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Summary sheet: Armodafinil
Chemical Nomenclature
Common names Armodafinil, Nuvigil, Waklert, Artvigil, R-Modawake, Neoresotyl
Substitutive name (R)-Modafinil
Systematic name 2-[(R)-benzhydrylsulfinyl]acetamide
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 20 mg
Light 40 - 100 mg
Common 100 - 200 mg
Strong 200 - 300 mg
Heavy 300 mg +
Total 8 - 15 hours
Onset 20 - 60 minutes
Come up 1 - 2.5 hours
Peak 4 - 7 hours
Offset 2 - 5 hours
After effects 2 - 12 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Hormonal birth control

(R)-Modafinil (also known as Armodafinil and by the brand names Artvigil and Waklert[1]) is a eugeroic substance of the benzhydryl class. Armodafinil is the enantiopure formulation of modafinil (brand name Provigil). As opposed to the racemic formulation, which contains a 50/50 mix of both the (S) and (R) enantiomers, armodafinil consists of just the (R)-enantiomer of modafinil.

Armodafinil was approved by the U.S. Food and Drug Administration (FDA) in June 2007 for the treatment of obstructive sleep apnea, shift work sleep disorder, and narcolepsy.[2]

In addition to its wakefulness-promoting effects and ability to increase locomotor activity in animals, armodafinil can produce rewarding psychoactive and euphoric effects such as alterations in mood, perception, thinking, and feelings typically observed with other central nervous system (CNS) stimulants in humans.

A study in which patients were administered modafinil, methylphenidate, and a placebo found that modafinil produces "psychoactive and euphoric effects and feelings consistent with methylphenidate."[3] Relative to modafinil, armodafinil reaches its peak concentration in the blood later after administration than modafinil does, which may make it more effective at improving wakefulness in patients with excessive daytime sleepiness.[citation needed]

The long-term risks of regular armodafinil intake have yet to be studied in detail.[citation needed]


Armodafinil, or (R)-modafinil, is a psychoactive molecule of the benzhydryl class. Benzhydryl compounds are comprised of two benzene rings attached to a single carbon molecule. Armodafinil is classified as a sulphinyl benzhydryl molecule, as it also contains a sulphinyl group, a sulfur molecule double-bonded to an oxygen molecule attached to the carbon of the benzhydryl group.

From this sulfur group at R2, an acetamide group is bound at its free carbon through a carbonyl group to a terminal amine group. Armodafinil has a center of chirality at its sulfur group. Armodafinil, unlike modafinil, consists of only the (−)-(R)-enantiomer of modafinil.


(R,S)-modafinil, mechanism of action.

Although the exact mechanisms by which modafinil and its R-enantiomer, armodafinil, decrease sleepiness are not fully understood, evidence suggests that these agents promote wakefulness by acting directly or indirectly on many components of the sleep / wake circuit. Modafinil and armodafinil are hypothesized to inhibit GABA and promote dopamine, norepinephrine, histamine, and hypocretin / orexin.[4][5][6][7]

Modafinil and its R-enantiomer, armodafinil, increase both norepinephrine (NE) and dopamine (DA), possibly via their blockade of both the NE and DA reuptake transporters (NET and DAT, respectively). The actions of NE at alpha-adrenergic receptors and DA at dopamine D2 receptors are thought to contribute to the wake-promoting properties of modafinil. Orexin is a key component of the arousal system; thus, the hypothesized action of modafinil on the orexinergic system may help increase alertness. Additionally, modafinil may indirectly increase histamine, either by reducing GABAergic inhibition of histaminergic neurons or via actions at orexinergic neurons. The increase in histamine may contribute to both the wake-promoting effects of modafinil as well as the potential of modafinil to increase alertness.[4][6][8]

In genetically engineered mice lacking the dopamine transporter (DAT), modafinil lacked wake-promoting activity, suggesting that this activity was DAT-dependent. However, the wake-promoting effects of modafinil, unlike those of amphetamine, were not reduced by the dopamine receptor antagonist haloperidol in rats. In addition, alpha-methyl-p-tyrosine, an inhibitor of dopamine synthesis, blocks the action of amphetamine but does not block locomotor activity induced by modafinil.

Subjective effects

In comparison to traditional stimulants such as amphetamine, this compound induces an experience which is far less forceful, recreational and euphoric. It instead focuses on general wakefulness and motivation enhancement. In comparison to regular modafinil it is usually considered to be less side effect intensive, more comfortable and with a longer duration.

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

The long-term safety and effectiveness of armodafinil has not been determined.[15]

Anecdotal evidence suggests a lack of adverse health effects when sparingly used at small to moderate doses, although this must not be assumed. This compound is a commonly prescribed prescription medication, thus is considerably less likely to have adverse health effects than that of a typical research chemical.

It is strongly recommended that one use harm reduction practices when using this substance.

