--- title: "Modafinil: Dosing & Vendor Prices — BodyHackGuide" description: "Modafinil: dosing protocols, mechanism & side effects, 3 PubMed studies. Compare verified vendor prices." lang: en json-ld: | [ { "@context": "https://schema.org", "@type": "BreadcrumbList", "itemListElement": [ { "@type": "ListItem", "position": 1, "name": "Home", "item": "https://www.bodyhackguide.co/" }, { "@type": "ListItem", "position": 2, "name": "Compounds", "item": "https://www.bodyhackguide.co/compare" }, { "@type": "ListItem", "position": 3, "name": "Modafinil" } ] }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "Modafinil", "description": "Modafinil is a prescription wakefulness-promoting agent approved by the US Food and Drug Administration in December 1998 under the brand name Provigil (Cephalon, now Teva) for the treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and as an adjunct to continuous positive airway pressure therapy in obstructive sleep apnea. It is a racemic mixture of R- and S-enantiomers; the R-enantiomer (armodafinil, brand name Nuvigil) was approved separately in 2007 as a longer-acting alternative. Modafinil became a Schedule IV controlled substance in the United States in 1999, reflecting a low but non-zero abuse potential that is substantially below that of amphetamines and classical stimulants. The compound is structurally unrelated to amphetamines, methylphenidate, and other stimulant classes — it is a diphenylmethylsulfinyl acetamide with a distinct pharmacology that produces wakefulness and cognitive effects without the catecholamine surge, appetite suppression, and cardiovascular profile of traditional stimulants. Modafinil's approved medical use base is narrow, but its off-label use is enormous. Physicians prescribe it off-label for ADHD (particularly in patients who do not tolerate or respond to stimulants), fatigue in multiple sclerosis and other neurologic conditions, cancer-related fatigue, depression augmentation (particularly for residual fatigue and cognitive symptoms), post-concussion cognitive dysfunction, jet lag, and age-related cognitive decline. Off-label and non-medical use as a cognitive enhancer — among students preparing for exams, professionals working long hours, military personnel during sustained operations, and the general nootropic community — has made modafinil one of the most-discussed cognitive enhancement compounds in both academic and lay media. The evidence base is substantial for approved indications and mixed for off-label use, with meta-analyses and systematic reviews documenting meaningful cognitive benefits in sleep-deprived users and healthy users performing complex cognitive tasks, alongside more modest or inconsistent effects on simple cognitive measures in rested users. Its safety profile across 25+ years of clinical use is generally favorable, though rare serious adverse events including Stevens-Johnson syndrome, toxic epidermal necrolysis, and DRESS syndrome (drug reaction with eosinophilia and systemic symptoms) require specific attention. This entry covers modafinil's mechanism of action and the ongoing uncertainty about which of its multiple pharmacologic effects drives wakefulness; the clinical evidence base for approved indications including narcolepsy, shift work disorder, and OSA; the off-label cognitive enhancement literature with its well-known heterogeneity between sleep-deprived and rested subjects; the side effect profile including common, serious, and rare adverse effects; the practical dosing conventions used in medical and non-medical contexts; its interactions with hormonal contraception and CYP450 substrates; contraindications based on cardiovascular, hepatic, and psychiatric history; how modafinil compares to and stacks with other nootropic compounds like Noopept, Piracetam, Sulbutiamine, Bromantane, Selank, Semax, Methylene Blue, NAD+, L-Theanine, and L-Tyrosine; and what responsible use looks like for someone considering modafinil for either medical or cognitive enhancement purposes. Modafinil remains the single most clinically validated cognitive enhancement compound available, with a body of evidence, safety data, and regulatory oversight that no research-chemical nootropic can match. For users who need demonstrably effective wakefulness promotion for legitimate medical reasons, it is a first-line option. For users considering it for cognitive enhancement, it is a serious drug with real effects and real side effects that deserves a serious evaluation rather than casual experimentation.", "lastReviewed": "2026-05-04T11:35:00.391+00:00", "url": "https://www.bodyhackguide.co/compound/modafinil", "author": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://x.com/bodyhackguide", "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "reviewedBy": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://x.com/bodyhackguide", "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "publisher": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" }, "mainContentOfPage": { "@type": "WebPageElement", "cssSelector": "main" }, "about": { "@type": "Drug", "name": "Modafinil", "alternateName": [ "Provigil", "Alertec", "Modalert", "Modvigil", "Modawake", "2-((diphenylmethyl)sulfinyl)acetamide", "CRL-40476" ], "description": "Modafinil is a prescription wakefulness-promoting agent approved by the US Food and Drug Administration in December 1998 under the brand name Provigil (Cephalon, now Teva) for the treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and as an adjunct to continuous positive airway pressure therapy in obstructive sleep apnea. It is a racemic mixture of R- and S-enantiomers; the R-enantiomer (armodafinil, brand name Nuvigil) was approved separately in 2007 as a longer-acting alternative. Modafinil became a Schedule IV controlled substance in the United States in 1999, reflecting a low but non-zero abuse potential that is substantially below that of amphetamines and classical stimulants. The compound is structurally unrelated to amphetamines, methylphenidate, and other stimulant classes — it is a diphenylmethylsulfinyl acetamide with a distinct pharmacology that produces wakefulness and cognitive effects without the catecholamine surge, appetite suppression, and cardiovascular profile of traditional stimulants. Modafinil's approved medical use base is narrow, but its off-label use is enormous. Physicians prescribe it off-label for ADHD (particularly in patients who do not tolerate or respond to stimulants), fatigue in multiple sclerosis and other neurologic conditions, cancer-related fatigue, depression augmentation (particularly for residual fatigue and cognitive symptoms), post-concussion cognitive dysfunction, jet lag, and age-related cognitive decline. Off-label and non-medical use as a cognitive enhancer — among students preparing for exams, professionals working long hours, military personnel during sustained operations, and the general nootropic community — has made modafinil one of the most-discussed cognitive enhancement compounds in both academic and lay media. The evidence base is substantial for approved indications and mixed for off-label use, with meta-analyses and systematic reviews documenting meaningful cognitive benefits in sleep-deprived users and healthy users performing complex cognitive tasks, alongside more modest or inconsistent effects on simple cognitive measures in rested users. Its safety profile across 25+ years of clinical use is generally favorable, though rare serious adverse events including Stevens-Johnson syndrome, toxic epidermal necrolysis, and DRESS syndrome (drug reaction with eosinophilia and systemic symptoms) require specific attention. This entry covers modafinil's mechanism of action and the ongoing uncertainty about which of its multiple pharmacologic effects drives wakefulness; the clinical evidence base for approved indications including narcolepsy, shift work disorder, and OSA; the off-label cognitive enhancement literature with its well-known heterogeneity between sleep-deprived and rested subjects; the side effect profile including common, serious, and rare adverse effects; the practical dosing conventions used in medical and non-medical contexts; its interactions with hormonal contraception and CYP450 substrates; contraindications based on cardiovascular, hepatic, and psychiatric history; how modafinil compares to and stacks with other nootropic compounds like Noopept, Piracetam, Sulbutiamine, Bromantane, Selank, Semax, Methylene Blue, NAD+, L-Theanine, and L-Tyrosine; and what responsible use looks like for someone considering modafinil for either medical or cognitive enhancement purposes. Modafinil remains the single most clinically validated cognitive enhancement compound available, with a body of evidence, safety data, and regulatory oversight that no research-chemical nootropic can match. For users who need demonstrably effective wakefulness promotion for legitimate medical reasons, it is a first-line option. For users considering it for cognitive enhancement, it is a serious drug with real effects and real side effects that deserves