Fladrafinil
CRL-40,941 / fluorafinil
Fladrafinil (CRL-40,941 / fluorafinil) is a cognitive & mood research compound. A bis-fluoro analog of adrafinil that converts to a modafinil-like active. Dopamine reuptake inhibition is the accepted mechanism for the wakefulness effect.
Fladrafinil quick facts
| Reported research dose (Oral) | 30–100mg (research) |
| Route | Oral |
| Frequency | 1x early · 2–3x |
| Half-life | Long — commonly 12–15 hours reported |
| Forms | Oral |
| Evidence level | No human trials; extrapolated from modafinil |
| Other forms available | Injectable — dosed differently |
Reported as more potent than adrafinil per milligram and without adrafinil's liver-enzyme burden, though that comparison rests on anecdote rather than data. Sleep disruption is the main practical issue given the duration — anything after midday is a bad idea. Modafinil is the version with actual trials behind it. Banned in competition, FYI: fladrafinil is a prodrug for flmodafinil and both are WADA class S6 stimulants, and the anti-doping work on them reports long urinary detection windows for the parent drugs and their metabolites (Krug 2026).
How Fladrafinil works
A bis-fluoro analog of adrafinil that converts to a modafinil-like active. Dopamine reuptake inhibition is the accepted mechanism for the wakefulness effect.
Proposed benefits
Researched for focus, memory, neuroprotection, mood and stress resilience.
Where to get Fladrafinil
The evidence for Fladrafinil
Graded by what exists behind each claim.
Human clinical evidence
- No human trials: development stopped at preclinical, so the ceiling on any claim here is a rodent model — and these transfer poorly.
📊 Correlative data
- Community use as a wakefulness agent. Reported experience is similar to adrafinil and modafinil but described as stronger, with more anxiety and irritability at higher doses.
- Modafinil's human safety record does not transfer to it. They are related but not the same molecule, and the fluorination changes both potency and metabolism.
🧪 How the mechanism reads
- A bis(4-fluoro) analog of adrafinil, a modafinil prodrug. Like the family it appears to act primarily as a weak dopamine reuptake inhibitor with effects on orexin and histamine signaling.
- Being an adrafinil-type prodrug means hepatic conversion, which is the mechanistic basis for the liver-enzyme caution that applies to adrafinil on long-term use.
Why an empty tier is not a verdict →
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Fladrafinil actually does
The chemistry on every other page about this compound is wrong, and the correction matters. Fladrafinil is CRL-40,941 = 2-[bis(4-fluorophenyl)methylsulfinyl]-N-hydroxyacetamide, C15H13F2NO3S, 325.33 Da. Its sibling flmodafinil is CRL-40,940 = 2-[bis(4-fluorophenyl)methylsulfinyl]acetamide, 309.33 Da. Both names and both structures are given in the 2026 doping-control study Krug 2026. The difference between them is a single N-hydroxyl: fladrafinil is a hydroxamic acid and flmodafinil is a plain amide, which is exactly the relationship adrafinil (289.35 Da) has to modafinil (273.35 Da). And the consequence that everyone gets backwards: fladrafinil is a prodrug for flmodafinil, not for modafinil Krug 2026. The two fluorines are never removed. Whatever this compound does, it does through a molecule that has itself never been characterized pharmacologically in a human.
Why the fluorines are there, mechanistically. Para-substitution of a phenyl ring with fluorine blocks the position most available to cytochrome-P450-mediated aromatic hydroxylation; blocking the soft spot is the standard medicinal-chemistry move for slowing oxidative clearance. That predicts a longer duration than the unfluorinated parent, which is what people report — and it has never been tested head to head against adrafinil or modafinil in any species. Flagged as extrapolation from the substitution pattern, not as a finding.
The stereocentre nobody sells. The sulfoxide sulfur is chiral. Modafinil is marketed as a racemate and its R-enantiomer, armodafinil, has a longer half-life and a different concentration profile. Fladrafinil and flmodafinil have the same stereocentre, and no vendor states an enantiomeric ratio on any certificate of analysis. Two batches with the same purity figure can therefore be pharmacokinetically different products.
