Modafinil
2-[(diphenylmethyl)sulfinyl]acetamide
Overview
Modafinil belongs to Nootropics.
Effects
- The core effect is wakefulness and reduced fatigue and sleepiness, with improved alertness and sustained attention: most robustly in sleep-deprived people.
- Users often report increased focus, motivation and mental stamina. Unlike amphetamine it produces little euphoria or 'rush', which is part of why it is experienced as subtle or 'flat'.
- In well-rested people the cognitive-enhancement effect is modest and inconsistent, and can come with over-focus, irritability, headache or difficulty sleeping later.
- Common unwanted effects are headache, dry mouth, reduced appetite, anxiety or jitteriness, and insomnia if taken late in the day.
Dosing & duration
Oral. Prescription doses for approved sleep disorders. Modafinil has roughly linear kinetics across 100–800 mg. Taking it late in the day disrupts night-time sleep. This is reference information, not medical advice: modafinil is a prescription-only, scheduled medicine.
Dose ranges
100–200 mg once daily (morning)
200 mg ~1 h before the shift
≈50–250 mg (≈50 mg ≈ 100 mg modafinil)
Duration
≈0.5–1 h (Tmax ≈2–4 h)
≈11–15 h (wakefulness across the day)
Chemical & Physical Properties
| Formula | C15H15NO2S |
| Molar mass | 273.35 g/mol |
| State | Solid |
| Melting point | 164–166 °C |
| Boiling point | Not reported |
| Density | Not reported |
| Vapor pressure | Not reported |
| pKa | Not reported |
| LogP | 0.6 |
| Solubility | Slightly soluble, Practically insoluble in water and cyclohexane. Sparingly to slightly soluble in methanol and acetone., 6.22×10⁻¹ g/L |
| Refractive index | Not reported |
Identifiers & Synonyms
| CAS | 68693-11-8 |
| CAS (enantiomer) | |
| PubChem CID | 4236 |
| InChIKey | YFGHCGITMMYXAQ-UHFFFAOYSA-N |
| InChI | InChI=1S/C15H15NO2S/c16-14(17)11-19(18)15(12-7-3-1-4-8-12)13-9-5-2-6-10-13/h1-10,15H,11H2,(H2,16,17) |
| SMILES | C1=CC=C(C=C1)C(C2=CC=CC=C2)S(=O)CC(=O)N |
Synonyms
- Provigil
- Modafinil
- 2-(diphenylmethylsulfinyl)acetamide
- Modasomil
- Modalert
- Armodafinil (R-enantiomer)
- Nuvigil
Pharmacodynamics & Biochemistry
Modafinil is a wakefulness-promoting agent ('eugeroic') whose pharmacology is distinct from that of classical stimulants. Its best-established molecular action is atypical, low-affinity inhibition of the dopamine transporter (DAT), which raises extracellular dopamine slowly and modestly, without the rapid surge, euphoria or strong reinforcement of amphetamine or cocaine. This DAT interaction appears necessary for its effect: modafinil does not promote wakefulness in dopamine-transporter-knockout mice. Downstream of that dopaminergic action it engages the brain's arousal networks: activating hypothalamic orexin (hypocretin) and histaminergic (tuberomammillary) wake-promoting neurons and raising noradrenergic tone, and at the cortical level tips the balance toward glutamatergic excitation and away from GABAergic inhibition. Its precise molecular mechanism is still not fully resolved despite decades of clinical use. It has little direct affinity for the noradrenaline or serotonin transporters or for classical monoamine receptors at therapeutic doses. Nonetheless the DAT occupancy seen on human PET imaging is enough to raise abuse-potential concerns, which is why modafinil is a scheduled drug. Modafinil is sold as the racemate: an equal mixture of (R)- and (S)-modafinil. The two enantiomers share a similar terminal half-life, but (S)-modafinil is cleared faster in the early phase, so at steady state the longer-lived (R)-enantiomer makes up the large majority of circulating drug and sustains higher late-day levels. (R)-modafinil is the more potent, longer-acting enantiomer and is marketed on its own, enantiopure, as armodafinil (Nuvigil): roughly 50 mg of armodafinil is equivalent to about 100 mg of racemic modafinil. Because armodafinil is simply this single enantiomer of modafinil, it is covered here rather than on a separate page.