a serious evaluation rather than casual experimentation.", "activeIngredient": "Modafinil", "mechanismOfAction": "Modafinil's mechanism of action is genuinely incompletely understood despite more than two decades of clinical use and extensive preclinical research. It is not a classical stimulant — it does not produce the catecholamine surge of amphetamines, the direct noradrenergic release of ephedrine, or the primary adenosine antagonism of caffeine. What modafinil does do, based on converging evidence from receptor binding, microdialysis, imaging, and knockout mouse studies, is produce a modest inhibition of the dopamine transporter (DAT) that elevates extracellular dopamine in specific brain regions including the prefrontal cortex, striatum, and nucleus accumbens. DAT binding studies show a functionally meaningful effect at clinically relevant doses — Volkow and colleagues demonstrated in 2009 using PET imaging with the DAT radioligand [11C]cocaine that modafinil occupies dopamine transporters in the human brain at doses used therapeutically, with occupancy levels that correlated with elevations in extracellular dopamine. This finding was important because it established that modafinil's dopaminergic effects, while milder than amphetamine's, are real rather than negligible. However, DAT inhibition alone does not fully explain modafinil's pharmacology. Methylphenidate is a more potent DAT inhibitor but has a different clinical profile, and modafinil's effects on vigilance and wakefulness appear to involve additional systems. The orexin/hypocretin system is a major focus. Orexin neurons in the lateral hypothalamus are the primary wake-promoting neurons, and their loss causes narcolepsy. Modafinil activates orexin-containing neurons and increases histamine release in the tuberomammillary nucleus, which is the major histaminergic wake-promoting system. Direct activation of the histaminergic system via H1 histamine receptors in the cortex and other wake-relevant regions contributes to modafinil's wakefulness effect and may explain why modafinil produces alertness without the subjective stimulation of amphetamines. Additional modafinil effects include modest noradrenergic activation through alpha-1 adrenergic receptors, partial inhibition of the norepinephrine transporter, modest effects on serotonergic transmission at higher doses, increased glutamate release in cortex and thalamus, and reduced GABA release in multiple brain regions. The net effect is a neurotransmitter milieu that favors cortical activation and vigilance without the blunt force of amphetamine-class drugs. The selectivity of modafinil's effects on specific wake-promoting circuits, rather than generalized catecholamine release, helps explain its relatively favorable subjective profile: less jitteriness, less appetite suppression, less cardiovascular activation, and less crash upon offset compared to traditional stimulants. The cognitive enhancement effects of modafinil are mechanistically linked to dopaminergic activity in the prefrontal cortex, which is the substrate for working memory, executive function, and attention. Enhanced prefrontal dopaminergic tone — whether produced by endogenous arousal, by direct catecholaminergic drugs, or by modafinil — improves performance on tasks requiring sustained attention, working memory, and cognitive flexibility, particularly when baseline arousal is low (as in sleep deprivation, fatigue, or poor baseline vigilance). This dose-response relationship is the inverted-U curve familiar from the broader catecholaminergic cognition literature: too little dopamine is bad for prefrontal function, an optimal zone produces peak performance, and excessive stimulation degrades performance again. Modafinil appears to produce effects in the lower or middle portion of this curve in most users at standard doses, which is why its cognitive effects are generally described as sharpening focus and improving sustained attention without the over-aroused, scattered quality of high-dose amphetamine. The pharmacokinetics of modafinil are reasonably well characterized. Oral bioavailability is high (>90%), though formal absolute bioavailability has not been determined because no intravenous formulation is approved. Peak plasma concentrations occur 2-4 hours after oral dosing, with food delaying absorption modestly without reducing total exposure. The terminal elimination half-life averages 12-15 hours with considerable inter-individual variability; the R-enantiomer (armodafinil) has a longer half-life of 15 hours versus the S-enantiomer at 4-5 hours, which is why armodafinil produces more sustained daytime alertness from a single morning dose. Metabolism is primarily hepatic via CYP3A4 oxidation and amide hydrolysis, with metabolites excreted renally. Modafinil is itself a CYP3A4 inducer and a CYP2C19 inhibitor, which produces clinically important drug interactions, most notably reduced efficacy of hormonal contraception and potentially altered levels of benzodiazepines, warfarin, and other CYP substrates.", "legalStatus": "Not approved for human use — research chemical", "warning": "For research purposes only. Not for human consumption." } }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "What is modafinil and what is it used for?", "acceptedAnswer": { "@type": "Answer", "text": "Modafinil (brand name Provigil) is a prescription wakefulness-promoting agent approved by the FDA in 1998 for treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and obstructive sleep apnea (as adjunct to CPAP therapy). It is widely used off-label for ADHD, fatigue in multiple sclerosis and other conditions, depression augmentation, and cognitive enhancement. The R-enantiomer armodafinil (Nuvigil) is a longer-acting alternative. Modafinil is a Schedule IV controlled substance in the United States." } }, { "@type": "Question", "name": "How does modafinil work?", "acceptedAnswer": { "@type": "Answer", "text": "Modafinil's mechanism is incompletely understood but involves modest dopamine transporter (DAT) inhibition, activation of orexin/hypocretin neurons in the hypothalamus, increased histamine release from the tuberomammillary nucleus, and effects on norepinephrine, glutamate, and GABA signaling. Unlike amphetamines, modafinil does not produce a dopamine surge — it subtly shifts the neurotransmitter balance toward wakefulness. Volkow and colleagues demonstrated dopamine transporter occupancy at therapeutic doses using PET imaging (PMID 19336573)." } }, { "@type": "Question", "name": "Does modafinil work for cognitive enhancement in healthy people?", "acceptedAnswer": { "@type": "Answer", "text": "Yes, with caveats. The 2015 systematic review by Battleday and Brem (PMID 26381811) analyzing 24 studies concluded that modafinil produces consistent cognitive improvements in healthy non-sleep-deprived subjects, particularly on complex tasks requiring sustained attention, working memory, and executive function. Effect sizes are modest — meaningful but not dramatic. Effects are larger in sleep-deprived or fatigued users and smaller in well-rested high-functioning individuals. Simple cognitive tasks show less benefit than demanding tasks that require sustained effort over time." } }, { "@type": "Question", "name": "What is the typical modafinil dose?", "acceptedAnswer": { "@type": "Answer", "text": "Standard adult dose is 200 mg once daily taken in the morning. Some users titrate from 100 mg to 200 mg over the first week. For shift work disorder, 200 mg is taken 30-60 minutes before the shift. Higher doses (300-400 mg daily, sometimes split into morning and early afternoon) are used for severe daytime sleepiness unresponsive to 200 mg. Armodafinil is dosed at 150-250 mg once daily. Afternoon dosing commonly causes insomnia and should be avoided unless intentional for overnight wakefulness." } }, { "@type": "Question", "name": "What are the main modafinil side effects?", "acceptedAnswer": { "@type": "Answer", "text": "Common side effects (5-10%+ of users): headache, nausea, nervousness, insomnia, dry mouth, dizziness. These are usually mild and often improve after the first week. Less common: modest blood pressure and heart rate elevation, anxiety, GI upset. Serious but rare: Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome, anaphylaxis (approximately 1 per million prescriptions). Psychiatric: anxiety, irritability, rare reports of mania, psychosis, or suicidal ideation. Any rash on modafinil warrants immediate discontinuation and medical evaluation." } }, { "@type": "Question", "name": "Does modafinil interact with birth control?", "acceptedAnswer": { "@type": "Answer", "text": "Yes, this is the most clinically important drug interaction. Modafinil induces CYP3A4, which reduces the plasma levels of combined oral contraceptives, progestin-only pills, and hormonal implants or IUDs (though to a lesser extent for IUDs). This can reduce contraceptive efficacy and result in unintended pregnancy. Women using hormonal contraception must use a backup non-hormonal method (condoms, copper IUD, abstinence) during modafinil