Modafinil
Provigil — sold as Modalert, Modvigil, Modafresh, Modawake, ModaXL, Vilafinil, Modaheal
Modafinil (Provigil — sold as Modalert, Modvigil, Modafresh, Modawake, ModaXL, Vilafinil, Modaheal) is a cognitive & mood research compound. A wake-promoting agent whose FDA label states plainly that the mechanism is unknown. The one action measured in a living human brain is dopamine transporter blockade: positron-emission tomography at 200-400mg found transporter binding potential reduced by 39.3% in nucleus accumbens, 47.2% in putamen and 53.8% in caudate, with extracellular dopamine rising most in the accumbens. It induces CYP3A4/5 and inhibits CYP2C19, which is why it can make steroidal contraceptives less effective and can raise exposure to phenytoin, diazepam, propranolol, omeprazole and clomipramine.
Modafinil quick facts
| Route | Oral |
| Frequency | 1x Daily · Per prescription |
| Half-life | ~15 hrs (effective half-life on multiple dosing) |
| Forms | Oral |
| Evidence level | FDA-approved for narcolepsy, obstructive sleep apnea and shift work disorder — Schedule IV controlled substance |
Prescription-only and a Schedule IV controlled substance in the US, and the trial evidence is narrower than the reputation. Pooled across nine randomized trials in diagnosed sleep disorders, objective wakefulness improved by 2.95 minutes on the Maintenance of Wakefulness Test while continuous Epworth sleepiness scores did not separate from placebo, and discontinuation for adverse events ran at about 2.5x placebo, with insomnia at 4.6x. No randomized trial has tested it in rested adults for productivity. The interaction that matters most in this readership is CYP3A4 induction: the label states steroidal contraceptives may be less effective during use and for one month after stopping.
How Modafinil works
A wake-promoting agent whose FDA label states plainly that the mechanism is unknown. The one action measured in a living human brain is dopamine transporter blockade: positron-emission tomography at 200-400mg found transporter binding potential reduced by 39.3% in nucleus accumbens, 47.2% in putamen and 53.8% in caudate, with extracellular dopamine rising most in the accumbens. It induces CYP3A4/5 and inhibits CYP2C19, which is why it can make steroidal contraceptives less effective and can raise exposure to phenytoin, diazepam, propranolol, omeprazole and clomipramine.
Proposed benefits
Researched for focus, memory, neuroprotection, mood and stress resilience.
Where to get Modafinil
Buy Modafinil at RUPharma →Prescription-only in the US and a Schedule IV controlled substance, approved for narcolepsy, shift-work disorder and sleep apnea — not for ordinary tiredness, which is the use nobody has run the trial on.
It is a CYP3A4 inducer, and that is the interaction that catches people: it can drop hormonal contraception below the effective level for a month after the last dose. If you run testosterone or estrogen therapy alongside it, the levels are the thing to actually look at.
Order these through my Marek link →The evidence for Modafinil
Graded by what exists behind each claim.
✅ Clinically validated
- FDA-approved since 1998 to improve wakefulness in adults with excessive sleepiness from narcolepsy, obstructive sleep apnea or shift work disorder. Schedule IV controlled substance. That is the entire approved footprint — three sleep disorders, in adults, at 200 mg once daily.
- A 2026 meta-analysis of 9 randomized trials, 1265 participants found objective wakefulness improved (Maintenance of Wakefulness Test +2.95 minutes, 95% CI 0.66 to 5.23) while continuous Epworth sleepiness scores did not separate from placebo. Discontinuation for adverse events ran at RR 2.50, insomnia at RR 4.64 (de Lima 2026).
- The largest network meta-analysis in sleep apnea — 14 trials, 3085 patients — put armodafinil-modafinil behind solriamfetol on both sleepiness and objective wakefulness, and found it probably raises the risk of stopping for side effects (Pitre 2023, Ann Intern Med).
- There is no randomized trial in healthy, well-rested adults with a pre-registered cognitive endpoint. Every number above comes from people with a diagnosed sleep disorder, already on treatment for it.
📊 Correlative data
- Positron-emission tomography in 10 healthy men at 200-400 mg found dopamine transporter binding potential down 39.3% to 53.8% across striatal regions, with extracellular dopamine rising most in nucleus accumbens. The authors' own conclusion called for heightened awareness of abuse and dependence potential (Volkow 2009, JAMA).
- Two decades of off-label use for fatigue in multiple sclerosis, depression, Parkinson's and cancer-related fatigue, plus large non-medical use as a study drug. Widely reported; almost none of it collected in a way that could show whether it helps a rested person.
