Lemborexant
Indications
| Indication | Approved Population | Therapy Type | Status |
|---|---|---|---|
| Insomnia characterized by difficulties with sleep onset and/or sleep maintenance | Adults | Monotherapy | FDA Approved |
Lemborexant is the second dual orexin receptor antagonist (DORA) approved by the FDA, following suvorexant. Its mechanism — selective competitive antagonism at both the OX1R and OX2R orexin receptors — suppresses wake drive rather than augmenting GABA-mediated sedation, which is reflected in its broad indication covering both sleep onset and sleep maintenance. Lemborexant was approved in December 2019, after the publication of the 2017 American Academy of Sleep Medicine (AASM) clinical practice guideline; it is therefore not specifically addressed in that guideline. Cognitive behavioral therapy for insomnia (CBT-I) remains first-line in both AASM and ACP guidance, with pharmacotherapy reserved for patients in whom CBT-I is unavailable, has failed, or is needed as a temporary adjunct. The pivotal program comprised two phase 3 trials: SUNRISE 1 (Study 304, FDA Study 2; 1-month placebo- and zolpidem-controlled trial in older adults using polysomnographic latency to persistent sleep as the primary endpoint) and SUNRISE 2 (Study 303, FDA Study 1; 12-month placebo-controlled trial in adults ≥18 years using patient-reported sleep diary outcomes). Both demonstrated statistically significant superiority to placebo for sleep onset and sleep maintenance endpoints.
Irregular sleep–wake rhythm disorder in mild-to-moderate Alzheimer disease dementia — A phase 2 dose-finding RCT in 62 patients with ISWRD and AD-D (Moline 2021) used 4 weeks of treatment with lemborexant 2.5–15 mg. Outcomes were assessed by actigraphy and clinical scales; significant improvements versus placebo were reported in selected circadian rhythm parameters. Unlike suvorexant — whose label was updated to incorporate AD-population insomnia data — the lemborexant label does not include AD-specific findings. Evidence quality: low.
Delirium prevention in hospitalized older adults — Smaller observational and quasi-experimental studies; the evidence base is less mature than for suvorexant or ramelteon. Evidence quality: very low to low.
Dosing
The labeled approach is to use the lowest effective dose. Recommended starting dose is 5 mg taken immediately before going to bed, only when at least 7 hours of sleep opportunity remain before activities requiring full alertness. The 5 mg dose may be increased to a maximum of 10 mg once daily based on clinical response and tolerability. Concurrent CYP3A inhibitors and hepatic impairment dictate specific dose ceilings, and concurrent strong or moderate CYP3A inducers should be avoided altogether. There is no genuine 20 mg option — unlike suvorexant, lemborexant has only two strengths (5 and 10 mg).
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| Adult insomnia (sleep onset and/or maintenance) — primary indication | 5 mg PO | 5–10 mg nightly | 10 mg/day | Take immediately before bed; ≥7 h before planned awakening Increase to 10 mg only if 5 mg is well tolerated but inadequate |
| Older adults (≥65 years) | 5 mg PO | 5–10 mg nightly | 10 mg/day | Per FDA label, exercise caution with doses >5 mg in patients ≥65 Somnolence at 10 mg: 9.8% in elderly vs 7.7% in younger adults |
| Mild hepatic impairment (Child-Pugh A) | 5 mg PO | 5–10 mg nightly | 10 mg/day | No formal adjustment; AUC increased Patients may experience increased somnolence |
| Moderate hepatic impairment (Child-Pugh B) | 5 mg PO | 5 mg nightly | 5 mg/day | Maximum 5 mg AUC, Cmax, and terminal half-life all increased |
| Severe hepatic impairment (Child-Pugh C) | Not recommended | — | — | Not studied; avoid use |
| Renal impairment (mild, moderate, severe) | 5 mg PO | 5–10 mg nightly | 10 mg/day | No dose adjustment required AUC increased in severe impairment; counsel on somnolence |
| Concomitant weak CYP3A inhibitor (e.g., chlorzoxazone, ranitidine) | 5 mg PO | 5 mg nightly | 5 mg/day | Maximum 5 mg PBPK modelling predicts <2-fold AUC increase with weak inhibitors |
| Concomitant strong or moderate CYP3A inhibitor (e.g., itraconazole, clarithromycin, fluconazole, verapamil) | Avoid | Use alternative hypnotic Substantial AUC increase expected | ||