treatment and for at least one month after discontinuation. This interaction should be discussed explicitly with the prescribing physician." } }, { "@type": "Question", "name": "Can I take modafinil with caffeine, L-theanine, or other nootropics?", "acceptedAnswer": { "@type": "Answer", "text": "Caffeine combinations are common but often worsen side effects; reducing rather than maintaining caffeine intake when starting modafinil is often better. L-Theanine 100-200 mg with the modafinil dose is well-tolerated and may reduce anxiety without blunting cognitive effects. L-Tyrosine supports catecholamine synthesis during demanding cognitive periods. Racetams like Piracetam and Noopept stack commonly with modafinil; co-supplement choline. Russian nootropics like Selank, Semax, and Bromantane pair through complementary mechanisms. Clinical evidence for most stack benefits is anecdotal rather than controlled." } }, { "@type": "Question", "name": "Is modafinil safe for long-term use?", "acceptedAnswer": { "@type": "Answer", "text": "Evidence from 25+ years of clinical use supports favorable long-term safety for approved indications. Patients with narcolepsy on chronic modafinil generally maintain efficacy without tolerance and without significant cumulative adverse effects. Blood pressure and cardiovascular monitoring are warranted, particularly in users with risk factors. For off-label cognitive enhancement use, daily chronic use is less clearly appropriate — many users adopt weekdays-only or demanding-days-only schedules to preserve baseline and avoid psychological dependence. Drug holidays of 1-2 weeks every 3-6 months can re-establish baseline and prevent subtle dependence." } }, { "@type": "Question", "name": "How does modafinil compare to Adderall or other stimulants?", "acceptedAnswer": { "@type": "Answer", "text": "Modafinil has lower abuse potential, less cardiovascular activation, less appetite suppression, and smaller mood-altering effects than Adderall or methylphenidate, while producing less dramatic cognitive effects. Adderall and methylphenidate are more potent cognitive enhancers with more noticeable subjective effects, more appetite suppression, more cardiovascular load, and higher abuse potential. For ADHD specifically, stimulants are typically more effective than modafinil; for wakefulness promotion, modafinil is better. The choice depends on indication, individual response, and tolerability. Users who need dramatic stimulant effects generally get them from classical stimulants; users who want clean sustained alertness often prefer modafinil." } }, { "@type": "Question", "name": "Is modafinil legal to buy online without a prescription?", "acceptedAnswer": { "@type": "Answer", "text": "In the United States, no. Modafinil is a Schedule IV controlled substance and importing it without a prescription is technically illegal, even for personal use. Enforcement has been inconsistent, and most personal-quantity imports are not intercepted, but users choosing this route accept legal risk, quality-control uncertainty with international generic sources, and the absence of medical oversight. The responsible path is a legitimate prescription from a licensed physician (in-person or through reputable telehealth) for an appropriate indication. Legitimate use through medical channels provides FDA-regulated quality, physician oversight, and legal protection that grey-market sourcing does not." } } ] }, { "@context": "https://schema.org", "@type": "Organization", "@id": "https://www.bodyhackguide.co#organization", "name": "BodyHackGuide", "alternateName": "BHG", "url": "https://www.bodyhackguide.co", "logo": { "@type": "ImageObject", "url": "https://www.bodyhackguide.co/logo.png", "width": 512, "height": 512 }, "description": "Evidence-based research reference for peptides and nootropics. 124+ compound profiles, interactive dosing calculators, real-time vendor pricing, and trust-scored vendor reviews scored on a public, reproducible methodology applied to every vendor. BodyHackGuide and BHG Labs share common ownership, and we earn a commission on purchases through our links.", "foundingDate": "2024", "founder": { "@id": "https://www.bodyhackguide.co/about#person" }, "sameAs": [ "https://x.com/bodyhackguide", "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher", "https://discord.gg/Mhq5UdRYBA" ], "knowsAbout": [ "Peptide research", "Nootropic research", "Biohacking", "Compound dosing", "Vendor transparency" ], "publishingPrinciples": "https://www.bodyhackguide.co/editorial-standards", "ethicsPolicy": "https://www.bodyhackguide.co/editorial-standards", "diversityPolicy": "https://www.bodyhackguide.co/editorial-standards" }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "Modafinil", "description": "Modafinil is a prescription wakefulness-promoting agent approved by the US Food and Drug Administration in December 1998 under the brand name Provigil (Cephalon, now Teva) for the treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and as an adjunct to continuous positive airway pressure therapy in obstructive sleep apnea. It is a racemic mixture of R- and S-enantiomers; the R-enantiomer (armodafinil, brand name Nuvigil) was approved separately in 2007 as a longer-acting alternative. Modafinil became a Schedule IV controlled substance in the United States in 1999, reflecting a low but non-zero abuse potential that is substantially below that of amphetamines and classical stimulants. The compound is structurally unrelated to amphetamines, methylphenidate, and other stimulant classes — it is a diphenylmethylsulfinyl acetamide with a distinct pharmacology that produces wakefulness and cognitive effects without the catecholamine surge, appetite suppression, and cardiovascular profile of traditional stimulants. Modafinil's approved medical use base is narrow, but its off-label use is enormous. Physicians prescribe it off-label for ADHD (particularly in patients who do not tolerate or respond to stimulants), fatigue in multiple sclerosis and other neurologic conditions, cancer-related fatigue, depression augmentation (particularly for residual fatigue and cognitive symptoms), post-concussion cognitive dysfunction, jet lag, and age-related cognitive decline. Off-label and non-medical use as a cognitive enhancer — among students preparing for exams, professionals working long hours, military personnel during sustained operations, and the general nootropic community — has made modafinil one of the most-discussed cognitive enhancement compounds in both academic and lay media. The evidence base is substantial for approved indications and mixed for off-label use, with meta-analyses and systematic reviews documenting meaningful cognitive benefits in sleep-deprived users and healthy users performing complex cognitive tasks, alongside more modest or inconsistent effects on simple cognitive measures in rested users. Its safety profile across 25+ years of clinical use is generally favorable, though rare serious adverse events including Stevens-Johnson syndrome, toxic epidermal necrolysis, and DRESS syndrome (drug reaction with eosinophilia and systemic symptoms) require specific attention. This entry covers modafinil's mechanism of action and the ongoing uncertainty about which of its multiple pharmacologic effects drives wakefulness; the clinical evidence base for approved indications including narcolepsy, shift work disorder, and OSA; the off-label cognitive enhancement literature with its well-known heterogeneity between sleep-deprived and rested subjects; the side effect profile including common, serious, and rare adverse effects; the practical dosing conventions used in medical and non-medical contexts; its interactions with hormonal contraception and CYP450 substrates; contraindications based on cardiovascular, hepatic, and psychiatric history; how modafinil compares to and stacks with other nootropic compounds like Noopept, Piracetam, Sulbutiamine, Bromantane, Selank, Semax, Methylene Blue, NAD+, L-Theanine, and L-Tyrosine; and what responsible use looks like for someone considering modafinil for either medical or cognitive enhancement purposes. Modafinil remains the single most clinically validated cognitive enhancement compound available, with a body of evidence, safety data, and regulatory oversight that no research-chemical nootropic can match. For users who need demonstrably effective wakefulness promotion for legitimate medical reasons, it is a first-line option. For users considering it for cognitive enhancement, it is a serious drug with real effects and real side effects that deserves a serious evaluation rather than casual experimentation.", "lastReviewed": "2026-05-04T11:35:00.391+00:00", "url": "https://www.bodyhackguide.co/compound/modafinil", "author": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://x.com/bodyhackguide", "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "reviewedBy": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://x.com/bodyhackguide", "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "publisher": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" }, "mainContentOfPage": { "@type": "WebPageElement", "cssSelector": "main" }, "about": { "@type": "Drug", "name": "Modafinil", "alternateName": [ "Provigil", "Alertec", "Modalert", "Modvigil", "Modawake", "2-((diphenylmethyl)sulfinyl)acetamide", "CRL-40476" ], "description": "Modafinil is a prescription wakefulness-promoting agent approved by the US Food and Drug Administration in December 1998 under the brand name Provigil (Cephalon, now Teva) for the treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and as an adjunct to continuous positive airway pressure therapy in obstructive sleep apnea. It is a racemic mixture of R- and S-enantiomers; the R-enantiomer (armodafinil, brand name Nuvigil) was approved separately in 2007 as a longer-acting alternative. Modafinil became a Schedule IV controlled substance in the United States in 1999, reflecting a low but non-zero abuse potential that is substantially below that of amphetamines and classical stimulants. The compound is structurally unrelated to amphetamines, methylphenidate, and other stimulant classes — it is a diphenylmethylsulfinyl acetamide with a distinct pharmacology that produces wakefulness and cognitive effects without the catecholamine surge, appetite suppression, and cardiovascular profile of traditional stimulants. Modafinil's approved medical use base is narrow, but its off-label use is enormous. Physicians prescribe it off-label for ADHD (particularly in patients who do not tolerate or respond to stimulants), fatigue in multiple sclerosis and other neurologic conditions, cancer-related fatigue, depression augmentation (particularly for residual fatigue and cognitive symptoms), post-concussion cognitive dysfunction, jet lag, and age-related cognitive decline. Off-label and non-medical use as a cognitive enhancer — among students preparing for exams, professionals working long hours, military personnel during sustained operations, and the general nootropic community — has made modafinil one of the most-discussed cognitive enhancement compounds in both academic and lay media. The evidence base is substantial for approved indications and mixed for off-label use, with meta-analyses and systematic reviews documenting meaningful cognitive benefits in sleep-deprived users and healthy users performing complex cognitive tasks, alongside more modest or inconsistent effects on simple cognitive measures in rested users. Its safety profile across 25+ years of clinical use is generally favorable, though rare serious adverse events including Stevens-Johnson syndrome, toxic epidermal necrolysis, and DRESS syndrome (drug reaction with eosinophilia and systemic symptoms) require specific attention. This entry covers modafinil's mechanism of action and the ongoing uncertainty about which of its multiple pharmacologic effects drives wakefulness; the clinical evidence base for approved indications including narcolepsy, shift work disorder, and OSA; the off-label cognitive enhancement literature with its well-known heterogeneity between sleep-deprived and rested subjects; the side effect profile including common, serious, and rare adverse effects; the practical dosing conventions used in medical and non-medical contexts; its interactions with hormonal contraception and CYP450 substrates; contraindications based on cardiovascular, hepatic, and psychiatric history; how modafinil compares to and stacks with other nootropic compounds like Noopept, Piracetam, Sulbutiamine, Bromantane, Selank, Semax, Methylene Blue, NAD+, L-Theanine, and L-Tyrosine; and what responsible use looks like for someone considering modafinil for either medical or cognitive enhancement purposes. Modafinil remains the single most clinically validated cognitive enhancement compound available, with a body of evidence, safety data, and regulatory oversight that no research-chemical nootropic can match. For users who need demonstrably effective wakefulness promotion for legitimate medical reasons, it is a first-line option. For users considering it for cognitive enhancement, it is a serious drug with real effects and real side effects that deserves a serious evaluation rather than casual experimentation.", "activeIngredient": "Modafinil", "mechanismOfAction": "Modafinil's mechanism of action is genuinely incompletely understood despite more than two decades of clinical use and extensive preclinical research. It is not a classical stimulant — it does not produce the catecholamine surge of amphetamines, the direct noradrenergic release of ephedrine, or the primary adenosine antagonism of caffeine. What modafinil does do, based on converging evidence from receptor binding, microdialysis, imaging, and knockout mouse studies, is produce a modest inhibition of the dopamine transporter (DAT) that elevates extracellular dopamine in specific brain regions including the prefrontal cortex, striatum, and nucleus accumbens. DAT binding studies show a functionally meaningful effect at clinically relevant doses — Volkow and colleagues demonstrated in 2009 using PET imaging with the DAT radioligand [11C]cocaine that modafinil occupies dopamine transporters in the human brain at doses used therapeutically, with occupancy levels that correlated with elevations in extracellular dopamine. This finding was important because it established that modafinil's dopaminergic effects, while milder than amphetamine's, are real rather than negligible. However, DAT inhibition alone does not fully explain modafinil's pharmacology. Methylphenidate is a more potent DAT inhibitor but has a different clinical profile, and modafinil's effects on vigilance and wakefulness appear to involve additional systems. The orexin/hypocretin system is a major focus. Orexin neurons in the lateral hypothalamus are the primary wake-promoting neurons, and their loss causes narcolepsy. Modafinil activates orexin-containing neurons and increases histamine release in the tuberomammillary nucleus, which is the major histaminergic wake-promoting system. Direct activation of the histaminergic system via H1 histamine receptors in the cortex and other wake-relevant regions contributes to modafinil's wakefulness effect and may explain why modafinil produces alertness without the subjective stimulation of amphetamines. Additional modafinil effects include modest noradrenergic activation through alpha-1 adrenergic receptors, partial inhibition of the norepinephrine transporter, modest effects on serotonergic transmission at higher doses, increased glutamate release in cortex and thalamus, and reduced GABA release in multiple brain regions. The net effect is a neurotransmitter milieu that favors cortical activation and vigilance without the blunt force of amphetamine-class drugs. The selectivity of modafinil's effects on specific wake-promoting circuits, rather than generalized catecholamine release, helps explain its relatively favorable subjective profile: less jitteriness, less appetite suppression, less cardiovascular activation, and less crash upon offset compared to traditional stimulants. The cognitive enhancement effects of modafinil are mechanistically linked to dopaminergic activity in the prefrontal cortex, which is the substrate for working memory, executive function, and attention. Enhanced prefrontal dopaminergic tone — whether produced by endogenous arousal, by direct catecholaminergic drugs, or by modafinil — improves performance on tasks requiring sustained attention, working memory, and cognitive flexibility, particularly when baseline arousal is low (as in sleep deprivation, fatigue, or poor baseline vigilance). This dose-response relationship is the inverted-U curve familiar from the broader catecholaminergic cognition literature: too little dopamine is bad for prefrontal function, an optimal zone produces peak performance, and excessive stimulation degrades performance again. Modafinil appears to produce effects in the lower or middle portion of this curve in most users at standard doses, which is why its cognitive effects are generally described as sharpening focus and improving sustained attention without the over-aroused, scattered quality of high-dose amphetamine. The pharmacokinetics of modafinil are reasonably well characterized. Oral bioavailability is high (>90%), though formal absolute bioavailability has not been determined because no intravenous formulation is approved. Peak plasma concentrations occur 2-4 hours after oral dosing, with food delaying absorption modestly without reducing total exposure. The terminal elimination half-life averages 12-15 hours with considerable inter-individual variability; the R-enantiomer (armodafinil) has a longer half-life of 15 hours versus the S-enantiomer at 4-5 hours, which is why armodafinil produces more sustained daytime alertness from a single morning dose. Metabolism is primarily hepatic via CYP3A4 oxidation and amide hydrolysis, with metabolites excreted renally. Modafinil is itself a CYP3A4 inducer and a CYP2C19 inhibitor, which produces clinically important drug interactions, most notably reduced efficacy of hormonal contraception and potentially