🧪 Theoretical / extrapolated
- The label says the mechanism is unknown, and that is not a hedge — it is the current state of the science. The orexin and histamine story comes from animal work; the transporter blockade is what has been measured in a person.
- It induces CYP3A4/5 and inhibits CYP2C19 at the same time. The induction is why steroidal contraceptives may fail during use and for a month after; the inhibition is why phenytoin, diazepam, propranolol, omeprazole and clomipramine exposures rise.
- A ~15-hour effective half-life is the mechanistic reason for the insomnia signal: a morning dose is still at roughly half its peak at bedtime. That is a design feature of the drug, not a side effect of misuse.
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 Modafinil actually does
Start with the sentence the regulator wrote, because every other page about this drug skips it. Provigil label 2025: “The mechanism(s) through which modafinil promotes wakefulness is unknown.” That is the FDA-approved labeling for a drug in its third decade of clinical use, and it is a more honest position than the orexin-and-histamine story the supplement internet tells. The label goes on to say only what has been shown: “In vitro, modafinil binds to the dopamine transporter and inhibits dopamine reuptake”, an activity associated in vivo with raised extracellular dopamine in some brain regions of animals.
The one measurement in a living human, and the numbers are large. Volkow 2009 gave 10 healthy men therapeutic doses — 200 mg and 400 mg orally — and imaged them twice. With [11C]cocaine, the dopamine transporter ligand, binding potential fell by 53.8% in caudate, 47.2% in putamen and 39.3% in nucleus accumbens: that is transporter occupancy, and roughly half of the caudate transporter pool was occupied. With [11C]raclopride, which reports endogenous dopamine, binding potential fell 6.1% in caudate, 6.7% in putamen and 19.4% in nucleus accumbens, meaning extracellular dopamine rose, most of all in the accumbens. The authors' own conclusion is printed in the abstract: because drugs that raise accumbens dopamine have abuse potential, the increasing use of this one warrants heightened awareness of abuse and dependence in vulnerable people.
How ‘low affinity’ and ‘half the transporter occupied’ are both true. Hersey 2024 frames modafinil as an atypical CNS stimulant: a weak dopamine transporter inhibitor, with additional and less understood actions across GABA, glutamate, serotonin and noradrenaline, and with strikingly few dependence reports relative to other transporter blockers. Weak affinity is not weak occupancy. Occupancy is set by concentration divided by affinity, and the dose that compensates is the reason this drug is taken in 200 mg units while methylphenidate is taken in 10 mg ones. The pharmacology is not gentle; the dose scale is where the gentleness lives.
The category itself was an argument, not a discovery. Scholte 2025 traces how modafinil came to be classified as something other than a stimulant, and the useful reading of that paper on a page like this one is that the word eugeroic did work the pharmacology could not. RUPharma files ten SKUs of it under a shelf with that name. The shelf is marketing history; the transporter occupancy above is measurement.
Cell, rodent, human — and where it stops
The cell rung is an in vitro binding assay and the label says so in one sentence Provigil label 2025. There is no cascade here worth narrating — the interesting part of this compound's translation chain is that it skipped straight to humans.
The human mechanism rung is real, small, and male. Ten men, one center, positron emission tomography, two doses Volkow 2009. Ten people is a pilot; the effect sizes were large enough to clear it, and no comparable study has been published in women, in older adults, or at the 100 mg dose that one of the SKUs on the shelf actually is.
The clinical rung is the biggest one and it is entirely inside diagnosed sleep disorders. Pitre 2023 pooled 14 randomized trials, 3085 patients with excessive daytime sleepiness in obstructive sleep apnea, all of them on or eligible for conventional therapy. At 4 weeks, armodafinil-modafinil improved the Epworth Sleepiness Scale by a mean difference of −2.25 points (95% CI −2.85 to −1.64), moderate certainty, and improved the Maintenance of Wakefulness Test by a standardized mean difference of 0.41 (0.27 to 0.55), high certainty. Solriamfetol beat it on both (ESS −3.85; SMD 0.90). And armodafinil-modafinil probably raises the risk of stopping the drug because of side effects: relative risk 2.01 (1.14 to 3.51).
A 2026 meta-analysis of modafinil on its own is less flattering, and its split result is the most useful thing on this page. de Lima 2026 pooled 9 randomized trials, 1265 participants in obstructive sleep apnea and shift work sleep disorder. Objective wakefulness moved: pooled Maintenance of Wakefulness Test endpoint +2.95 minutes (95% CI 0.66 to 5.23, p = 0.01, I² = 36%), moderate certainty. Subjective sleepiness did not: continuous Epworth analyses, both change-from-baseline and endpoint, showed no statistically significant difference from placebo, low certainty, although responder analyses using predefined criteria favored the drug. Tolerability was unambiguous: discontinuation for adverse events RR 2.50 (1.24 to 5.07), insomnia RR 4.64 (2.21 to 9.75), anxiety or nervousness RR 3.08 (1.49 to 6.39), nausea RR 2.57 (1.33 to 4.97), headache RR 1.38 (1.10 to 1.72).
