We use essential cookies (authentication, your saved goals/stack) by default. With your permission we'll also enable privacy-respecting analytics (Vercel Web Analytics, anonymous load-time metrics) and error-replay diagnostics (Sentry — DOM snapshots only when an error fires) so we can fix bugs faster. Learn more about cookies
Research compound — not a dietary supplement
Fladrafinil (CRL-40,941) is a research compound, not a regulated dietary supplement. It is sold for research or off-label use. The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most Fladrafinil (CRL-40,941) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality randomised trials published 1997–2026.
Based on 5 studies · 2 RCTs
Confidence
LowBy outcome
The current evidence for Fladrafinil (CRL-40,941) is insufficient to assign an evidence score, based on 5 indexed studies, including 1 meta-analysis. A grey-market 'research chemical' sold online as a wakefulness-promoting nootropic — fladrafinil (fluorafinil / CRL-40,941) is a fluorinated analogue of adrafinil/modafinil and, critically, a PRODRUG that converts in the body to flmodafinil (CRL-40,940), which is itself an unstudied modafinil analogue catalogued here. The defining fact is the ABSENCE of evidence: there are essentially NO published human efficacy or safety trials of fladrafinil. The only direct human data is a single 2026 doping-control paper in which six volunteers ingested 20 mg of fladrafinil (or flmodafinil) so its metabolism and detection could be mapped — human pharmacokinetics, but nothing about whether it works or is safe. Everything else marketers cite is the MODAFINIL literature — a related but DIFFERENT drug — which cannot be transferred to an unstudied analogue of unknown purity and dose. By extrapolation from modafinil (and via its active metabolite flmodafinil) expect modafinil-like effects and harms only: insomnia, headache, anxiety, raised blood pressure and heart rate, the rare-but-serious skin reactions seen with modafinil, and dependence/misuse potential — all UNMONITORED, with grey-market product of unverified identity and dosing. It is reputed (anecdotally only) to be more 'anti-aggressive' than adrafinil, but that too is unproven. It is NOT an approved medicine, NOT a dietary supplement, and there is no human use this library can recommend. Informational, harm-reduction entry only — the honest takeaway is that fladrafinil's benefit and safety are unstudied in humans. Representative study: PMID 26381811.
Sarcosine
Mostly mechanism / observationalAn endogenous glycine derivative that inhibits the type-1 glycine transporter (GlyT-1), enhancing NMDA-receptor co-agonism. It is studied as a prescription-style PSYCHIATRIC ADJUNCT — with genuine add-on RCTs in schizophrenia (and smaller signals in OCD and depression) — not as a casual nootropic. Evidence is real but narrow and emerging.
Tianeptine
Last reviewed June 2026 · evidence from 5 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Fladrafinil (fluorafinil; CRL-40,941; N-hydroxy / bis(4-fluorophenyl) analogue of adrafinil) — a grey-market 'research chemical' wakefulness-promoter and PRODRUG of flmodafinil, with essentially NO published human efficacy or safety trials of its own
A grey-market 'research chemical' sold online as a wakefulness-promoting nootropic — fladrafinil (fluorafinil / CRL-40,941) is a fluorinated analogue of adrafinil/modafinil and, critically, a PRODRUG that converts in the body to flmodafinil (CRL-40,940), which is itself an unstudied modafinil analogue catalogued here. The defining fact is the ABSENCE of evidence: there are essentially NO published human efficacy or safety trials of fladrafinil. The only direct human data is a single 2026 doping-control paper in which six volunteers ingested 20 mg of fladrafinil (or flmodafinil) so its metabolism and detection could be mapped — human pharmacokinetics, but nothing about whether it works or is safe. Everything else marketers cite is the MODAFINIL literature — a related but DIFFERENT drug — which cannot be transferred to an unstudied analogue of unknown purity and dose. By extrapolation from modafinil (and via its active metabolite flmodafinil) expect modafinil-like effects and harms only: insomnia, headache, anxiety, raised blood pressure and heart rate, the rare-but-serious skin reactions seen with modafinil, and dependence/misuse potential — all UNMONITORED, with grey-market product of unverified identity and dosing. It is reputed (anecdotally only) to be more 'anti-aggressive' than adrafinil, but that too is unproven. It is NOT an approved medicine, NOT a dietary supplement, and there is no human use this library can recommend. Informational, harm-reduction entry only — the honest takeaway is that fladrafinil's benefit and safety are unstudied in humans.