altered levels of benzodiazepines, warfarin, and other CYP substrates.", "legalStatus": "Not approved for human use — research chemical", "warning": "For research purposes only. Not for human consumption." } }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "What is modafinil and what is it used for?", "acceptedAnswer": { "@type": "Answer", "text": "Modafinil (brand name Provigil) is a prescription wakefulness-promoting agent approved by the FDA in 1998 for treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and obstructive sleep apnea (as adjunct to CPAP therapy). It is widely used off-label for ADHD, fatigue in multiple sclerosis and other conditions, depression augmentation, and cognitive enhancement. The R-enantiomer armodafinil (Nuvigil) is a longer-acting alternative. Modafinil is a Schedule IV controlled substance in the United States." } }, { "@type": "Question", "name": "How does modafinil work?", "acceptedAnswer": { "@type": "Answer", "text": "Modafinil's mechanism is incompletely understood but involves modest dopamine transporter (DAT) inhibition, activation of orexin/hypocretin neurons in the hypothalamus, increased histamine release from the tuberomammillary nucleus, and effects on norepinephrine, glutamate, and GABA signaling. Unlike amphetamines, modafinil does not produce a dopamine surge — it subtly shifts the neurotransmitter balance toward wakefulness. Volkow and colleagues demonstrated dopamine transporter occupancy at therapeutic doses using PET imaging (PMID 19336573)." } }, { "@type": "Question", "name": "Does modafinil work for cognitive enhancement in healthy people?", "acceptedAnswer": { "@type": "Answer", "text": "Yes, with caveats. The 2015 systematic review by Battleday and Brem (PMID 26381811) analyzing 24 studies concluded that modafinil produces consistent cognitive improvements in healthy non-sleep-deprived subjects, particularly on complex tasks requiring sustained attention, working memory, and executive function. Effect sizes are modest — meaningful but not dramatic. Effects are larger in sleep-deprived or fatigued users and smaller in well-rested high-functioning individuals. Simple cognitive tasks show less benefit than demanding tasks that require sustained effort over time." } }, { "@type": "Question", "name": "What is the typical modafinil dose?", "acceptedAnswer": { "@type": "Answer", "text": "Standard adult dose is 200 mg once daily taken in the morning. Some users titrate from 100 mg to 200 mg over the first week. For shift work disorder, 200 mg is taken 30-60 minutes before the shift. Higher doses (300-400 mg daily, sometimes split into morning and early afternoon) are used for severe daytime sleepiness unresponsive to 200 mg. Armodafinil is dosed at 150-250 mg once daily. Afternoon dosing commonly causes insomnia and should be avoided unless intentional for overnight wakefulness." } }, { "@type": "Question", "name": "What are the main modafinil side effects?", "acceptedAnswer": { "@type": "Answer", "text": "Common side effects (5-10%+ of users): headache, nausea, nervousness, insomnia, dry mouth, dizziness. These are usually mild and often improve after the first week. Less common: modest blood pressure and heart rate elevation, anxiety, GI upset. Serious but rare: Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome, anaphylaxis (approximately 1 per million prescriptions). Psychiatric: anxiety, irritability, rare reports of mania, psychosis, or suicidal ideation. Any rash on modafinil warrants immediate discontinuation and medical evaluation." } }, { "@type": "Question", "name": "Does modafinil interact with birth control?", "acceptedAnswer": { "@type": "Answer", "text": "Yes, this is the most clinically important drug interaction. Modafinil induces CYP3A4, which reduces the plasma levels of combined oral contraceptives, progestin-only pills, and hormonal implants or IUDs (though to a lesser extent for IUDs). This can reduce contraceptive efficacy and result in unintended pregnancy. Women using hormonal contraception must use a backup non-hormonal method (condoms, copper IUD, abstinence) during modafinil treatment and for at least one month after discontinuation. This interaction should be discussed explicitly with the prescribing physician." } }, { "@type": "Question", "name": "Can I take modafinil with caffeine, L-theanine, or other nootropics?", "acceptedAnswer": { "@type": "Answer", "text": "Caffeine combinations are common but often worsen side effects; reducing rather than maintaining caffeine intake when starting modafinil is often better. L-Theanine 100-200 mg with the modafinil dose is well-tolerated and may reduce anxiety without blunting cognitive effects. L-Tyrosine supports catecholamine synthesis during demanding cognitive periods. Racetams like Piracetam and Noopept stack commonly with modafinil; co-supplement choline. Russian nootropics like Selank, Semax, and Bromantane pair through complementary mechanisms. Clinical evidence for most stack benefits is anecdotal rather than controlled." } }, { "@type": "Question", "name": "Is modafinil safe for long-term use?", "acceptedAnswer": { "@type": "Answer", "text": "Evidence from 25+ years of clinical use supports favorable long-term safety for approved indications. Patients with narcolepsy on chronic modafinil generally maintain efficacy without tolerance and without significant cumulative adverse effects. Blood pressure and cardiovascular monitoring are warranted, particularly in users with risk factors. For off-label cognitive enhancement use, daily chronic use is less clearly appropriate — many users adopt weekdays-only or demanding-days-only schedules to preserve baseline and avoid psychological dependence. Drug holidays of 1-2 weeks every 3-6 months can re-establish baseline and prevent subtle dependence." } }, { "@type": "Question", "name": "How does modafinil compare to Adderall or other stimulants?", "acceptedAnswer": { "@type": "Answer", "text": "Modafinil has lower abuse potential, less cardiovascular activation, less appetite suppression, and smaller mood-altering effects than Adderall or methylphenidate, while producing less dramatic cognitive effects. Adderall and methylphenidate are more potent cognitive enhancers with more noticeable subjective effects, more appetite suppression, more cardiovascular load, and higher abuse potential. For ADHD specifically, stimulants are typically more effective than modafinil; for wakefulness promotion, modafinil is better. The choice depends on indication, individual response, and tolerability. Users who need dramatic stimulant effects generally get them from classical stimulants; users who want clean sustained alertness often prefer modafinil." } }, { "@type": "Question", "name": "Is modafinil legal to buy online without a prescription?", "acceptedAnswer": { "@type": "Answer", "text": "In the United States, no. Modafinil is a Schedule IV controlled substance and importing it without a prescription is technically illegal, even for personal use. Enforcement has been inconsistent, and most personal-quantity imports are not intercepted, but users choosing this route accept legal risk, quality-control uncertainty with international generic sources, and the absence of medical oversight. The responsible path is a legitimate prescription from a licensed physician (in-person or through reputable telehealth) for an appropriate indication. Legitimate use through medical channels provides FDA-regulated quality, physician oversight, and legal protection that grey-market sourcing does not." } } ] }, { "@context": "https://schema.org", "@type": "Organization", "@id": "https://www.bodyhackguide.co#organization", "name": "BodyHackGuide", "alternateName": "BHG", "url": "https://www.bodyhackguide.co", "logo": { "@type": "ImageObject", "url": "https://www.bodyhackguide.co/logo.png", "width": 512, "height": 512 }, "description": "Evidence-based research reference for peptides and nootropics. 124+ compound profiles, interactive dosing calculators, real-time vendor pricing, and trust-scored vendor reviews scored on a public, reproducible methodology applied to every vendor. 