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Adrafinil (Olmifon, CRL-40028) — a modafinil prodrug
A discontinued French wakefulness drug (Olmifon, CRL-40028) the liver converts into modafinil — essentially a less-efficient, slower way to take modafinil. Once prescribed for vigilance and attention in the elderly, it was withdrawn from the market and now circulates grey-market as an unregulated 'nootropic.' Direct human evidence is old and thin, chronic use can raise liver enzymes, and it is NOT a dietary supplement and NOT a longevity drug.
Research compound — not a dietary supplement
Adrafinil (Olmifon) 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 Adrafinil (Olmifon) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from medium-quality studies published 2000–2020.
Based on 6 studies
Confidence
Low confidenceBy outcome
Adrafinil is essentially a less-efficient, liver-converted prodrug of modafinil — its ceiling of benefit is modafinil's, reached more slowly and less predictably with an added hepatic-conversion step. Direct human evidence is old and thin (it was withdrawn from the market, with no modern controlled efficacy trials), the cleanest direct data are in aged dogs and are mixed (improved discrimination learning in one study, disrupted working-memory performance in another), chronic use can raise liver enzymes, and it circulates grey-market with no approval — so it stays low/emerging.
Adrafinil (Olmifon; lab code CRL-40028) is a wakefulness-promoting agent — a eugeroic — first identified by the French firm Laboratoire L. Lafon in 1974.
Its key pharmacological fact is that adrafinil itself is largely a prodrug: after oral dosing the liver metabolizes it into modafinil (plus inactive modafinilic acid), and that active metabolite is what actually drives wakefulness.
Modafinil was in fact discovered THROUGH adrafinil — chasing adrafinil's pharmacokinetics led Lafon to its active metabolite, which became the better-characterized drug.
The honest framing for this collection: adrafinil is a less-efficient, hepatically-converted, slower-onset way of taking modafinil, so its ceiling of benefit is modafinil's, reached less predictably and with an extra liver-conversion step.
The direct human evidence for adrafinil is genuinely thin and dated — it was once marketed in France (as Olmifon) for vigilance, attention, and mood in elderly patients, but Michel Jouvet's early prescribing was reported to give 'inconsistent results,' there are no modern controlled efficacy trials in healthy adults, and most of the modern literature is pharmacology, doping-control assay development, and case reports rather than outcome trials.
The cleanest direct efficacy data are actually in aged dogs, and even there the picture is mixed: adrafinil improved simple discrimination learning in aged beagles in one study but DISRUPTED performance on a delayed-nonmatching-to-position memory task in another.
Adrafinil was withdrawn from the market (Olmifon was discontinued in 2011) and is banned in sport by WADA; it is now sold grey-market online as an unregulated 'nootropic.' The principal distinctive risk versus modafinil is hepatic: chronic adrafinil use can elevate liver enzymes (the conversion happens in the liver), which is a stated reason it is unsuited to long-term use, and case reports document persistent orofacial dyskinesia.
It is not a dietary supplement, not approved anywhere today, and there is no lifespan or healthspan evidence — it is not a longevity drug. The low score reflects thin, old, and mixed direct evidence, an active metabolite that is simply modafinil, grey-market status, and a real hepatotoxicity signal.
Adrafinil is largely a prodrug — the liver metabolizes it into modafinil (and inactive modafinilic acid), so the active wakefulness effect is modafinil's, reached after an extra conversion step.
Via the modafinil metabolite, it raises cortical catecholamine (noradrenaline/dopamine) tone and engages orexin and histamine arousal circuitry to promote vigilance.
Because it must be converted in the liver, adrafinil acts more slowly and less predictably than modafinil and requires a higher milligram dose for an equivalent effect.
How Adrafinil (Olmifon) 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.
Avoid — the hepatic-conversion step and liver-enzyme elevation make adrafinil a poor choice; modafinil is a more direct option under medical supervision.
Banned in sport by WADA (adrafinil and modafinil) — do not use in competition.
Not suited to chronic use because of cumulative liver-enzyme elevation.
Adrafinil is converted in the liver and can raise liver enzymes; combining with other hepatotoxic agents or alcohol compounds the risk.
Via its modafinil metabolite (a CYP3A4 inducer), adrafinil may reduce hormonal-contraceptive efficacy — use additional/alternative contraception.
Additive cardiovascular and CNS stimulation; use with caution.
Tip: The hallmark distinctive risk versus modafinil; avoid chronic use and monitor liver function if used at all.
Tip: Shared with modafinil; dose earlier in the day and reduce dose.
Tip: Take earlier in the day; reduce dose.
Tip: A case report describes persistent orofacial dyskinesia that did not resolve on withdrawal; discontinue and seek neurological care if abnormal movements appear.
Adrafinil (Olmifon) has an evidence score of 3.4/10 — emerging evidence based on 6 indexed studies. A discontinued French wakefulness drug (Olmifon, CRL-40028) the liver converts into modafinil — essentially a less-efficient, slower way to take modafinil. Once prescribed for vigilance and attention in the elderly, it was withdrawn from the market and now circulates grey-market as an unregulated 'nootropic.' Direct human evidence is old and thin, chronic use can raise liver enzymes, and it is NOT a dietary supplement and NOT a longevity drug. Representative study: PMID 30174215.
The commonly studied dose of Adrafinil (Olmifon) is Historically Olmifon was dosed around 600–1200 mg/day (in divided doses, earlier in the day) — roughly 3–4× a modafinil dose because of incomplete hepatic conversion. There is no approved or standardized regimen today; it is an unapproved grey-market chemical and not a clinician-supervised drug.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
The best time to take Adrafinil (Olmifon) is in the morning. It can be taken on an empty stomach. Like its modafinil metabolite, adrafinil is long-acting, so it is taken earlier in the day to avoid disrupting nighttime sleep.
Adrafinil (Olmifon) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are elevated liver enzymes, headache / insomnia / anxiety, gastric / abdominal discomfort. Use caution if any of these apply to you: Liver disease or elevated baseline liver enzymes (hepatic conversion step); Concurrent hepatotoxic drugs or heavy alcohol use; Uncontrolled hypertension or arrhythmia (use with caution).
Caffeine
Likely helpsBlocks adenosine receptors to boost alertness, reaction time, and endurance — one of the most proven ergogenic aids.
Citicoline
Probably helpsDual precursor to acetylcholine and phosphatidylcholine — enhances memory, focus, and brain cell membrane repair.
Nicotinamide Riboside
Mostly mechanism / observationalA vitamin B3 precursor that reliably raises cellular NAD+ levels and is well tolerated — but human trials have so far shown mostly null or mixed results on the functional outcomes (muscle, metabolism, blood pressure, cognition) that elevation is meant to drive.
Theacrine
Mostly mechanism / observationalCaffeine-like purine alkaloid from kucha tea. Small RCTs suggest subjective energy and mood benefits and good safety, but objective performance gains are inconsistent.
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Reviewed by Dr. Baher Al Hakim · Last reviewed June 2026 · evidence from 6 studies · how we score · editorial policy
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.
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