Fladrafinil (fluorafinil / CRL-40,941) is a grey-market 'research chemical' analogue of modafinil and a PRODRUG that converts in the body to flmodafinil. It has essentially NO published human efficacy or safety trials of its own. The only fladrafinil-specific literature is a 2026 human doping-control study in which six volunteers ingested 20 mg of fladrafinil (or flmodafinil), mapping its metabolism/conversion/detection (Krug 2026) — which gives human pharmacokinetics and confirms the fladrafinil→flmodafinil conversion, but shows neither efficacy nor safety. The nearest mechanistic evidence is a mouse wakefulness study of the active metabolite flmodafinil/lauflumide (Luca 2018). The supporting modafinil studies cited here (Battleday & Brem 2015 systematic review; Broughton 1997 and US Modafinil Study Group 2000 RCTs) are the PARENT compound, NOT fladrafinil, and cannot be transferred to an unstudied fluorinated analogue/prodrug of unknown purity and dose. The dominant signal is therefore an ABSENCE of human efficacy or safety evidence, against an extrapolated modafinil-like harm profile (insomnia, anxiety, raised BP/HR, rare serious skin reactions, misuse/dependence) and grey-market quality risk — so the score sits low.
Fladrafinil — also called fluorafinil and known by its development code CRL-40,941 — is a synthetic fluorinated analogue of adrafinil and modafinil in which the two phenyl rings carry 4-fluoro substituents and the molecule retains an N-hydroxy (hydroxamic) group; chemically it is 2-[bis(4-fluorophenyl)methylsulfinyl]-N-hydroxyacetamide.
Crucially, fladrafinil is a PRODRUG: in the body it converts to flmodafinil (CRL-40,940), the bis(4-fluorophenyl) analogue of modafinil, so a person who takes fladrafinil is ultimately exposed to flmodafinil and its metabolites.
Like the rest of the modafinil family it is presumed to act largely as a dopamine-reuptake inhibitor and wakefulness-promoting agent of the (diphenylmethylsulfinyl)acetamide class, and it is sold online — alongside flmodafinil — as a grey-market 'research chemical' marketed as a more potent, reputedly more 'anti-aggressive' nootropic than adrafinil.
The honest description of its evidence base is that it BARELY HAS ONE. There are essentially NO published randomized controlled trials of fladrafinil in humans, no approved indication anywhere, and no pharmacovigilance data on the material people actually buy.
The only direct, fladrafinil-specific literature is a 2026 doping-control paper in which six volunteers ingested 20 mg of fladrafinil (or flmodafinil) to characterize how it is metabolized, converted and detected for sports-doping control — direct human pharmacokinetic data confirming the fladrafinil→flmodafinil prodrug conversion, but nothing about whether it works or is safe.
The nearest mechanistic evidence is for its active metabolite: a single 2018 mouse study in which the related analogue lauflumide (NLS-4 / flmodafinil) produced significantly longer wakefulness than a much larger dose of modafinil — preclinical potency, not human efficacy.
Everything else that fladrafinil vendors and nootropic forums lean on is the MODAFINIL literature — the parent compound — which is a related but genuinely different molecule.
That modafinil evidence is real: a systematic review of modafinil for cognitive neuroenhancement in healthy non-sleep-deprived adults found modest, task-dependent benefits to executive function and attention (Battleday & Brem 2015), and randomized trials established modafinil for the excessive daytime sleepiness of narcolepsy (Broughton 1997; US Modafinil in Narcolepsy Multicenter Study Group 2000).
But it would be dishonest to pass any of that off as fladrafinil evidence — a different fluorinated analogue and prodrug, made and sold outside any quality system, may differ in potency, pharmacokinetics, metabolites and toxicity, and the doses on a research-chemical label are not the doses used in those trials.