Lethal dosage

The median lethal dose at which 50% of participants die (LD50) from either armodafinil or modafinil for human beings has never been reached. No life-threatening effects have taken place in clinical trials involving the administration of 1000mg to 1600mg of modafinil per day for 7 to 21 consecutive days. Intentional acute overdoses of 4500mg and 4000mg in two adult subjects and an accidental ingestion of 800mg by a three-year-old child did not result in any life-threatening effects or death.[16] After overdosing on 5000mg of modafinil in a suicide attempt, a fifteen-year-old female reported a severe headache, nausea, and tachycardia, but did not appear to have any lethal or long-term effects.[17]

Tolerance and addiction potential

Armodafinil, like racemic modafinil, may also possess addiction reinforcing properties, as evidenced by its self-administration in monkeys previously trained to administer cocaine; armodafinil was also partially discriminated as stimulant-like. The chronic use of armodafinil can be considered as mildly addictive with a low potential for abuse. It does not seem to be capable of causing psychological dependence among certain users.

Tolerance to many of the effects of armodafinil develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Armodafinil may present a cross-tolerance with all benzhydryl nootropics, meaning that after the consumption of modafanil certain nootropics such as modafanil and adrafanil may have a reduced effect.

Dangerous interactions

Disclaimer: Psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous or even life-threatening when combined with other substances. The following list includes some known dangerous interactions (although it is not guaranteed to include all of them).

Independent research (e.g. Google, DuckDuckGo) should always be conducted to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • 25x-NBOMe & 25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be handled with extreme care due to DXM's effects on serotonin and norepinephrine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome with stimulants that increase levels of serotonin (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other stimulants. There is also a risk of excessive heart strain.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Stimulants - Armodafinil can be potentially dangerous in combination with other stimulants like cocaine as they can increase one's heart rate and blood pressure to dangerous levels.
  • Tramadol - Tramadol lowers the seizure threshold.[18] Combinations with stimulants may further increase this risk.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, and some antidepressants.[19]
  • Hormonal birth control - Modafinil reduces the effectiveness of hormonal birth control for up to a month after use by increasing the activity of the enzyme CYP3A4/5.[20] Notably, the same enzyme is inhibited by grapefruit juice.[21]

Legal status

Armodafinil is legally approved for medical purposes worldwide. However, it is illegal to sell and possess without a prescription in most countries.

  • Canada: Modafinil is listed as a Schedule F prescription drug in Canada and it can be prescribed for human and veterinary use.[22]
  • Germany: Modafinil is a prescription medicine, according to Anlage 1 AMVV.[23]
  • United Kingdom: Armodafinil is not a licensed medicine in the United Kingdom and is not covered by the Misuse of Drugs Act 1971 so it may be considered illegal to produce, supply, or import under the Psychoactive Substances Act.[24] However, it may not be covered by the Psychoactive Substances Act as it is a licensed medicine in many other countries[citation needed] and modafinil, the non-enantiopure substance that is comprised of armodafinil and the S-enantiomer of modafinil in equal proportions, is a licensed prescription-only medicine (POM) in the United Kingdom.[25] In this case it would not be considered a criminal offence to possess this substance without a valid prescription and it could be legally be obtained with a valid prescription or through legal import of the substance for personal use as outlined in Section 13 of the Medicines Act 1968.[26]
  • United States: Armodafinil is a Schedule IV controlled substance in the United States. It is illegal to buy, sell, or possess the drug without a prescription or DEA license.[27]

See also

External links


  • Darwish, M., Kirby, M., D’Andrea, D. M., Yang, R., Hellriegel, E. T., & Robertson, P. (2010). Pharmacokinetics of armodafinil and modafinil after single and multiple doses in patients with excessive sleepiness associated with treated obstructive sleep apnea: A randomized, open-label, crossover study. Clinical Therapeutics, 32(12), 2074–2087.
  • Fuller, P., Vetrivelan, R., & Saper, C. (2014). Armodafinil-induced wakefulness in animals with ventrolateral preoptic lesions. Nature and Science of Sleep, 6, 57.
  • Greve, D. N., Duntley, S. P., Larson-Prior, L., Krystal, A. D., Diaz, M. T., Drummond, S. P. A., … Thomas, R. J. (2014). Effect of Armodafinil on Cortical Activity and Working Memory in Patients with Residual Excessive Sleepiness Associated with CPAP-Treated OSA: A Multicenter fMRI Study. Journal of Clinical Sleep Medicine, 10(2), 143–153.
  • Loland, C. J., Mereu, M., Okunola, O. M., Cao, J., Prisinzano, T. E., Mazier, S., … Newman, A. H. (2012). R-modafinil (armodafinil): A unique dopamine uptake inhibitor and potential medication for psychostimulant abuse. Biological Psychiatry, 72(5), 405–413.
  • Niemegeers, P., Maudens, K. E., Morrens, M., Patteet, L., Joos, L., Neels, H., & Sabbe, B. G. (2012). Pharmacokinetic evaluation of armodafinil for the treatment of bipolar depression. Expert Opinion on Drug Metabolism & Toxicology, 8(9), 1189–1197.
  • Ramachandra, B. (2016). A Critical Review of Properties of Modafinil and Analytical, Bioanalytical Methods for its Determination. Critical Reviews in Analytical Chemistry, 46(6), 482–489.
  • T., M., M., M., N., S., & S., N. (2016). The pathogenesis of narcolepsy, current treatments, and prospective therapeutic targets. Expert Opinion on Orphan Drugs, 4(1), 63–82.