The target, borrowed from the parent because there is no other option. In 10 healthy men given therapeutic doses of 200–400 mg of modafinil, PET showed decreased [11C]raclopride binding in caudate, putamen and nucleus accumbens — meaning extracellular dopamine rose — and decreased [11C]cocaine binding, meaning dopamine transporter occupancy; the authors' own conclusion was that the abuse and dependence potential in vulnerable people needs to be recognized Volkow 2009. A 2024 review frames modafinil as an ‘atypical’ stimulant: a low-affinity dopamine transporter inhibitor with unusually few dependence reports, plus actions across GABA, glutamate, serotonin and noradrenaline and regionally selective activation Hersey 2024. None of that has been measured for fladrafinil or flmodafinil.
The analytical fact that belongs on every page about this molecule and is on none of them. Modafinil, modafinic acid, adrafinil, CRL-40,940 and CRL-40,941 all thermally degrade in the hot injector of a gas chromatograph, producing diphenylmethanol and 1,1,2,2-tetraphenylethane — and, for the fluorinated members, its tetrafluoro analog — confirmed by synthesis and X-ray crystallography Dowling 2017. Two consequences for a buyer. First, a GC-MS certificate of analysis for this compound can show peaks that were never in the vial. Second, and worse, fladrafinil and flmodafinil converge on the same tetrafluoro degradation product, so GC-MS is a poor method for telling the two apart — which is precisely the distinction the market gets wrong.
Cell, rodent, human — and where it stops
The receptor rung is empty. There is no published binding or uptake assay for fladrafinil or flmodafinil at the dopamine transporter or anywhere else. Everything mechanistic on this page above is either structural or borrowed from modafinil Volkow 2009 Hersey 2024.
The rodent rung is empty too. No animal pharmacology, no animal toxicology, no behavioral study for either fluorinated compound has been published.
And then, unusually, the human rung exists — and it is brand new. Six volunteers each ingested 20 mg of either flmodafinil or fladrafinil; urine and blood were analyzed by liquid chromatography high-resolution mass spectrometry with detection limits of 0.2 to 4 ng/mL. After flmodafinil, flmodafinil acid and flmodafinil sulfone were detected; because fladrafinil is a prodrug for flmodafinil, the same two metabolites appeared after fladrafinil. Urinary maximum concentrations were 191–891 ng/mL for flmodafinil and 52–111 ng/mL for fladrafinil; blood concentrations reached 45–98 ng/mL and 11–35 ng/mL respectively. Both compounds are S6 stimulants on the WADA Prohibited List, banned in competition, and the authors note that the relatively long detection windows of both intact drugs and their metabolites require careful interpretation of findings Krug 2026.
The obstacles, and the first three are numbers. (1) The only human study used 20 mg. This site lists 30–100 mg. Nothing above 20 mg has ever been characterized in a person, so the top of the commonly used range is five-fold outside the only data that exists. (2) Twenty milligrams produced an 11 to 35 ng/mL blood range across six people Krug 2026 — a three-fold spread at an identical dose. That is a large inter-individual variation and it is the concrete reason the same capsule is unremarkable for one person and too much for another. (3) Not one pharmacodynamic measurement was taken. The study's endpoint was detection for doping control: no wakefulness scale, no cognitive battery, no heart rate, no blood pressure. So fladrafinil now has human pharmacokinetics and still has zero human pharmacodynamics. (4) Everything anyone believes about the effect is imported from 200–400 mg of modafinil Volkow 2009 — a ten- to twenty-fold higher dose of a different molecule that is not even in the metabolic pathway.
Fladrafinil pharmacokinetics — how much of it actually gets in
The catalog says ‘Long — commonly 12–15 hours reported’. As of 2026 there are real human numbers to put beside that report, and they are not the same kind of number.
What degrades it, in sequence. Three transformations, two of them oxidative. First the hydroxamic acid is reduced or hydrolyzed to the plain amide, converting fladrafinil into flmodafinil — this is the activation step and it is the same relationship adrafinil has to modafinil. Then the amide is hydrolyzed to flmodafinil acid, and separately the sulfoxide is oxidized to flmodafinil sulfone. Both of those were the metabolites actually detected in human urine and blood Krug 2026. Note what is not on that list: no defluorination, and no conversion to modafinil or modafinic acid.