The expected harm profile is likewise extrapolated from modafinil rather than measured for fladrafinil: insomnia, headache, nausea, anxiety and nervousness, raised blood pressure and heart rate, and — rarely but seriously — severe cutaneous reactions (Stevens-Johnson syndrome / DRESS have prompted regulatory warnings for modafinil), plus the dependence and misuse potential of a wakefulness-promoting psychostimulant.
Layered on top is the grey-market reality: a 'research chemical' of unverified identity, purity and dose, taken with no medical supervision, no monitoring of blood pressure or skin reactions, and unknown drug interactions (modafinil induces CYP3A4 and can reduce the effectiveness of hormonal contraceptives, among others).
The evidence score sits low and the level is 'Emerging' precisely because the dominant signal here is an ABSENCE — no human efficacy or safety data on fladrafinil at all, only a single human pharmacokinetic/detection study.
This is an informational, harm-reduction entry: the responsible conclusion is that fladrafinil is an essentially unstudied modafinil-analogue prodrug sold as a nootropic, not a supported intervention, and there is no human use this library endorses.
Fladrafinil (CRL-40,941) is a prodrug: in the body it converts to flmodafinil (CRL-40,940), the bis(4-fluorophenyl) analogue of modafinil. A 2026 human doping-control study confirmed this conversion — after fladrafinil ingestion, the flmodafinil metabolites (flmodafinil acid and sulfone) were detected, with a slight offset until peak flmodafinil. So fladrafinil's pharmacology is effectively that of flmodafinil, which is itself an unstudied modafinil analogue.
Fladrafinil is a fluorinated analogue of adrafinil/modafinil from the (diphenylmethylsulfinyl)acetamide family of wakefulness-promoting agents, acting through its active metabolite flmodafinil. By extrapolation from modafinil it is expected to promote sustained wakefulness and arousal. The nearest direct evidence is a mouse study of the metabolite (lauflumide / flmodafinil) showing longer wakefulness than a far larger dose of modafinil — preclinical evidence of potency, not a human-efficacy result.
Modafinil-class wakefulness agents act substantially as dopamine-reuptake inhibitors, raising synaptic dopamine in wake-regulating circuits. Fladrafinil (via flmodafinil) is assumed to share this mechanism, which also underlies the misuse/dependence potential of the class. This is inferred from the parent drug; fladrafinil's own pharmacology in humans is uncharacterised.
How Fladrafinil (CRL-40,941) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
There is no established or legitimate human dose. Fladrafinil is an essentially UNSTUDIED grey-market 'research chemical' analogue of modafinil and a prodrug of flmodafinil, with no human clinical trials, no approval, and no pharmacovigilance — this library does NOT provide a dosing protocol. Vendors and forums quote figures in the tens-to-low-hundreds of milligrams orally, extrapolated from modafinil/adrafinil, but these are unverified for a product of unknown purity and identity, taken without medical supervision or monitoring. The only human datapoint is a 2026 doping-control study in which six volunteers ingested 20 mg of fladrafinil (or flmodafinil) to map metabolism, prodrug conversion and detection — a detection study, NOT a dosing or efficacy recommendation.
Can be taken without food
| Form | Type |
|---|---|
| 💊No human form is endorsed — fladrafinil is an unstudied 'research chemical' analogue/prodrug of modafinil with no approved or supplement form | Recommended |
There is no over-the-counter, supplement or prescription form of fladrafinil. Grey-market powder/capsules are of unverified identity and purity and are frequently sold 'not for human consumption'. As a prodrug, fladrafinil converts to flmodafinil in the body.
Minimum: 1 weeks
Optimal: 4 weeks
Cycling: Not required
Note: No human timing is endorsed. Fladrafinil is an unstudied grey-market modafinil-analogue prodrug with no human trials and an extrapolated stimulant harm profile (insomnia, anxiety, raised BP/HR, rare serious skin reactions). Morning-only framing is harm-reduction to limit insomnia if exposure occurs; this library does not schedule its use.
Dose-response data unavailable. The current published research for Fladrafinil (CRL-40,941) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
There are essentially no published human efficacy or safety trials of fladrafinil — no demonstrated cognitive, wakefulness or performance benefit in people. The only direct human study mapped its metabolism, prodrug conversion and detection in six volunteers (a doping-control paper); the nearest efficacy-relevant evidence is a mouse study of its active metabolite flmodafinil/lauflumide. Any 'benefit' claimed for fladrafinil is extrapolated from the separate modafinil literature, not measured for this compound.