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[Home](/) 3. [Compounds](/compare) 5. Modafinil # Modafinil Nootropics Preclinical Download PDF Also known as: Provigil, Alertec, Modalert, Modvigil, Modawake, 2-((diphenylmethyl)sulfinyl)acetamide, CRL-40476 Modafinil is a prescription wakefulness-promoting agent approved by the US Food and Drug Administration in December 1998 under the brand name Provigil (Cephalon, now Teva) for the treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and as an adjunct to continuous positive airway pressure therapy in obstructive sleep apnea. It is a racemic mixture of R- and S-enantiomers; the R-enantiomer (armodafinil, brand name Nuvigil) was approved separately in 2007 as a longer-acting alternative. [3 PubMed Studies](https://pubmed.ncbi.nlm.nih.gov/?term=modafinil%20cognitive%20enhancement%20narcolepsy%20wakefulness) Last reviewed: May 4, 2026 [ 3 PubMed Studies ](https://pubmed.ncbi.nlm.nih.gov/?term=modafinil%20cognitive%20enhancement%20narcolepsy%20wakefulness)[ Nootropics Category ](/wiki#cat-nootropics) Preclinical Research Stage OverviewChemical InfoDosing & ProtocolsInteractionsResearchCompare PricesRelated ## Overview ### At A Glance Mechanism Modafinil's mechanism of action is genuinely incompletely understood despite more than two decades of clinical use and extensive preclinical research. It is not a classical stimulant — it does not produce the catecholamine surge of amphetamines, the direct noradrenergic release o… ### Overview Modafinil is a prescription wakefulness-promoting agent approved by the US Food and Drug Administration in December 1998 under the brand name Provigil (Cephalon, now Teva) for the treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and as an adjunct to continuous positive airway pressure therapy in obstructive sleep apnea. It is a racemic mixture of R- and S-enantiomers; the R-enantiomer (armodafinil, brand name Nuvigil) was approved separately in 2007 as a longer-acting alternative. Modafinil became a Schedule IV controlled substance in the United States in 1999, reflecting a low but non-zero abuse potential that is substantially below that of amphetamines and classical stimulants. The compound is structurally unrelated to amphetamines, methylphenidate, and other stimulant classes — it is a diphenylmethylsulfinyl acetamide with a distinct pharmacology that produces wakefulness and cognitive effects without the catecholamine surge, appetite suppression, and cardiovascular profile of traditional stimulants. Modafinil's approved medical use base is narrow, but its off-label use is enormous. Physicians prescribe it off-label for ADHD (particularly in patients who do not tolerate or respond to stimulants), fatigue in multiple sclerosis and other neurologic conditions, cancer-related fatigue, depression augmentation (particularly for residual fatigue and cognitive symptoms), post-concussion cognitive dysfunction, jet lag, and age-related cognitive decline. Off-label and non-medical use as a cognitive enhancer — among students preparing for exams, professionals working long hours, military personnel during sustained operations, and the general nootropic community — has made modafinil one of the most-discussed cognitive enhancement compounds in both academic and lay media. The evidence base is substantial for approved indications and mixed for off-label use, with meta-analyses and systematic reviews documenting meaningful cognitive benefits in sleep-deprived users and healthy users performing complex cognitive tasks, alongside more modest or inconsistent effects on simple cognitive measures in rested users. Its safety profile across 25+ years of clinical use is generally favorable, though rare serious adverse events including Stevens-Johnson syndrome, toxic epidermal necrolysis, and DRESS syndrome (drug reaction with eosinophilia and systemic symptoms) require specific attention. This entry covers modafinil's mechanism of action and the ongoing uncertainty about which of its multiple pharmacologic effects drives wakefulness; the clinical evidence base for approved indications including narcolepsy, shift work disorder, and OSA; the off-label cognitive enhancement literature with its well-known heterogeneity between sleep-deprived and rested subjects; the side effect profile including common, serious, and rare adverse effects; the practical dosing conventions used in medical and non-medical contexts; its interactions with hormonal contraception and CYP450 substrates; contraindications based on cardiovascular, hepatic, and psychiatric history; how modafinil compares to and stacks with other nootropic compounds like [Noopept](/compound/noopept), [Piracetam](/compound/piracetam), [Sulbutiamine](/compound/sulbutiamine), [Bromantane](/compound/bromantane), [Selank](/compound/selank), [Semax](/compound/semax), [Methylene Blue](/compound/methylene-blue), [NAD+](/compound/nad), [L-Theanine](/compound/l-theanine), and [L-Tyrosine](/compound/l-tyrosine); and what responsible use looks like for someone considering modafinil for either medical or cognitive enhancement purposes. Modafinil remains the single most clinically validated cognitive enhancement compound available, with a body of evidence, safety data, and regulatory oversight that no research-chemical nootropic can match. For users who need demonstrably effective wakefulness promotion for legitimate medical reasons, it is a first-line option. For users considering it for cognitive enhancement, it is a serious drug with real effects and real side effects that deserves a serious evaluation rather than casual experimentation. ## Chemical Information IUPAC Name Not yet available CAS Number Not yet available Molecular Formula Not yet available Molecular Mass Not yet available Chemical data is being compiled for this compound. ## Dosing & Protocols ### Unlock Dosing Protocols Free account gets you: - View beginner, intermediate & advanced protocols - See weight-based dosing calculations - Access cycle length & frequency data [Create free account](/auth)[Sign in](/auth) 2,800+ researchers already in ## Research ### Unlock Research Data Free account gets you: - Browse PubMed study summaries - See clinical trial phases & results - Access mechanism of action details [Create free account](/auth)[Sign in](/auth) 2,800+ researchers already in ## Interactions ### Contraindications Modafinil has a well-defined contraindication profile from 25+ years of clinical use and complete FDA labeling. Absolute contraindications include: known hypersensitivity to modafinil, armodafinil, or any component of the formulation; history of severe cutaneous drug reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome) to modafinil, armodafinil, or chemically similar compounds; severe hypersensitivity, angioedema, or anaphylactic reactions with prior use. These hypersensitivity contraindications exist because recurrence on rechallenge is potentially life-threatening. Serious cardiovascular contraindications include: recent myocardial infarction or unstable angina within the past 6 months; serious cardiac arrhythmias including atrial fibrillation with rapid ventricular response, ventricular tachycardia, or symptomatic bradyarrhythmias; severe uncontrolled hypertension; left ventricular hypertrophy; mitral valve prolapse with previous mitral valve prolapse syndrome on CNS stimulants; and recent history of ischemic ECG changes, chest pain, or arrhythmia. Modafinil's modest cardiovascular effects (small increases in heart rate and blood pressure) are well-tolerated in most users but may be significant in patients with cardiovascular instability. Patients with stable, well-controlled cardiovascular disease may use modafinil with physician oversight and monitoring. Pregnancy is a significant consideration. Modafinil crosses the placenta and animal studies have shown developmental toxicity at high doses. The FDA previously classified modafinil as Category C and labels now advise that it should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Pregnancy registries have collected limited data suggesting possible increased risk of congenital malformations and intrauterine growth restriction with modafinil exposure, leading to a 2019 FDA safety advisory recommending women of reproductive potential use reliable non-hormonal contraception during treatment. Pregnancy is a relative to strong contraindication unless the indication is compelling (severe narcolepsy affecting maternal safety) and alternative management is insufficient. Breastfeeding should be avoided or the infant monitored carefully — modafinil is excreted in breast milk at low concentrations and effects on the nursing infant are not fully characterized. Children and adolescents should not use modafinil because Stevens-Johnson syndrome has appeared at higher rates in pediatric trials, leading to withdrawal of pediatric indication from the label. Severe hepatic impairment requires dose reduction (typically halved) but is a relative contraindication for full-dose use. Severe renal impairment does not contraindicate use but warrants monitoring. Psychiatric history requires careful evaluation. History of psychosis, severe mania, or schizophrenia are relative to absolute contraindications depending on current stability — modafinil can rarely unmask psychotic symptoms. History of severe anxiety, panic disorder, or significant anxiety-inducing medications may be exacerbated. Bipolar disorder has reports of modafinil-induced mania in case series, though it is also used in some bipolar depression augmentation protocols under psychiatric oversight. Bipolar patients should use modafinil only under psychiatric supervision with careful monitoring. History of suicidal ideation or behavior is a relative contraindication due to rare reports of emergent suicidal ideation on modafinil. Substance use disorder history is a relative contraindication. While modafinil has lower abuse potential than classical stimulants, it is still a controlled substance and users with active or recent substance use disorder