The numbers, converted into something comparable. A 20 mg oral dose gave blood fladrafinil of 11–35 ng/mL Krug 2026. At 325.33 Da, 35 ng/mL is about 108 nM; the flmodafinil figure of 98 ng/mL at 309.33 Da is about 317 nM. Hold that against the pharmacology: modafinil is characterized as a low-affinity dopamine transporter inhibitor Hersey 2024, which is why it is dosed at 200–400 mg Volkow 2009. Circulating concentrations in the low hundreds of nanomolar from a 20 mg dose are therefore hard to reconcile with transporter occupancy by the parent, and are a further argument that the active species is the metabolite and that 20 mg is a small dose for this family rather than a large one.
The oral barrier. A neutral, moderately lipophilic sulfoxide of 325 Da has no absorption problem: no ionized group, no peptide bond for brush-border peptidases, no ester for gut esterases. The rate-limiting step is not getting in — it is first-pass conversion, and for a prodrug that step is the point rather than the loss. This is also why the ‘without adrafinil's liver burden’ claim is chemically odd: a hydroxamic acid prodrug requires hepatic conversion by definition.
Route, and the number an athlete needs. Oral only. Detection limits in the doping-control assay are 0.2–4 ng/mL for the parents and metabolites, and the detection windows are described as relatively long Krug 2026. Set that beside urinary concentrations of 52–891 ng/mL after a single 20 mg dose and the implication is arithmetic: the assay can see this compound at a fraction of a percent of its peak, so a single use is detectable for a long time after the effect has gone.
What would have to be true, and how you would know it was not
Four predictions. The fourth contradicts this compound's main selling point.
1. Actigraphy will show the duration claim is real or is not, and nobody has looked. Wear a sleep tracker. Compare total sleep time and sleep-onset latency on a day with a single morning dose against matched non-dosed days in the same week. Prediction: if the 12–15 hour figure is accurate, a 09:00 dose measurably delays sleep onset that night. If it does not, the duration number is a folk figure and the ‘nothing after midday’ rule is being followed for the wrong reason.
2. Resting heart rate and blood pressure will rise. Dopamine transporter blockade raises both across this family Volkow 2009. Use the seven-day average resting heart rate from a wearable and a home cuff at 2–4 hours post dose, before and during a block of use. This is the cheapest safety measurement on the page and the one most people skip.
3. A tested athlete will fail, and this is a prediction with a number. Both fladrafinil and flmodafinil are S6 stimulants prohibited in competition, the assay detects them at 0.2–4 ng/mL, and detection windows for the parents and the acid and sulfone metabolites are long Krug 2026. Nothing about this is physiological and it is the prediction most likely to change a reader's decision. Check the current Prohibited List rather than this paragraph.
4. Against the product: GGT and a CMP should be drawn, because the ‘no liver burden’ claim has the chemistry backwards. Adrafinil's reputation for raising liver enzymes on long-term use is attributed to its hydroxamic acid and the hepatic conversion it requires. Fladrafinil is also a hydroxamic acid — N-hydroxyacetamide is in its systematic name Krug 2026 — and also requires hepatic conversion. So the mechanistic expectation is that on this axis fladrafinil behaves like adrafinil, not like modafinil, and the widely repeated claim that it spares the liver is asserted about a molecule that carries the same functional group. Draw GGT with a CMP at baseline and at 12 weeks of regular use. Nobody has ever measured it, in anyone.
What nobody has tested yet
Five experiments. The second is the one a buyer would most want and the fifth is the one the marketing depends on.
1. Nobody has measured a single pharmacodynamic endpoint. Six people have now taken 20 mg under study conditions and the only thing recorded was what appeared in their urine Krug 2026. Adding a psychomotor vigilance task, a Karolinska sleepiness scale and a blood pressure cuff to that same protocol would create the compound's entire pharmacodynamic literature at essentially no extra cost.
2. Nobody has surveyed what research-chemical ‘fladrafinil’ actually contains. Fladrafinil and flmodafinil differ by one oxygen atom, both are sold under overlapping names and code numbers, and the GC method a vendor is most likely to use degrades both to a shared tetrafluoro product Dowling 2017. A twenty-sample LC-HRMS survey would say how often the bottle matches the label. The broader market surveillance that does exist — 159 samples, 34 molecules, 69% from illegal supply Vanhee 2025 — did not resolve this pair.
3. Nobody has addressed the enantiomers. The sulfoxide is chiral, the single-enantiomer version of the parent compound in this family has a different half-life, and no product on the market states a ratio. A chiral LC method on five batches would tell you whether ‘fladrafinil’ is even one consistent substance.