| Concomitant strong or moderate CYP3A inducer (e.g., rifampin, carbamazepine, St. John’s wort, bosentan, efavirenz, etravirine, modafinil) | Avoid | Choose a non-CYP3A-dependent hypnotic Efficacy substantially reduced | ||
| Pediatric (<18 years) | Not established | — | — | Safety and effectiveness not established |
Lemborexant has a longer half-life than other hypnotics in routine use (~17 h at 5 mg, ~19 h at 10 mg), and steady-state accumulation is 1.5- to 3-fold. The FDA label is explicit that lemborexant should not be administered unless ≥7 hours remain before required awakening, and that the 10 mg dose carries a labeled caution regarding next-morning driving. CNS depressant effects may persist for several days after discontinuation. Patients who routinely cannot guarantee a full 7-hour sleep opportunity, on-call clinicians, and shift workers are not appropriate candidates.
If insomnia fails to remit after 7–10 days of treatment, the FDA label advises re-evaluation for an underlying psychiatric or medical disorder rather than continued empiric treatment.
Pharmacology of Lemborexant
Mechanism of Action
Lemborexant is a competitive antagonist at the orexin OX1R and OX2R receptors with in vitro IC50 values of 6.1 nM and 2.6 nM, respectively. The orexin (hypocretin) signaling system originates in the lateral hypothalamus and projects to monoaminergic and cholinergic wake-promoting nuclei; orexin A and orexin B are the principal endogenous neuropeptides driving arousal. By blocking their binding at OX1R and OX2R, lemborexant suppresses wake drive rather than augmenting sleep drive. The major metabolite, M10, is pharmacologically active with comparable in vitro affinity to the parent compound (IC50 4.2 nM at OX1R and 2.9 nM at OX2R), and contributes to overall pharmacodynamic effect. The clinical signature of orexin antagonism is the labeled signal for narcolepsy-spectrum events — sleep paralysis, hypnagogic/hypnopompic hallucinations, and cataplexy-like leg weakness — which increase in incidence with dose; loss of orexin neurons is the pathological substrate of human narcolepsy with cataplexy, which is why narcolepsy is the only labeled contraindication.
ADME Profile
| Parameter | Value | Clinical Implication |
|---|---|---|
| Absorption | Tmax ~1–3 h fasted; less-than-proportional Cmax/AUC across 2.5–75 mg; high-fat meal decreases Cmax by 23%, increases AUC by 18%, and delays Tmax by ~2 h | Take on an empty stomach for fastest sleep-onset effect; avoid taking immediately after a heavy meal |
| Distribution | Vd ~1,970 L (very large — extensive tissue distribution); plasma protein binding ~94% in vitro; blood-to-plasma ratio 0.65 | High-volume distribution explains long effective half-life; hemodialysis is not expected to remove drug in overdose |
| Metabolism | Hepatic; CYP3A4 is the major enzyme with minor contribution from CYP3A5; major circulating active metabolite is M10. M10 induces CYP3A and has weak inhibitory potential at CYP3A and inductive potential at CYP2B6 | CYP3A is the dominant determinant of drug interactions. Lemborexant decreases exposure of CYP2B6 substrates (e.g., bupropion, methadone) |
| Elimination | ~57% feces, ~29% urine (<1% unchanged); effective t½ 17 h (5 mg) and 19 h (10 mg); accumulation 1.5- to 3-fold; steady-state by ~7 days | Long half-life means CNS effects may persist for several days after discontinuation; clinically meaningful for transitions in care or surgery |
Side Effects
The pivotal lemborexant development program — comprising FDA Study 1 (also known as SUNRISE 2: 6-month placebo-controlled adult trial with 6-month extension) and FDA Study 2 (also known as SUNRISE 1: 1-month placebo- and zolpidem-controlled trial in older adults) — enrolled 1,418 adults with insomnia disorder. The most common adverse event was somnolence (combined preferred term: somnolence/lethargy/fatigue/sluggishness) at 6.9% on 5 mg and 9.6% on 10 mg, versus 1.3% on placebo. Most CNS adverse events show a clear dose response. The narcolepsy-spectrum events (sleep paralysis, hypnagogic/hypnopompic hallucinations, cataplexy-like leg weakness) — although uncommon — are mechanistically distinctive and dose-related. Lemborexant is a Schedule IV controlled substance, with abuse-liability profile in recreational sedative users statistically similar to zolpidem 30 mg and suvorexant 40 mg.