  1. "Sun Pharma Product Listing". Retrieved 2017-06-03. Product Name: Waklert 150, Waklert 50. Molecule: Armodafinily. Therapy area: Neurology and Psychiatry. 
  2. Nuvigil (Manufacturer's Website) |
  4. 4.0 4.1 Morrissette, D. A. (2013). Twisting the night away: a review of the neurobiology, genetics, diagnosis, and treatment of shift work disorder. CNS Spectrums, 18(s1), 42–54.
  5. Touitou, Y., & Bogdan, A. (2007). Promoting adjustment of the sleep-wake cycle by chronobiotics. Physiology and Behavior, 90(2–3), 294–300.
  6. 6.0 6.1 Darwish, M., Kirby, M., D'Andrea, D. M., Yang, R., Hellriegel, E. T., & Robertson, P. (2010). Pharmacokinetics of armodafinil and modafinil after single and multiple doses in patients with excessive sleepiness associated with treated obstructive sleep apnea: A randomized, open-label, crossover study. Clinical Therapeutics, 32(12), 2074–2087.
  7. Erman MK, Yang R, Seiden DJ. The effect of armodafinil on patient-reported functioning and quality of life in patients with excessive sleepiness associated with shift work disorder: a randomized, double-blind, placebo-controlled trial. Prim Care Companion CNS Disord. 2012;14(4) . doi:10.4088/pcc.12m01345. PMID: 23251870; PMCID: PMC3505139.
  8. He, B., Peng, H., Zhao, Y., Zhou, H., & Zhao, Z. (2011). Modafinil treatment prevents REM sleep deprivation-induced brain function impairment by increasing MMP-9 expression. Brain Research, 1426, 38–42.
  9. Davis, C., Levitan, R. D., Kaplan, A. S., Carter, J., Reid, C., Curtis, C., … Kennedy, J. L. (2007). Dopamine transporter gene (DAT1) associated with appetite suppression to methylphenidate in a case-control study of binge eating disorder. Neuropsychopharmacology, 32(10), 2199–2206.
  10. Blundell, J. (1991). Pharmacological approaches to appetite suppression. Trends in Pharmacological Sciences, 12(April), 147–157.
  11. Heal, D. J., Smith, S. L., Gosden, J., & Nutt, D. J. (2013). Amphetamine, past and present--a pharmacological and clinical perspective. Journal of Psychopharmacology (Oxford, England), 27(6), 479–96.
  12. Udert, K. M., Larsen, T. A., & Gujer, W. (2006). Fate of major compounds in source-separated urine. Water Science and Technology, 54(11–12), 413–420.
  13. Rammsayer, T. (1989). Is there a common dopaminergic basis of time perception and reaction time? Neuropsychobiology, 21(1), 37–42. Retrieved from
  14. Sessi, P., Di Sante, D., Szczerbakow, A., Glott, F., Wilfert, S., Schmidt, H., … Bode, M. (2016). Robust spin-polarized midgap states at step edges of topological crystalline insulators. Science, 354(6317), 1269–1273.
  15. Pharmacotherapy for excessive daytime sleepiness |
  16. The National Library of Medicine - PROVIGIL |
  17. Journal of Clinical Sleep Medicine - Unsuccessful Suicide Attempt of a 15 Year Old Adolescent with Ingestion of 5000 mg Modafinil
  18. Talaie, H.; Panahandeh, R.; Fayaznouri, M. R.; Asadi, Z.; Abdollahi, M. (2009). "Dose-independent occurrence of seizure with tramadol". Journal of Medical Toxicology. 5 (2): 63–67. doi:10.1007/BF03161089. eISSN 1937-6995. ISSN 1556-9039. OCLC 163567183. 
  19. Gillman, P. K. (2005). "Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity". British Journal of Anaesthesia. 95 (4): 434–441. doi:10.1093/bja/aei210Freely accessible. eISSN 1471-6771. ISSN 0007-0912. OCLC 01537271. PMID 16051647. 
  20. Robertson, P (2002). "Effect of modafinil on the pharmacokinetics of ethinyl estradiol and triazolam in healthy volunteers". Clinical Pharmacology & Therapeutics. Springer Nature. 71 (1): 46–56. doi:10.1067/mcp.2002.121217. ISSN 0009-9236. 
  21. Bailey, D. G.; Dresser, G.; Arnold, J. M. O. (2012-11-26). "Grapefruit-medication interactions: Forbidden fruit or avoidable consequences?". Canadian Medical Association Journal. Joule Inc. 185 (4): 309–316. doi:10.1503/cmaj.120951. ISSN 0820-3946. 
  22. National Association of Pharmacy Regulatory Authorities Regulations Amending the Food and Drug Regulations (1184 — Modafinil) |
  24. Psychoactive Substances Act 2016 ( |
  25. MHRA (April 3, 2013). "MHRA license for Modafinil in UK" (PDF). MHRA. 
  26. "Medicines Act 1968 Section 13". 
  27. Placement of Modafinil Into Schedule IV - U.S. Department of Justice |