4. There is no dose-response above 20 mg. The published human study used a single 20 mg dose Krug 2026; the market runs 30–100 mg. Three doses, six people each, plasma and a vigilance endpoint, would put a curve where there is currently a range copied between vendor pages.
5. Nobody has run the liver comparison the marketing rests on. Adrafinil against fladrafinil, same subjects, crossover, GGT and a full metabolic panel at twelve weeks. The claim that fladrafinil delivers adrafinil-like effects without adrafinil's liver-enzyme cost is the single most repeated selling point for this compound, it is made about a molecule bearing the same hydroxamic acid functional group, and there is not one measurement behind it in either direction.
Fladrafinil — its own safety story, not its class's
The class block covers stimulants generally. Five things here belong to this molecule, and the first is a correction rather than a warning.
1. It converts to flmodafinil, not to modafinil, and modafinil's safety record does not come with it. Fladrafinil is the hydroxamic acid prodrug of CRL-40,940 Krug 2026. Modafinil has been given to hundreds of thousands of patients under regulatory surveillance; flmodafinil has been given to six volunteers in one published study. Importing one record onto the other is the central error people make with this compound.
2. Anti-doping is the dominant risk for anyone who competes. S6 stimulant, prohibited in competition, detected at 0.2–4 ng/mL with long detection windows for both parent compounds and their acid and sulfone metabolites Krug 2026. That is a career-level consequence with a published assay behind it, and it outranks every pharmacological consideration on this page.
3. The three-fold spread at a fixed dose is a reason not to titrate by other people's reports. Twenty milligrams gave blood concentrations of 11 to 35 ng/mL across six people Krug 2026. Somebody describing 50 mg as mild may be at the bottom of that distribution, and copying their dose is copying their metabolism, which you do not have.
4. Two warnings imported from the parent drug's regulatory labeling, flagged as imports. Modafinil's approved labeling carries a warning about serious rash including Stevens-Johnson syndrome, and a warning that it induces CYP3A4 and can reduce the effectiveness of hormonal contraceptives. Neither has been studied for fladrafinil or flmodafinil, and neither can be assumed absent: there is no adverse-event reporting system for a research chemical, so an absence of case reports here is an absence of anyone collecting them. Anyone relying on hormonal contraception while using a modafinil-family compound should treat the interaction as live until somebody measures it.
5. The liver claim is unearned in both directions. The selling point is that this spares the liver relative to adrafinil; the chemistry says it carries the same hydroxamic acid and needs the same hepatic conversion Krug 2026. Neither position has a measurement. That is not a claim that it damages the liver — it is a statement that the reassurance being offered is a marketing sentence with the chemistry pointing the other way, and that a baseline liver panel before a long block costs almost nothing.
Sources read for this page
- Krug O, Guddat S, Görgens C, Walpurgis K, Toma F, Thomas A, Thevis M. Investigations Into the Metabolism and Elimination of Flmodafinil and Fladrafinil for Sports Drug Testing Purposes. Drug Testing and Analysis 2026 · PMID 42210629
- Dowling G, Kavanagh PV, Talbot B, O'Brien J, Hessman G, McLaughlin G, Twamley B, Brandt SD. Outsmarted by nootropics? An investigation into the thermal degradation of modafinil, modafinic acid, adrafinil, CRL-40,940 and CRL-40,941 in the GC injector: formation of 1,1,2,2-tetraphenylethane and its tetra fluoro analog. Drug Testing and Analysis 2017;9(3):518-528 · PMID 27928893
- Volkow ND, Fowler JS, Logan J, Alexoff D, Zhu W, Telang F, Wang GJ, Jayne M, Hooker JM, Wong C, et al. Effects of modafinil on dopamine and dopamine transporters in the male human brain: clinical implications. JAMA 2009;301(11):1148-1154 · PMID 19293415
- Hersey M, Tanda G. Modafinil, an atypical CNS stimulant?. Advances in Pharmacology 2024;99:287-326 · PMID 38467484
- Napoletano F, Schifano F, Corkery JM, Guirguis A, Arillotta D, Zangani C, Vento A. The Psychonauts' World of Cognitive Enhancers. Frontiers in Psychiatry 2020;11:546796 · PMID 33024436
- Vanhee C, Deconinck E, George M, Hansen A, Hackl A, Wollein U, El-Atma O, Beerbaum N, Aureli F, Borioni A, et al. The Occurrence of Illicit Smart Drugs or Nootropics in Europe and Australia and Their Associated Dangers: Results from a Market Surveillance Study by 12 Official Medicines Control Laboratories. Journal of Xenobiotics 2025;15(3):88 · PMID 40558871
Fladrafinil — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- This group acts directly on established CNS receptors — GABA-B (phenibut), serotonergic and histaminergic (trazodone, doxepin), beta-adrenergic (propranolol), dopaminergic (cabergoline, apomorphine). These are pharmacological drugs, not research peptides, and the predicted problems are the known ones for each receptor.