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| None reported at this frequency in pivotal trials at the recommended doses | — | The composite somnolence/fatigue endpoint at 10 mg approached this threshold (9.6%) but did not exceed it in pooled first-30-day data |
| Adverse Effect | Incidence (5 mg / 10 mg) | Clinical Note |
|---|---|---|
| Somnolence / lethargy / fatigue / sluggishness (combined) | 6.9% / 9.6% | Placebo 1.3%. Higher in elderly at the 10 mg dose (9.8% vs 7.7% in younger adults) |
| Headache | 5.9% / 4.5% | Placebo 3.4%; usually mild and self-limiting |
| Nightmare or abnormal dreams | 0.9% / 2.2% | Placebo 0.9%; clear dose-related signal at 10 mg; inquire on follow-up |
| Sleep paralysis | 1.3% / 1.6% | Placebo 0%; counsel patients proactively about the nature of these events |
| Adverse Effect | Estimated Frequency | Typical Onset | Required Action |
|---|---|---|---|
| Daytime impairment / impaired driving | Documented in some subjects taking 10 mg in driving studies | Morning after dose; may persist for several days after discontinuation | Counsel patients on 10 mg about next-morning driving; reduce dose or discontinue if daytime somnolence develops |
| Complex sleep behaviors (sleep-walking, sleep-driving, preparing/eating food, phone calls, sex with amnesia) | 2 events in pivotal trials, both on 10 mg | Any time during therapy, including first dose | Discontinue immediately if any episode occurs; risk increased by alcohol and other CNS depressants |
| Worsening depression and emergence of suicidal ideation | By questionnaire: 0.4% (5 mg) and 0.3% (10 mg) vs 0.2% placebo | Variable | Immediately evaluate any new behavioral signs or suicidal ideation; prescribe smallest feasible quantity in patients with depression |
| Sleep paralysis (inability to move/speak during sleep–wake transitions) | 1.3% (5 mg) and 1.6% (10 mg); placebo 0% | Sleep–wake transitions | Reassure if isolated and brief; consider dose reduction or discontinuation if recurrent or distressing |
| Hypnagogic / hypnopompic hallucinations | 0.1% (5 mg) and 0.7% (10 mg); placebo 0% | Falling asleep or waking | Counsel proactively about the nature of these events; consider dose reduction or discontinuation if recurrent |
| Cataplexy-like symptoms (transient leg weakness, day or night) | Per labeled effect; not necessarily emotion-triggered | Variable | Consider dose reduction or discontinuation; assess fall risk in older adults |
| Falls (related to drowsiness) | Increased risk per label, particularly in elderly | Any time | Assess gait stability before dose escalation; lower dose in patients with prior falls |
| Respiratory depression in compromised patients | Cannot be excluded in moderate-to-severe OSA or COPD | Variable | Not studied in moderate-to-severe OSA or COPD; consider risks before prescribing in these populations and in combination with opioids |
| Abuse and dependence (Schedule IV) | Subjective abuse-liability similar to zolpidem 30 mg and suvorexant 40 mg | Variable | Screen substance-use history; monitor for misuse; prescribe limited quantities in at-risk patients. No physical dependence in clinical trials |
| Reason for Discontinuation (6-Month Period, FDA Study 1 / SUNRISE 2) | Incidence (5 mg / 10 mg) | Context |
|---|---|---|
| Somnolence | 1.0% / 2.9% | Placebo 0.6%; the dominant dose-related discontinuation signal |
| Nightmares | 0.3% / 1.3% | Placebo 0%; if mild, 5 mg dose may be tolerated |
| Palpitations | 0% / 0.6% | Placebo 0%; class effect not described — investigate alternative cardiac causes |
Lemborexant’s effective half-life of 17–19 hours is materially longer than older hypnotics and longer than suvorexant. Per the FDA label, CNS depressant effects may persist for several days after discontinuation. This is clinically meaningful for patients undergoing surgery, sedation procedures, or transitions of care. When a patient stops lemborexant, schedule reassessment of mental status and driving capacity within the first week rather than assuming washout is complete after a single missed dose.
