Narcolepsy (NT) is a rare central disorder of hypersomnolence, categorized as type 1 or type 2 depending on whether there is loss of hypothalamic orexinergic neurons. Its core clinical features—excessive daytime sleepiness (EDS) and abnormalities in REM sleep—significantly interfere with patients' educational attainment, work productivity, and activities of daily living. Currently, wake-promoting agents (WPAs) remain the cornerstone of EDS symptom management. This article provides a systematic review of advances over the past decade in the treatment of NT-related EDS with WPAs. Traditional central nervous system stimulants—amphetamine , methyphenidate, modafinil and armodafinil—have the longest history of use, yet research progress on their pharmacological mechanisms and therapeutic optimization has been limited in recent years. Novel WPAs, such as the dopamine and norepinephrine reuptake inhibitor solriamfetol and the histamine H3 receptor antagonist/inverse agonist pitolisant, significantly improve both subjective and objective assessment indices of NT-related EDS by modulating monoaminergic and histaminergic wake-promoting pathways. The gamma-hydroxybutyrate (GHB) prodrug sodium oxybate, which consolidates nocturnal sleep and regulates cataplexy by activating gama-aminobutyric acid_B (GABA_B) receptors and modulating noradrenergic and dopaminergic neuronal activity, has demonstrated equivalent efficacy to conventional formulations while reducing dosing frequency and cardiometabolic burden through its controlled-release and low-sodium formulations. Network meta-analyses indicate that the aforementioned WPAs exhibit favorable therapeutic efficacy in narcolepsy, and all three are recommended as first-line agents for NT-related EDS by domestic and international guideline consensus. Notably, orexin type 2 receptor agonists—the first etiology-targeted therapy—have completed Phase III clinical trials, demonstrating sustained wake-promoting effects and favorable safety profiles in patients with NT1, heralding a breakthrough in pathogenesis-oriented treatment.