And here is exactly where it stops. Read those two paragraphs again and notice what population they describe: people with a diagnosed sleep disorder, already on treatment for it. That is not who buys the ten SKUs. There is no trial in this evidence base of a rested adult taking modafinil to work harder, and the objective gain that does exist in the sick population is measured in single-digit minutes of sleep latency. Anyone extrapolating a three-minute wakefulness effect in apnea into a cognitive transformation in a healthy person is doing the extrapolation themselves, without a paper underneath it.
Modafinil pharmacokinetics — how much of it actually gets in
What degrades it, and the answer is mostly not a cytochrome. Provigil label 2025 lists the routes: hydrolytic deamidation, S-oxidation, aromatic ring hydroxylation and glucuronide conjugation, with less than 10% of a dose excreted as the parent compound. Amide hydrolysis to modafinic acid is the dominant step. It is about 60% bound to plasma protein, mainly albumin, which is low enough that displacement interactions are not the story here; enzyme induction is.
The oral barrier, and there is essentially none. This is a neutral, small, moderately lipophilic sulfinyl acetamide with no ionizable group, no peptide bond for brush-border peptidases and no ester for gut esterases. Food does not change overall bioavailability; it delays peak concentration by about one hour. Peak plasma concentrations arrive at 2 to 4 hours, and the effective elimination half-life after multiple doses is about 15 hours Provigil label 2025. No injectable form of modafinil has ever been marketed anywhere, and an injection would buy nothing: absorption is not the limiting step for this molecule, unlike every peptide on this site.
The arithmetic that decides when you take it. Fifteen hours means a dose at 07:00 has fallen to roughly half its peak by 22:00 and is not functionally gone until the following afternoon. Five half-lives is 75 hours. That single number explains the insomnia relative risk of 4.64 in de Lima 2026 better than any discussion of receptors: the drug is still there at bedtime because it was designed to be.
The enzyme interaction that matters most in this readership, and it is not the one people worry about. Modafinil induces CYP3A4/5, so substrates of that enzyme are cleared faster and reach lower systemic exposure — and the label states the consequence plainly: “The effectiveness of steroidal contraceptives may be reduced when used with PROVIGIL and for one month after discontinuation of therapy” Provigil label 2025. One month after stopping, not one day. In the opposite direction it inhibits CYP2C19, prolonging elimination of phenytoin, diazepam, propranolol, omeprazole and clomipramine and raising their exposure. A drug that is both an inducer and an inhibitor on the same prescription list is an unusual object and neither half is optional reading.
The dose ceiling, stated by the regulator and contradicted by the shelf. Provigil label 2025: “Doses up to 400 mg/day, given as a single dose, have been well tolerated, but there is no consistent evidence that this dose confers additional benefit beyond that of the 200 mg/day dose.” One of the ten SKUs a partner stocks is a 400 mg tablet. The label says the second 200 mg has no demonstrated benefit and the same adverse-event profile.
What would have to be true, and how you would know it was not
Four predictions. The first two cut against the reason most people buy this.
1. Against the product: in a rested adult, a validated sleepiness scale will not move. The Epworth is free, takes two minutes and is the instrument the trials used. de Lima 2026 found that even in people with obstructive sleep apnea, continuous Epworth analyses did not separate from placebo. Score it for a week off and a week on, at the same hour. Prediction: no change beyond the scale's own noise. If somebody's Epworth drops five points on modafinil while they are sleeping normally, that is a finding worth having and it contradicts the pooled trial data.
2. Against the product: an executive-function battery will not move either. Trail making, part B, and a MoCA are both free, both take under fifteen minutes, and both are sensitive to the kind of change the smart-drug market claims. No published randomized trial has shown modafinil improving either in a healthy, well-rested adult with a pre-registered endpoint. Run them at baseline and at 2 hours post dose. Alertness is not the same measurement as executive function, and conflating the two is the whole marketing move.
3. Actigraphy will show the 15-hour half-life operating, and most users have never checked. Wear a tracker. Compare sleep-onset latency and total sleep time on dosed days against matched undosed days in the same week. Prediction, straight from the pharmacokinetics: a 07:00 dose measurably delays sleep onset that night. This is the cheapest way to find out whether the fatigue somebody is medicating on day four is the drug's own doing.