Drug Interactions
Lemborexant is a CYP3A4 substrate (with minor CYP3A5 contribution), so CYP3A inhibitors and inducers dominate its pharmacokinetic interaction profile. The labeled interaction strategy is more restrictive than for suvorexant: even moderate CYP3A inhibitors should be avoided, and weak inhibitors require a dose ceiling of 5 mg. In addition, lemborexant is a CYP2B6 inducer that can reduce exposure of CYP2B6 substrates such as bupropion and methadone. Pharmacodynamic additivity with alcohol and other CNS depressants is the dominant non-PK concern.
Compared with suvorexant — where moderate CYP3A inhibitors require a dose reduction (5 mg, max 10 mg) — lemborexant takes a stricter position: moderate CYP3A inhibitors should be avoided altogether. Among commonly prescribed agents this is most likely to affect patients on diltiazem, verapamil, or fluconazole. Switching to a non-CYP3A inhibitor or selecting an alternative hypnotic is generally more practical than discontinuing the cardiovascular or antifungal therapy.
Monitoring
The FDA label does not specify routine laboratory monitoring for lemborexant. Clinical follow-up should focus on therapeutic response, daytime function, dose-related neuropsychiatric and narcolepsy-spectrum events, falls (especially in older adults), and — because lemborexant is a controlled substance — appropriate use and abuse-screening.
-
Sleep response
Reassess at 7–10 days, then periodically
Routine Track sleep latency, wake after sleep onset, total sleep time, and daytime function. Per the FDA label, failure of insomnia to remit after 7–10 days should prompt re-evaluation for an underlying psychiatric or medical disorder. -
Daytime somnolence and driving
Each follow-up visit
Routine Specifically inquire about morning grogginess, near-misses while driving, and cognitive function. CNS depressant effects may persist for several days after discontinuation. Step down to 5 mg or discontinue if daytime impairment develops. -
Falls and balance (older adults)
Each follow-up visit
Routine Per FDA label, increased drowsiness raises fall risk, particularly in elderly. Assess gait stability and consider home safety review before increasing to 10 mg in patients ≥65. -
Mood and suicidal ideation
Each follow-up visit
Routine Suicidal ideation by questionnaire was higher with lemborexant than placebo (0.3–0.4% vs 0.2%). PHQ-9 with item 9 review or C-SSRS is appropriate, particularly in patients with prior depression. -
Complex sleep behaviors
Each follow-up visit
Routine Ask directly about sleep-walking, sleep-eating, sleep-driving, and unrecalled night-time activity. The label directs immediate discontinuation after any reported episode. -
Narcolepsy-spectrum events
Each follow-up visit
Routine Inquire specifically about sleep paralysis, vivid hallucinations on falling asleep or waking, and transient leg weakness. Sleep paralysis was reported in 1.3–1.6% in pivotal trials; dose reduction or discontinuation if recurrent. -
Substance-use risk
Baseline; ongoing as indicated
Routine Lemborexant is a Schedule IV controlled substance. Screen for prior alcohol or sedative misuse before initiation; monitor for early refill requests or self-escalation. -
CYP2B6 substrate efficacy
When co-administered
Trigger-based For patients on bupropion, methadone, or other CYP2B6 substrates, monitor for adequate clinical response to the substrate; consider dose adjustment if efficacy is reduced. -
Respiratory status
Baseline if compromised
Trigger-based Lemborexant has not been studied in moderate-to-severe OSA or COPD. Weigh hypnotic need against potential respiratory effects in compromised patients.
