Modafinil
Weak dopamine transporter (DAT) inhibitor that elevates synaptic dopamine, with secondary activation of orexin/hypocretin neurons in the lateral hypothalamus. Also modulates norepinephrine, serotonin, and histamine systems. Unlike amphetamines, does not cause vesicular dopamine release or significant peripheral sympathetic activation.
Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.
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- PMID:26381811Modafinil for cognitive neuroenhancement in healthy non-sleep-deprived subjects: A systematic review — Eur Neuropsychopharmacol, 2015
- PMID:18729534Effects of modafinil on dopamine and dopamine transporters in the male human brain — JAMA, 2009
- PMID:14725734Mechanisms of modafinil: a review of current research — Neuropsychiatr Dis Treat, 2004
Modafinil is the compound that made cognitive enhancement a mainstream conversation. Not because it is the most powerful stimulant. Because it is the most tolerable one. The 15-hour half-life is both its strength and its constraint. Take it after noon and you have purchased insomnia. The pharmacology is subtle. Weak DAT inhibition plus orexin activation creates wakefulness without the jittery dopamine surge of amphetamines. This is a precision tool for sleep-deprived performance, not a substitute for sleep architecture.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
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