- Phenibut is the one that needs saying plainly: it is physically addictive. GABA-B agonism produces tolerance within days of regular use, and withdrawal is genuinely severe — anxiety, insomnia, tremor, and in heavy users, psychosis and seizures. It is closer to a benzodiazepine than to a nootropic in this respect, and it is sold as though it were the latter.
- Propranolol blunts the physical symptoms of adrenaline. That predicts the useful effect and also the problem — it blunts the training response and masks hypoglycemia.
- Dopamine agonists predict nausea, orthostatic hypotension and, at the doses used in Parkinson's, impulse-control problems. Cabergoline's half-life is very long, so effects persist well past a dose.
What has actually been reported
- Phenibut dependence and withdrawal are well documented in case reports and poison-center data.
- Trazodone: sedation, orthostatic hypotension, and rarely priapism — which is a medical emergency.
- Abrupt propranolol cessation causes rebound tachycardia and hypertension. Do not stop a beta-blocker suddenly.
- Cabergoline at high cumulative doses is associated with cardiac valve changes; at the low doses used for prolactin this has not been shown.
How to reduce the risk
Same mechanism as the prediction.
- For phenibut, the only reliable mitigation is frequency: occasional use does not produce dependence, regular use does. There is no dose that makes daily use safe.
- Taper anything in this group rather than stopping abruptly.
- Take the first dose of anything with orthostatic effects at home, sitting down.
What it does to your bloodwork
A fact about the assay.
- Prolactin if using cabergoline (it is usually why you are). Otherwise blood pressure and heart rate are the monitoring that matters.
Don't run this if
- You already take a sedative, a benzodiazepine, or drink regularly — the CNS depressant effects are additive and this is where respiratory depression comes from.
- You are on an antidepressant and considering trazodone — serotonergic combinations need a prescriber, not a forum.
The honest unknown
- Most of this group is well characterized for its licensed use. What is NOT characterized is the off-label use most people here are making of it, at doses and durations nobody studied.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Fladrafinil — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Fladrafinil moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Most of this class has no predicted marker movement at all, and saying so is more useful than listing markers that will not move.
What to do: A baseline liver panel is reasonable for anything taken daily and long-term. Beyond that there is nothing specific to chase.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- How the forms differ in dose
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Fladrafinil in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Fladrafinil
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| TSH (Thyroid-Stimulating Hormone) | Thyroid disease imitates every cognitive complaint there is |
| Vitamin B12 | Deficiency causes fog long before it causes anemia |
| Methylmalonic Acid (MMA) | Catches the deficiency a normal B12 hides |
| Ferritin | Low iron flattens cognition at levels most labs call fine |
| Vitamin D (25-Hydroxy) | Commonly low, cheap to correct, associated with mood |
The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.
Check results you already have → · All 103 markers A–Z
Fladrafinil — frequently asked questions
What is Fladrafinil?
Fladrafinil (CRL-40,941 / fluorafinil) is a cognitive & mood research compound. A bis-fluoro analog of adrafinil that converts to a modafinil-like active. Dopamine reuptake inhibition is the accepted mechanism for the wakefulness effect.
Is the full Fladrafinil protocol on this page?
The reported research dose is on this page, along with how Fladrafinil works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Fladrafinil?
Fladrafinil has an approximate half-life of Long — commonly 12–15 hours reported, which is part of what determines how often it's dosed.
What's the evidence behind Fladrafinil?
Current evidence level: No human trials; extrapolated from modafinil. Fladrafinil is offered for research purposes only and is not an approved medicine.
Fladrafinil inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Fladrafinil is used for
Fladrafinil appears under 1 goal in the goal router.
Related Cognitive & Mood compounds
Where this goes next
Fladrafinil is the dopaminergic arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.