should use it only with specialist oversight. Concurrent use with classical stimulants, other Schedule IV substances, or with medications having significant CYP3A4/CYP2C19 interactions warrants specific caution. Drug interactions of clinical importance include: hormonal contraception — modafinil reduces efficacy and backup non-hormonal contraception is required during treatment and for one month after; cyclosporine, sirolimus, tacrolimus — modafinil may reduce levels requiring dose adjustment; antiepileptic drugs (phenytoin, carbamazepine) — complex interactions with modafinil may require TDM; warfarin — possible INR effects requiring more frequent monitoring; benzodiazepines, tricyclic antidepressants — possible level elevations through CYP2C19 inhibition; MAO inhibitors — theoretical serotonin syndrome risk though modafinil's direct serotonergic effects are modest; and classical stimulants — additive cardiovascular and psychiatric effects. Absence of appropriate clinical oversight is the final contraindication. Modafinil should be obtained through a prescription from a licensed physician who has evaluated the indication, assessed contraindications, discussed risks and benefits, and is available for ongoing monitoring and management. Self-prescribing without appropriate medical infrastructure is not responsible use of a Schedule IV medication with real adverse effect potential. Research Disclaimer This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds. [Sign in for alerts ](/auth) No listings found for Modafinil. Get Modafinil Price Drop Alerts Set a target price and we'll notify you when any vendor drops below it. [Sign in to set alerts](/auth) ### Sign in to leave a review Reviews on BodyHackGuide are tied to verified user accounts and moderated before publishing. Sign in (free, no spam) to share your experience with Modafinil. [Sign in](/auth) ### Related Compounds [View All](/wiki) [ ### 9-Me-BC (9-Methyl-β-carboline) Nootropics Preclinical 9-Methyl--carboline (9-Me-BC) is a synthetic -carboline alkaloid that has drawn nootropic-community interest for a preclinical property that is genuinely unusual among -carbolines: in rodent and cell-culture studies it appears to stimulate the dopaminergic phenotype - raising tyrosine hydroxylase, the number of differentiated dopamine neurons and dopamine content - while also showing neuroprotective, neurorestorative and anti-inflammatory effects, plus in-vitro MAO-A/MAO-B inhibition \[PMID:17913302, PMID:20374418, PMID:32285253\]. t½ Not characterized in humans (no pharmacokinetic data). Community/anecdotal only: ~5-25 mg per day, oral. No validated or approved human dose exists. 6 studies View Profile ](/compound/9-mbc)[ ### Bromantane Nootropics Russia Approved Bromantane is an atypical psychostimulant and anxiolytic developed in the 1980s at the Zakusov Institute of Pharmacology of the Russian Academy of Medical Sciences, originally created as an adaptogen for Soviet military and elite athletic use and later approved in Russia for the treatment of neurasthenic and asthenic disorders under the trade name Ladasten. 34 studies View Profile ](/compound/bromantane)[ ### Dihexa Nootropics Preclinical Dihexa is a synthetic peptide analogue of the angiotensin IV metabolite LVV-hemorphin-7, developed at Washington State University. t½ Not characterized in humans. Dihexa was engineered for metabolic stability (resistant to plasma and enzymatic degradation) and blood-brain-barrier penetration; in preclinical work its central procognitive effects appear to outlast its plasma presence. 5 to 40 mg oral per day (anecdotal range; no established human dose) 1 studies View Profile ](/compound/dihexa)[ ### Kavain Nootropics Preclinical for isolated kavain (in-vitro and animal mechanistic data). Human randomized controlled trials exist for the parent standardized kava extract, of which kavain is the principal kavalactone; the single molecule itself has not been trialed alone. Kavain (kawain) is the principal kavalactone in kava (Piper methysticum) and the main compound behind kava's calming, anxiolytic effect. t½ Not firmly established for isolated kavain in humans. Kavalactones are lipophilic and rapidly absorbed, with subjective effects generally lasting a few hours. Limited pharmacokinetic data preclude a precise elimination half-life. 50000-250000 Preclinical View Profile ](/compound/kavain)[ ### KW-6356 Nootropics Phase 2b (program discontinued) KW-6356 is a selective adenosine A2A receptor antagonist/inverse agonist developed by Kyowa Kirin and studied for Parkinson's disease, both as monotherapy and as an add-on to levodopa. Preclinical View Profile ](/compound/kw-6356)[ ### L-Theanine Nootropics FDA Approved L-Theanine is a non-proteinogenic amino acid found almost exclusively in tea (Camellia sinensis) and a handful of edible mushrooms, and it has become the single most widely-used calm-focus nootropic in the modern supplement market — both on its own at 100-400mg doses and, even more prominently, as the classic 1:1 or 2:1 pair with caffeine that defines the "calm-focus" experiential signature of green tea and of virtually every serious nootropic stack. t½ 1-3 hours (plasma); central CNS effect 3-5 hours 1226 studies View Profile ](/compound/l-theanine) ### Side-by-Side Comparisons [All Comparisons](/compare) [Modafinil vs Phenylpiracetam](/compare/modafinil-vs-phenylpiracetam "Modafinil vs Phenylpiracetam")[Modafinil vs Bromantane](/compare/bromantane-vs-modafinil "Bromantane vs Modafinil") [ View Full Dosage Guide → Protocols, calculator & safety for Modafinil ](/guides/dosage/modafinil) ### Related Articles [All Posts](/blog) [ #### Cognitive Enhancers by Mechanism and Safety: A Reference Guide A mechanism-first reference that groups cognitive enhancers into seven pharmacological classes and compares each on how it works and its main safety consideration, with a master table and honest evidence labels. Not a ranking, and not medical advice. 7/1/2026 ](/blog/cognitive-enhancers-by-mechanism-and-safety)[ #### We Compared 8 Focus Nootropics for 90 Days — Here's What Actually Works We tested 8 popular focus nootropics over 90 days using objective metrics — reaction time, deep work hours, and daily focus ratings. Here are the honest results, including costs and side effects. 4/3/2026 ](/blog/best-focus-nootropics-90-day-comparison) ### Research Score 15 3 PubMed studies ### Quality Indicators Data Completeness 63% Description Mechanism of Action Chemical Data Dosing Protocols Safety Profile PubMed Studies Interactions Vendor Listings Research Credibility 3 PubMed studies Limited research available ### Quick Facts Trial Phase Preclinical [Full Dosage Guide](/guides/dosage/modafinil)[Calculate Your Dose](/tools/reconstitution) Research Disclaimer This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use. ## Frequently Asked Questions What is modafinil and what is it used for? Modafinil (brand name Provigil) is a prescription wakefulness-promoting agent approved by the FDA in 1998 for treatment of excessive daytime sleepiness associated with narcolepsy, shift work sleep disorder, and obstructive sleep apnea (as adjunct to CPAP therapy). It is widely used off-label for ADHD, fatigue in multiple sclerosis and other conditions, depression augmentation, and cognitive enhancement. The R-enantiomer armodafinil (Nuvigil) is a longer-acting alternative. Modafinil is a Schedule IV controlled substance in the United States. How does modafinil work? Modafinil's mechanism is incompletely understood but involves modest dopamine transporter (DAT) inhibition, activation of orexin/hypocretin neurons in the hypothalamus, increased histamine release from the tuberomammillary nucleus, and effects on norepinephrine, glutamate, and GABA signaling. Unlike amphetamines, modafinil does not produce a dopamine surge — it subtly shifts the neurotransmitter balance toward wakefulness. Volkow and colleagues demonstrated dopamine transporter occupancy at therapeutic doses using PET imaging (PMID 19336573). Does modafinil work for cognitive enhancement in healthy people? Yes, with caveats. The 2015 systematic review by Battleday and Brem (PMID 26381811) analyzing 24 studies concluded that modafinil produces consistent cognitive improvements in healthy non-sleep-deprived subjects, particularly on complex tasks requiring sustained attention, working memory, and executive function. Effect sizes are modest — meaningful but not dramatic. Effects are larger in sleep-deprived or fatigued users and smaller in well-rested high-functioning individuals. Simple cognitive tasks show less benefit than demanding tasks that require sustained effort over time. What is the typical modafinil dose? Standard adult dose is 200 mg once daily taken in the morning. Some users titrate from 100 mg to 200 mg over the first week. For shift work disorder, 200 mg is taken 30-60 minutes before the shift. Higher doses (300-400 mg daily, sometimes split into morning and early afternoon) are used for severe daytime sleepiness unresponsive to 200 mg. Armodafinil is dosed at 150-250 mg once daily. Afternoon