4. The falsification with real-world stakes: contraceptive failure. The CYP3A4 induction claim is testable in the least pleasant way possible. Anyone on an ethinyl-estradiol contraceptive who takes this drug and does not add a non-hormonal method — during use and for a month afterwards Provigil label 2025 — is running the experiment on themselves. This is not a bloodwork prediction and it is the single most consequential line on the page.
What nobody has tested yet
Nobody has mapped the occupancy curve below 200 mg. Volkow 2009 imaged 200 mg and 400 mg. A partner sells a 100 mg tablet, and a large part of the community practice around this drug is splitting tablets further. The dopamine transporter occupancy at 50 mg and at 100 mg has never been measured in anybody. That is one more PET arm on an existing protocol, and it is the difference between a dose-response curve and folklore.
The trial that would settle the actual question has never been run. Healthy, well-rested adults; pre-registered executive-function primary endpoint; placebo; enough people to detect a small effect. Every trial in Pitre 2023 and de Lima 2026 enrolled people with a sleep disorder, so the entire evidence base answers a question adjacent to the one buyers are asking. The absence is not evidence the effect is absent — it is the reason nobody can say either way, which is exactly what a page like this owes a reader.
Nobody has published what is actually in the tablets. Vanhee 2025 is the closest thing that exists: a market surveillance study by 12 official medicines control laboratories across Europe and Australia, 159 samples, 166 identification entries, 34 distinct molecules, January 2020 to September 2024. 69% came from the illegal market, and prescription drugs were found in pharmacological quantities. That study did not analyze the specific SKUs on this shelf, and no published assay has. A generic modafinil tablet from a licensed pharmacy is a known quantity; the same molecule ordered from an unlicensed seller is an assumption, and the assumption has never been checked.
Extrapolation, labeled as such. If the wakefulness effect really runs through the transporter occupancy in Volkow 2009, three things should follow that nobody has looked for. The effect should be blunted by a D2 antagonist. It should track occupancy rather than plasma concentration, which are not the same curve. And it should be larger in people with lower baseline transporter density, which is measurable and varies with age. None of those three experiments appears in the published record, and each is an ordinary imaging study.
Modafinil — its own safety story, not its class's
Four things specific to this molecule, and none of them is in a class block.
The rash is the reason this drug has a warning at all, and the timing is the useful part. Provigil label 2025 reports that nearly all cases of serious rash occurred within 1 to 5 weeks of starting, that the incidence of rash leading to discontinuation was approximately 0.8%, 13 per 1,585, in pediatric trial participants under 17, and that the background rate of Stevens-Johnson syndrome and toxic epidermal necrolysis in the general population is 1 to 2 cases per million person-years. Hold those two figures side by side: a fraction of a percent against one in a million. Any rash in the first five weeks is a reason to stop and be seen, not a reason to wait and watch.
Multi-organ hypersensitivity, with a number for how long you have to stay alert. The label records reactions occurring in close temporal association with starting, median time to detection 13 days, range 4 to 33, including at least one fatality in postmarketing experience. Kasitinon 2022 is a published case of modafinil-induced DRESS — drug reaction with eosinophilia and systemic symptoms — which is the syndrome that presents as rash plus fever plus something wrong in the bloods, and which is missed when a rash is treated as a skin problem.
The psychiatric column, with the trial rates and the postmarketing list kept apart. In trials, psychiatric symptoms leading to discontinuation at a frequency of 0.3% or more were anxiety 1%, nervousness 1%, with insomnia, confusion, agitation and depression each under 1% Provigil label 2025. Postmarketing reports are a different kind of evidence and a different severity: mania, delusions, hallucinations, suicidal ideation and aggression, some resulting in hospitalization. Uncounted, unrated, and real.
The legal fact, stated plainly because it changes what the rest of the page means. Modafinil is a prescription drug and a Schedule IV controlled substance in the United States Provigil label 2025. The label's own abuse section says it produces psychoactive and euphoric effects and alterations in mood, perception and thinking typical of other CNS stimulants; Volkow 2009 provides the accumbens dopamine measurement that explains why. Nothing on this page is instruction for obtaining or using it outside a prescription, and the honest summary of the evidence above is that the measured benefit in people who need it is a few minutes of sleep latency while the measured cost is a doubled chance of stopping because of side effects.