As a modafinil-analogue prodrug of flmodafinil, fladrafinil is expected to promote wakefulness and alertness; the nearest direct evidence is a mouse study where the metabolite (lauflumide / flmodafinil) out-lasted modafinil for wakefulness. In humans this is UNPROVEN for fladrafinil specifically — it is an inference from the parent drug and metabolite, not a trial result, and comes bundled with the stimulant harms below.
Modafinil itself showed modest, task-dependent gains in executive function and attention in healthy adults (Battleday & Brem 2015) — but that is the parent compound, NOT fladrafinil. No human study has tested fladrafinil for focus or attention, so any benefit is assumed, not shown, and may not transfer to a different fluorinated analogue/prodrug at unknown doses.
Wakefulness-promoting agents of the modafinil family commonly cause difficulty falling asleep and reduced sleep, especially when taken later in the day. By extrapolation, fladrafinil (via flmodafinil) is expected to disrupt sleep; the metabolite's longer wakefulness duration in the mouse study suggests this risk could be at least as pronounced as with modafinil.
Modafinil-class stimulation commonly produces headache, nausea, nervousness and anxiety. Fladrafinil, an unstudied analogue/prodrug at uncertain doses, carries the same expected CNS-overstimulation risks with no human dose-finding or monitoring to bound them. Its reputed (anecdotal) 'anti-aggressive' character is unproven and does not remove these risks.
Modafinil raises blood pressure and heart rate and carries rare-but-serious cutaneous reactions (Stevens-Johnson syndrome / DRESS prompted regulatory warnings). These hazards are extrapolated to fladrafinil, which is taken without blood-pressure monitoring or medical oversight; a severe rash on any modafinil-family agent is a medical emergency.
Avoid — fladrafinil is unstudied in humans, of unverified identity and dose, a prodrug of the also-unstudied flmodafinil, and carries an extrapolated modafinil-like harm profile (insomnia, anxiety, raised BP/HR, rare serious skin reactions, misuse potential). There is no human evidence of benefit.
Avoid — modafinil-class agents raise blood pressure and heart rate, and fladrafinil is taken with no monitoring.
Avoid — modafinil-class CYP3A4 induction can reduce contraceptive efficacy; fladrafinil's effect is uncharacterised, so contraceptive failure cannot be excluded.
Avoid — modafinil carries psychiatric and severe-cutaneous-reaction warnings; fladrafinil is assumed to share them with no human safety data.
Avoid entirely — no human safety data; modafinil is associated with possible fetal risk and reduced contraceptive efficacy.
Modafinil induces CYP3A4 and can reduce the effectiveness of hormonal contraceptives (pill, patch, ring, some implants), risking unintended pregnancy; fladrafinil (via flmodafinil) is assumed to share this and is entirely uncharacterised, so the interaction is unpredictable and unmonitored.
Combining fladrafinil with caffeine, ADHD stimulants or other sympathomimetics compounds the expected rise in blood pressure, heart rate, anxiety and insomnia; the additive effect is uncharacterised in a product of unknown potency.
Tip: Expected of any wakefulness-promoting modafinil-family agent; the metabolite flmodafinil's longer animal wakefulness duration suggests pronounced sleep disruption. There is no validated human dosing to limit this — the only harm-reduction note is that evening exposure is worse than morning.
Tip: These are the most common modafinil adverse effects and are extrapolated to fladrafinil. With an unstudied analogue/prodrug of uncertain potency there is no dose-finding to bound them; stop use if they occur.
Tip: Modafinil-class agents raise BP and HR; fladrafinil is taken without any cardiovascular monitoring. Anyone with heart disease, arrhythmia or hypertension should avoid it entirely.
Tip: Modafinil carries regulatory warnings for severe, potentially life-threatening cutaneous and hypersensitivity reactions. The risk for fladrafinil is unknown but assumed shared — any rash, blistering, mucosal lesions or fever after use is a medical emergency: stop and seek urgent care.