dosing commonly causes insomnia and should be avoided unless intentional for overnight wakefulness. What are the main modafinil side effects? Common side effects (5-10%+ of users): headache, nausea, nervousness, insomnia, dry mouth, dizziness. These are usually mild and often improve after the first week. Less common: modest blood pressure and heart rate elevation, anxiety, GI upset. Serious but rare: Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome, anaphylaxis (approximately 1 per million prescriptions). Psychiatric: anxiety, irritability, rare reports of mania, psychosis, or suicidal ideation. Any rash on modafinil warrants immediate discontinuation and medical evaluation. Does modafinil interact with birth control? Yes, this is the most clinically important drug interaction. Modafinil induces CYP3A4, which reduces the plasma levels of combined oral contraceptives, progestin-only pills, and hormonal implants or IUDs (though to a lesser extent for IUDs). This can reduce contraceptive efficacy and result in unintended pregnancy. Women using hormonal contraception must use a backup non-hormonal method (condoms, copper IUD, abstinence) during modafinil treatment and for at least one month after discontinuation. This interaction should be discussed explicitly with the prescribing physician. Can I take modafinil with caffeine, L-theanine, or other nootropics? Caffeine combinations are common but often worsen side effects; reducing rather than maintaining caffeine intake when starting modafinil is often better. [L-Theanine](/compound/l-theanine) 100-200 mg with the modafinil dose is well-tolerated and may reduce anxiety without blunting cognitive effects. [L-Tyrosine](/compound/l-tyrosine) supports catecholamine synthesis during demanding cognitive periods. Racetams like [Piracetam](/compound/piracetam) and [Noopept](/compound/noopept) stack commonly with modafinil; co-supplement choline. Russian nootropics like [Selank](/compound/selank), [Semax](/compound/semax), and [Bromantane](/compound/bromantane) pair through complementary mechanisms. Clinical evidence for most stack benefits is anecdotal rather than controlled. Is modafinil safe for long-term use? Evidence from 25+ years of clinical use supports favorable long-term safety for approved indications. Patients with narcolepsy on chronic modafinil generally maintain efficacy without tolerance and without significant cumulative adverse effects. Blood pressure and cardiovascular monitoring are warranted, particularly in users with risk factors. For off-label cognitive enhancement use, daily chronic use is less clearly appropriate — many users adopt weekdays-only or demanding-days-only schedules to preserve baseline and avoid psychological dependence. Drug holidays of 1-2 weeks every 3-6 months can re-establish baseline and prevent subtle dependence. How does modafinil compare to Adderall or other stimulants? Modafinil has lower abuse potential, less cardiovascular activation, less appetite suppression, and smaller mood-altering effects than Adderall or methylphenidate, while producing less dramatic cognitive effects. Adderall and methylphenidate are more potent cognitive enhancers with more noticeable subjective effects, more appetite suppression, more cardiovascular load, and higher abuse potential. For ADHD specifically, stimulants are typically more effective than modafinil; for wakefulness promotion, modafinil is better. The choice depends on indication, individual response, and tolerability. Users who need dramatic stimulant effects generally get them from classical stimulants; users who want clean sustained alertness often prefer modafinil. Is modafinil legal to buy online without a prescription? In the United States, no. Modafinil is a Schedule IV controlled substance and importing it without a prescription is technically illegal, even for personal use. Enforcement has been inconsistent, and most personal-quantity imports are not intercepted, but users choosing this route accept legal risk, quality-control uncertainty with international generic sources, and the absence of medical oversight. The responsible path is a legitimate prescription from a licensed physician (in-person or through reputable telehealth) for an appropriate indication. Legitimate use through medical channels provides FDA-regulated quality, physician oversight, and legal protection that grey-market sourcing does not. ## Research Tools [ ### Peptide Calculator Reconstitution & syringe units ](/tools/reconstitution)[ ### Reconstitution Guide How to mix, step by step ](/guides/how-to-reconstitute-peptides)[ ### Nasal Spray Calc mL per actuation ](/tools/intranasal)[ ### Half-Life Visualizer Decay curves ](/tools/halflife) ## Related Compounds [View All](/wiki) [ ### 9-Me-BC (9-Methyl-β-carboline) Nootropics Preclinical 9-Methyl--carboline (9-Me-BC) is a synthetic -carboline alkaloid that has drawn nootropic-community interest for a preclinical property that is genuinely unusual among -carbolines: in rodent and cell-culture studies it appears to stimulate the dopaminergic phenotype - raising tyrosine hydroxylase, the number of differentiated dopamine neurons and dopamine content - while also showing neuroprotective, neurorestorative and anti-inflammatory effects, plus in-vitro MAO-A/MAO-B inhibition \[PMID:17913302, PMID:20374418, PMID:32285253\]. t½ Not characterized in humans (no pharmacokinetic data). Community/anecdotal only: ~5-25 mg per day, oral. No validated or approved human dose exists. 6 studies View Profile ](/compound/9-mbc)[ ### Bromantane Nootropics Russia Approved Bromantane is an atypical psychostimulant and anxiolytic developed in the 1980s at the Zakusov Institute of Pharmacology of the Russian Academy of Medical Sciences, originally created as an adaptogen for Soviet military and elite athletic use and later approved in Russia for the treatment of neurasthenic and asthenic disorders under the trade name Ladasten. 34 studies View Profile ](/compound/bromantane)[ ### Dihexa Nootropics Preclinical Dihexa is a synthetic peptide analogue of the angiotensin IV metabolite LVV-hemorphin-7, developed at Washington State University. t½ Not characterized in humans. Dihexa was engineered for metabolic stability (resistant to plasma and enzymatic degradation) and blood-brain-barrier penetration; in preclinical work its central procognitive effects appear to outlast its plasma presence. 5 to 40 mg oral per day (anecdotal range; no established human dose) 1 studies View Profile ](/compound/dihexa)[ ### Kavain Nootropics Preclinical for isolated kavain (in-vitro and animal mechanistic data). Human randomized controlled trials exist for the parent standardized kava extract, of which kavain is the principal kavalactone; the single molecule itself has not been trialed alone. Kavain (kawain) is the principal kavalactone in kava (Piper methysticum) and the main compound behind kava's calming, anxiolytic effect. t½ Not firmly established for isolated kavain in humans. Kavalactones are lipophilic and rapidly absorbed, with subjective effects generally lasting a few hours. Limited pharmacokinetic data preclude a precise elimination half-life. 50000-250000 Preclinical View Profile ](/compound/kavain)[ ### KW-6356 Nootropics Phase 2b (program discontinued) KW-6356 is a selective adenosine A2A receptor antagonist/inverse agonist developed by Kyowa Kirin and studied for Parkinson's disease, both as monotherapy and as an add-on to levodopa. Preclinical View Profile ](/compound/kw-6356)[ ### L-Theanine Nootropics FDA Approved L-Theanine is a non-proteinogenic amino acid found almost exclusively in tea (Camellia sinensis) and a handful of edible mushrooms, and it has become the single most widely-used calm-focus nootropic in the modern supplement market — both on its own at 100-400mg doses and, even more prominently, as the classic 1:1 or 2:1 pair with caffeine that defines the "calm-focus" experiential signature of green tea and of virtually every serious nootropic stack. t½ 1-3 hours (plasma); central CNS effect 3-5 hours 1226 studies View Profile ](/compound/l-theanine) ## Side-by-Side Comparisons [All Comparisons](/compare) Compare Modafinil head-to-head: mechanism, half-life, dosing, safety, and live pricing. [Modafinil vs Phenylpiracetam](/compare/modafinil-vs-phenylpiracetam "Modafinil vs Phenylpiracetam")[Modafinil vs Bromantane](/compare/bromantane-vs-modafinil "Bromantane vs Modafinil") Free 2026 Peptide Cheat Sheet — 50 pages, PDF Reconstitution math, concentration charts, half-lives, and vendor trust tiers. The reference we wish we had on day one. [Download Free](/guides/peptide-cheat-sheet-download?utm_source=compound-modafinil) ### Need bloodwork before starting? Full hormone + metabolic panels from Anabolic Insights. Code CHONCH for first-order discount. [Order Bloodwork](https://anabolicinsights.ai/?ref=nwm2zjb) ![BodyHackGuide](/assets/bodyhackguide-logo-DOzZNUyh.webp) ### BodyHackGuide Your biohacking research hub — compound pricing, brain health protocols, dosing tools, and vendor reviews. 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