Biological targets
- DAT
Binding & functional measurements
| Target | Measurement | Species |
|---|---|---|
| DAT | pKi 5.4 | Rat |
Pharmacokinetics
| Bioavailability | High (oral) |
| Tmax | ≈2–4 h |
| Half-life | ≈12–15 h |
| Vd | Not reported |
| Protein binding | ≈60% |
| Metabolism | Hepatic hydrolysis and CYP3A4. Modest CYP3A4 induction and CYP2C19 inhibition |
| Excretion | Renal (mainly as metabolites) |
Toxicology & Safety
2513 mg/kg (rat, oral)
Modafinil is generally well tolerated. Headache is the most common side effect, with nausea, anxiety, insomnia, dizziness and reduced appetite also frequent, plus modest increases in heart rate and blood pressure. Its serious risk is rare but important: severe cutaneous and hypersensitivity reactions (Stevens–Johnson syndrome, toxic epidermal necrolysis, DRESS and multi-organ hypersensitivity), which led the EMA (2011) to restrict its EU licence to narcolepsy only. It is contraindicated in pregnancy after data linked in-utero exposure to congenital malformations (cardiac defects, hypospadias, torticollis). Dependence potential is low but real and it is a controlled medicine. People with a history of substance misuse or serious cardiac disease/arrhythmia should avoid it. It is a prescription drug, not a benign 'smart drug'.[3][4]
Legal Status
US: Schedule IV. UK: Prescription only (POM). DE: Prescription only (Rx)
Interactions & Contraindications
Drug interactions
Contraindications
No interactions or contraindications listed.
Usage & Context
- Prescribed for excessive daytime sleepiness in narcolepsy, and as an adjunct in obstructive sleep apnoea and shift-work sleep disorder (the EU licence is restricted to narcolepsy only).
- Widely used off-label as a cognitive enhancer / 'smart drug' by students, shift workers and professionals, and studied by militaries for sustained operations, though its benefit in well-rested people is modest and inconsistent.
- The single (R)-enantiomer is marketed separately as armodafinil (Nuvigil), and the prodrug adrafinil is metabolised to modafinil in the body.
Sources & Evidence
- PubChem: Modafinil (CID 4236) — identifiers & properties
- Wikipedia: Modafinil (pharmacology, enantiomers, effects & legal status) CC BY-SA 4.0
- Ballon JS, Feifel D (2006). A systematic review of modafinil: Potential clinical uses and mechanisms of action. J Clin Psychiatry 67:554-66.
PMID 16669720 · doi:10.4088/jcp.v67n0406
- Minzenberg MJ, Carter CS (2008). Modafinil: a review of neurochemical actions and effects on cognition. Neuropsychopharmacology 33:1477-502.
PMID 17712350 · doi:10.1038/sj.npp.1301534
- Volkow ND, Fowler JS, Logan J, et al. (2009). Effects of modafinil on dopamine and dopamine transporters in the male human brain: clinical implications. JAMA 301:1148-54.
PMID 19293415 · doi:10.1001/jama.2009.351
- Darwish M, Kirby M, Hellriegel ET, et al. (2009). Armodafinil and modafinil have substantially different pharmacokinetic profiles despite having the same terminal half-lives: analysis of data from three randomized, single-dose, pharmacokinetic studies. Clin Drug Investig 29:613-23.
PMID 19663523 · doi:10.2165/11315280-000000000-00000
- FDA / DailyMed: Modafinil prescribing information — pharmacokinetics & metabolism
- IUPHAR/BPS Guide to PHARMACOLOGY: modafinil (ligand 7555) — DAT data CC BY-SA 4.0
- Zhou J, He R, Johnson KM, et al. (2004). Piperidine-based nocaine/modafinil hybrid ligands as highly potent monoamine transporter inhibitors: efficient drug discovery by rational lead hybridization. J Med Chem 47:5821-4.
PMID 15537337 · doi:10.1021/jm040117o