The commonly studied dose of Fladrafinil (CRL-40,941) is There is no established or legitimate human dose. Fladrafinil is an essentially UNSTUDIED grey-market 'research chemical' analogue of modafinil and a prodrug of flmodafinil, with no human clinical trials, no approval, and no pharmacovigilance — this library does NOT provide a dosing protocol. Vendors and forums quote figures in the tens-to-low-hundreds of milligrams orally, extrapolated from modafinil/adrafinil, but these are unverified for a product of unknown purity and identity, taken without medical supervision or monitoring. The only human datapoint is a 2026 doping-control study in which six volunteers ingested 20 mg of fladrafinil (or flmodafinil) to map metabolism, prodrug conversion and detection — a detection study, NOT a dosing or efficacy recommendation.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
The best time to take Fladrafinil (CRL-40,941) is in the morning. It can be taken on an empty stomach. Wakefulness-promoting agents of the modafinil family are taken in the morning to avoid insomnia; fladrafinil's metabolite flmodafinil showed long wakefulness duration in animal work, making evening dosing especially likely to disrupt sleep.
Fladrafinil (CRL-40,941) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are insomnia / disrupted sleep, headache, nausea, anxiety & nervousness, raised blood pressure & heart rate. Use caution if any of these apply to you: Any human use — fladrafinil is an essentially UNSTUDIED grey-market 'research chemical' and a prodrug of flmodafinil, with no human trials, no approval, and product of unverified identity, purity and dose; it is NOT a dietary supplement and NOT an approved medicine; Anyone seeking it for focus, wakefulness or 'nootropic' enhancement — there is no human evidence of benefit for fladrafinil and an extrapolated modafinil-like harm profile; Anyone with cardiovascular disease, arrhythmia, uncontrolled hypertension, or left-ventricular hypertrophy — modafinil-class agents raise blood pressure and heart rate.
An atypical antidepressant — brand Stablon/Coaxil/Tatinol — approved and prescribed for major depression (and anxious depression) in parts of Europe, Asia and Latin America, where randomized trials show efficacy comparable to SSRIs and tricyclics, often with better tolerability at the therapeutic dose (12.5 mg three times daily). Mechanistically it is unusual: it modulates the stress system and enhances glutamatergic/hippocampal plasticity, and — the critical fact for harm reduction — it is a FULL MU-OPIOID RECEPTOR AGONIST. That opioid action explains both its antidepressant effect AND its abuse potential. In the United States it is NOT FDA-approved; the FDA has warned about it, and it is sold illicitly as an unapproved 'nootropic'/'supplement' ('Tianaa', 'Za Za', 'Pegasus') nicknamed 'gas station heroin'. The dominant recent US literature is not efficacy but ABUSE, DEPENDENCE, opioid-like WITHDRAWAL, overdose/toxicity (usually at supratherapeutic doses far above the clinical dose), and rising poison-center exposures. The honest framing: a genuine antidepressant abroad with proven short-term efficacy at the prescribed dose, but a mu-opioid agonist carrying real dependence/abuse/withdrawal/overdose risk and no US approval. Informational, harm-reduction entry only — not a recommendation, and not a substitute for clinician-supervised treatment.
Because fladrafinil is sold as an unregulated 'research chemical', the substance, its purity, its actual dose and its metabolites are not assured. A human doping-control study (six volunteers) characterized how fladrafinil converts to flmodafinil and how both are metabolized and detected — useful for doping control, but underscoring that what a buyer ingests, and how the body handles it, is not guaranteed to match any label or any modafinil reference.
Modafinil modulates CYP enzymes (3A4 induction, 2C19 inhibition), altering levels of many co-medications. Fladrafinil's enzyme effects are uncharacterised, so any concurrent prescription is an unmonitored, unpredictable interaction.
Stacking a CNS stimulant of unknown pharmacology with antidepressants, antipsychotics or MAOIs risks additive cardiovascular and psychiatric effects; fladrafinil has no interaction data, so the combination is uncharacterised and unsafe to assume benign.
Tip: As a dopamine-reuptake-inhibiting wakefulness psychostimulant (via flmodafinil), fladrafinil carries misuse and psychological-dependence potential by extrapolation from the class; unsupervised escalating use in a grey-market setting compounds the risk.