-theanine, or step down one tier.
- Cold peripheries and mild vasoconstriction — expected sympathomimetic effect. Mitigation: warm-up time before training, no stacking with other vasoconstrictors (yohimbine, ephedrine, high-dose caffeine).
- Flat / anhedonic comedown 12–24 h post-dose — particularly visible on consecutive-day use, which is why the community frequency cap exists. Mitigation: ≥48 h between exposures, ≤2 days per week, and a tyrosine/B-complex morning the day after dosing.
Uncommon (dose-dependent or individual)#
These cluster at 20–30 mg, on stacked stimulant days, or in cardiovascular-naïve users.
- Tachycardia and elevated resting BP — Docherty's review of the aminorex–oxazolinone family characterises the chemotype as having "relatively low cardiovascular toxicity compared to amphetamines," but "lower" is not "none." Resting HR ≥100 or systolic ≥140 on a dosing day is a signal to drop a tier and abandon any concurrent sympathomimetic.
- Tremor and motor restlessness — early dose-dependent dopaminergic sign. Back off immediately; this is the same axis that produced choreiform movement in the high-dose case report.
- Mild transaminase elevation — pemoline, the closest licensed analog, was withdrawn for hepatotoxicity, and ALT was elevated to 104 U/L in the published NMC case. Baseline and follow-up LFTs (ALT, AST, ALP, GGT, bilirubin) are the prudent monitoring cadence. ALT/AST climbing above 2× ULN ends the protocol.
- Persistent insomnia across multiple nights — indicates the frequency cap is being exceeded. The fix is a 1–2 week washout, not a sleep aid stacked on top.
- Headache, mild dehydration — vasoconstriction plus reduced fluid intake from anorexia. Front-load electrolytes on dosing days.
Rare but serious#
The single published toxicology case (Basile et al., CFSRE 2022) is the reference point for the high-end toxidrome, and it was produced by roughly 1 g/day of NMC for 5 days — two orders of magnitude beyond any defensible community dose. The relevant warning signs:
The individual developed generalized choreiform motions, QRS and QTc prolongation, elevated transaminases, and rhabdomyolysis following repeated high-dose N-methyl-cyclazodone exposure. — Basile et al., CFSRE 2022
- Choreoathetoid / dyskinetic movements ("St. Vitus dance" presentation) — discontinue immediately; this is the hallmark of the high-exposure toxidrome.
- QRS widening and QTc prolongation — palpitations, presyncope, or any documented arrhythmia warrants discontinuation and ECG workup.
- Rhabdomyolysis — dark urine, severe muscle pain disproportionate to training load, or CK ≥5× ULN. Stop, hydrate aggressively, and seek workup.
- Hepatocellular injury — jaundice, RUQ pain, dark urine, nausea, or any ALT/AST elevation beyond 2–3× ULN. The pemoline precedent makes this the single most important watchpoint for anyone running the compound at any frequency.
- Seizure — the chemotype lowers seizure threshold; a first-ever seizure on the protocol ends the protocol permanently.
- Serotonergic crisis when stacked with SSRIs/SNRIs/MAOIs — the published case ran NMC alongside fluoxetine, which is mechanistically relevant to the autonomic instability observed.
Hard contraindications#
These are not negotiable.
- Baseline hepatic impairment, elevated LFTs, or any concurrent hepatotoxic compound — 17α-alkylated orals (superdrol, anavar, tbol, winstrol), high-dose paracetamol, isotretinoin, or any other liver-loading agent. Cyclazodone shares the oxazolinone backbone of pemoline, which was pulled from the market for fulminant hepatic failure. The protocol does not coexist with an oral AAS cycle.
- MAOIs — hypertensive crisis via potentiated monoamine release.
- SSRIs / SNRIs at therapeutic dose — the only published toxicity case ran this combination and developed autonomic instability with serotonergic features.
- Uncontrolled hypertension, structural heart disease, prior MI, or known QT prolongation — the case data shows clear conduction effects at high exposure, and the chemotype is sympathomimetic.
- Concurrent strong sympathomimetics — amphetamines, methylphenidate, ephedrine, clenbuterol, yohimbine, cocaine. Additive cardiovascular and hyperthermic risk with no upside.
- Seizure history — the oxazolinone family lowers seizure threshold.
- Tested athletes in-competition — cyclazodone and its analogs are detectable in urine by LC-MS/MS for several days post-dose and appear on WADA panels (Monfort et al. 2015). Not a side effect, but a career-ending consequence that belongs in this list.
Gender and PCT considerations#
Cyclazodone is non-hormonal. There is no aromatase, 5α-reductase, or androgen receptor activity, no documented endocrine impact, and no PCT requirement. The compound is dose-equivalent across sexes on a per-kg basis, so smaller subjects should anchor to the lower end of each tier (5–10 mg is the prudent starting range). There are no pregnancy data — the absence of any reproductive toxicology work, combined with the hepatic risk profile, means the compound has no place anywhere near pregnancy or potential conception. Bloodwork cadence is identical regardless of sex: baseline LFT panel, follow-up at 4–6 weeks of intermittent use, and CK added once frequency exceeds occasional.
FAQ — Cyclazodone
Research & citations
5 studies cited on this page.
Conclusion
Cyclazodone sits in a unique niche among research stimulants: a dopaminergic/noradrenergic nootropic with pronounced focus, wakefulness, and appetite-suppression, but a biochemical and hepatic risk profile that demands respect.
Key takeaways:
- Community protocols center on 10–15 mg oral doses, as-needed, never daily — typically ≤2 times per week with ≥48 h between exposures
- Acute cognitive enhancement, task motivation, and reduced fatigue are the standout effects, peaking around 2.5 hours post-dose and lasting 6–10 hours
- Stacking is most common with racetams (oxiracetam, aniracetam) and a choline donor; avoid combining with other stimulants or hepatotoxic compounds
- Aggressive dieting protocols use 5–10 mg as an anorectic adjunct, always with attention to liver health
- Bloodwork (LFT panel) prior to and after a cycle is highly recommended — treat it with the same caution as pemoline
- Only oral administration is documented; volumetric dosing from accurately weighed powder is the community-prudent method
For productivity sprints, cut support, or as an alternative to amphetamine-class agents, cyclazodone remains a tool for disciplined, low-frequency applications — not a daily driver.