Latest research on Eszopiclone

Eszopiclone, marketed by Sepracor under the brand-name Lunesta, is a nonbenzodiazepine hypnotic agent (viz., a sedative) used as a treatment for insomnia. Eszopiclone is the active stereoisomer of zopiclone, and belongs to the class of drugs known as cyclopyrrones. Its main selling point is that it is approved by the U.S. Food and Drug Administration for long-term use, unlike almost all other hypnotic sedatives, which are approved only for the relief of short-term (6-8 weeks) insomnia.

Eszopiclone side effects

Taken together, these data suggest that increased activity at GABAergic receptors is beneficial in a few cases, eg, with Alprazolam as a standalone treatment and Eszopiclone as an adjuvant. [source, 2015]
To decrease biased results, patients who had prescriptions of other nonbenzodiazepine hypnotic agents including Zopiclone, Zaleplon, and EsZopiclone were excluded from this study. [source, 2015]
For example, 1 μM Diazepam or 0.1 μM flunitrazepam significantly increased the decay time constants of IPSCs mediated by α2-containing GABAARs (Dixon et al., 2014) and 1 μM Zolpidem or 1 μM Eszopiclone increased IPSC magnitudes and decay time constants of IPSCs mediated by α1-containing GABAARs (Dixon et al., 2015). [source, 2015]
Sex differences in their pharmacokinetics and side effect profiles, including increased risk of cognitive impairment in the morning and motor vehicle accidents, led the US Food and Drug Administration to require the manufacturers of Ambien and Lunesta to lower recommended starting doses in women. [source, 2015]
Because of the widespread use of drugs by military personnel and veterans, a New York Magazine article dubbed this, “The Prozac, Paxil, Zoloft, Wellbutrin, Celexa, Effexor, Valium, Klonopin, Ativan, Restoril, Xanax, Adderall, Ritalin, Haldol, Resperdal, Seroquel, Ambien, Lunesta, Elavil, Trazodone War” [68]. [source, 2015]
Furthermore, administration of the atypical antipsychotic Olanzapine increased SWS, and the GABA agonist Eszopiclone enhanced the number of sleep spindles in schizophrenia; yet both treatments failed to normalize memory consolidation in these patients (Göder et al., 2008; Wamsley et al., 2013). [source, 2014]
Following active-phase treatment with Eszopiclone (10 mg/kg), the time course of NREM was significantly increased relative to both active-phase vehicle (F1,10 = 76.72, P < 0.0001, 2-way ANOVA; P < 0.0001, Tukey HSD) and that occurring during the onset of the inactive phase (F1,10 = 7.68, P = 0.0197, 2-way ANOVA; P < 0.0001, Tukey HSD), whereas REM sleep was significantly decreased relative to both control conditions (active phase: F1,10 = 8.86, P = 0.0139, 2-way ANOVA; P < 0.0001, Tukey HSD; inactive phase: F1,10 = 51.92, P < 0.0001, 2-way ANOVA; P < 0.0001, Tukey HSD). [source, 2014]
In contrast, Eszopiclone treatment during the active phase resulted in large increases in qEEG power in the beta band (19–30 Hz) (12 h) as well as sigma frequencies (12–16 Hz) (5.5 h) whereas minimal decreases were seen in theta and alpha power (4–7 Hz and 8–12 Hz, respectively). [source, 2014]
Relative to vehicle, Eszopiclone induced little-to-no change in gamma and delta powers until the onset of the inactive phase 6.5 h later, when levels of gamma, delta, and theta power were maintained even though vehicle-treated animals exhibited substantial decreases in gamma power and increases in delta and theta power associated with sleep onset. [source, 2014]
Compared with Eszopiclone alone, the combination induced no clear decreases in active wake or increases in delta sleep with the possible exceptions of light and REM sleep (Figure  6B). [source, 2014]