Sources read for this page
- U.S. Food and Drug Administration. PROVIGIL (modafinil) tablets, C-IV - full prescribing information, including the serious rash warning, the mechanism-of-action statement, the CYP3A4/5 induction and CYP2C19 inhibition sections and the drug abuse and dependence section. DailyMed, U.S. National Library of Medicine; Cephalon LLC label version 23, revised March 2025
- 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
- Pitre T. Comparative Efficacy and Safety of Wakefulness-Promoting Agents for Excessive Daytime Sleepiness in Patients With Obstructive Sleep Apnea: A Systematic Review and Network Meta-analysis. Annals of Internal Medicine 2023 · PMID 37155992
- de Lima MS. Modafinil for excessive daytime sleepiness: A systematic review and meta-analysis of randomized controlled trials. Sleep Medicine 2026 · PMID 42468246
- Kasitinon SY. Modafinil-induced drug reaction with eosinophilia and systemic symptoms syndrome. JAAD Case Reports 2022 · PMID 36046806
- Scholte SJ. Making modafinil: Classification and serendipity in drug development. Social Studies of Science 2025 · PMID 40099909
- 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
Modafinil — 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 class is broad, but the predicted problems cluster by mechanism rather than by molecule. Cholinergics (racetams, and anything raising acetylcholine) predict headache — the classic one, from choline demand outrunning supply. Dopaminergics and eugeroics predict tolerance, sleep disruption and a flat mood on the days off. Anything glutamatergic or AMPA-facing carries a theoretical excitotoxicity concern at high doses.
- The pattern worth internalizing: anything that borrows performance from tomorrow eventually presents the bill. Sleep is the most common currency it gets paid in.
What has actually been reported
- Headache is the most reported effect across the racetam family and usually responds to added choline.
- Irritability, blunted affect and a rebound low on cessation are commonly reported with the stimulant-adjacent members.
- Most of this class has little or no controlled human safety data at the doses actually used.
How to reduce the risk
Same mechanism as the prediction.
- Take a choline source with any racetam. The headache is the mechanism running out of substrate, and it is largely preventable rather than something to push through.
- Dose in the morning. Almost everything in this class has a longer functional tail than its half-life suggests, and sleep is the first thing you lose.
- Use them for something, not as a habit. The compounds that carry tolerance genuinely reward intermittent use aimed at a task, and genuinely punish daily use aimed at feeling normal.
- One at a time, and long enough to judge it. This is the class where people stack five and cannot tell you which one is doing anything — and the effects are subjective, so attribution is already hard enough.
- If you need it to feel normal, stop. That is the line where a tool has become a dependency, and it is the one worth watching for.
What it does to your bloodwork
A fact about the assay.
- No routine marker tracks these. Sleep is the assay — if it is degrading, the compound is costing more than it is producing, and that shows up before anything else does.
Don't run this if
- A seizure history — several of these lower the threshold at least theoretically, and it is not worth establishing empirically.
- Bipolar disorder, for the dopaminergic members especially.
- Alongside prescribed psychiatric medication without knowing exactly how the mechanisms overlap.
The honest unknown
- Chronic use is essentially uncharacterized. The specific unmeasured thing is what daily cholinergic or dopaminergic pressure does to baseline function over years — not whether a few weeks is tolerable.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Modafinil — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Modafinil 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.
- Dose range and how to work up to it
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- 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 — Modafinil in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Modafinil
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
Modafinil — frequently asked questions
What is Modafinil?
Modafinil (Provigil — sold as Modalert, Modvigil, Modafresh, Modawake, ModaXL, Vilafinil, Modaheal) is a cognitive & mood research compound. A wake-promoting agent whose FDA label states plainly that the mechanism is unknown. The one action measured in a living human brain is dopamine transporter blockade: positron-emission tomography at 200-400mg found transporter binding potential reduced by 39.3% in nucleus accumbens, 47.2% in putamen and 53.8% in caudate, with extracellular dopamine rising most in the accumbens. It induces CYP3A4/5 and inhibits CYP2C19, which is why it can make steroidal contraceptives less effective and can raise exposure to phenytoin, diazepam, propranolol, omeprazole and clomipramine.
Where can I find Modafinil dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Modafinil protocol are available to members inside Skool. This public page covers what Modafinil is, how it works and the evidence.
What is the half-life of Modafinil?
Modafinil has an approximate half-life of ~15 hrs (effective half-life on multiple dosing), which is part of what determines how often it's dosed.
What's the evidence behind Modafinil?
Current evidence level: FDA-approved for narcolepsy, obstructive sleep apnea and shift work disorder — Schedule IV controlled substance. Modafinil is offered for research purposes only and is not an approved medicine.
What Modafinil is used for
Modafinil appears under 1 goal in the goal router.
Related Cognitive & Mood compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.