Contraindications & Cautions
Absolute Contraindications (per FDA Label)
- Narcolepsy — the only labeled contraindication. Orexin antagonism could exacerbate the underlying loss of orexin signaling that produces the disorder.
Not Recommended / Specialist Input Suggested
- Concomitant strong or moderate CYP3A inhibitors — the FDA label directs avoidance of co-administration.
- Concomitant strong or moderate CYP3A inducers — the FDA label directs avoidance of co-administration; efficacy is substantially reduced.
- Severe hepatic impairment (Child-Pugh C) — not studied; the FDA label states lemborexant is not recommended.
- Active major depression with suicidal ideation — a small dose-related signal in suicidal ideation by questionnaire was observed in pivotal trials. Prescribe the lowest feasible quantity per label.
- Pediatric patients — safety and effectiveness have not been established.
- Combination with other hypnotics — the FDA label specifically states use of lemborexant with other drugs to treat insomnia is not recommended.
Use with Caution
- Older adults — exercise caution at doses above 5 mg per FDA label; falls and somnolence are more frequent.
- Moderate hepatic impairment — maximum dose 5 mg.
- Mild hepatic impairment or severe renal impairment — increased AUC and somnolence risk; consider lower dose.
- Concomitant weak CYP3A inhibitor — maximum 5 mg.
- Moderate or severe respiratory disease (OSA, COPD) — not studied; respiratory effects cannot be excluded.
- History of substance use disorder — Schedule IV; abuse-liability comparable to zolpidem 30 mg in recreational users.
- Patients who cannot guarantee 7 hours of sleep opportunity — risk of next-day impairment is materially increased.
- Pregnancy and lactation — no human data are available. Animal teratogenicity occurred only at very high multiples of human exposure. The drug is present in rat milk; monitor breastfed infants for excessive sedation. A pregnancy exposure registry is available (1-888-274-2378).
In April 2019, the FDA required a Boxed Warning on eszopiclone, zaleplon, and zolpidem for rare but serious complex sleep behaviors (sleep-driving, sleep-walking, sleep-eating, and others) that have resulted in injuries and deaths. Lemborexant was approved in December 2019 — after the 2019 Boxed Warning — and is not included in it, but its FDA label states that complex sleep behaviors have been reported with lemborexant and directs immediate discontinuation if any patient experiences such an episode. Two complex sleep behavior events were reported in pivotal trials, both at the 10 mg dose. The risk is increased by alcohol and other CNS depressants. Counsel every patient on this risk before the first dose.
Patient Counselling
Purpose of Therapy
Lemborexant is approved for adults with insomnia involving difficulty falling asleep, staying asleep, or both. It works differently from older sleeping pills: rather than enhancing the brain’s sleep-promoting signals, it blocks the brain’s own wake-promoting signals (orexin). Lemborexant is a federally controlled substance because it can be misused; keep it in a secure place and do not share it. Cognitive behavioural therapy for insomnia (CBT-I) is the recommended first-line treatment for chronic insomnia and should ideally be offered or continued alongside any drug therapy.
How to Take It
Take one tablet immediately before going to bed, and only when you can stay in bed for at least 7 hours before being active again. The recommended starting dose is 5 mg; the maximum is 10 mg per night. Avoid taking it with or shortly after a heavy or fatty meal — food, especially a high-fat dinner, slows how quickly the medication starts working by about 2 hours. Do not drink alcohol on evenings you take lemborexant.
Sources
- U.S. Food and Drug Administration. Dayvigo (lemborexant) prescribing information — initial approval December 2019 (Reference ID 4538172). accessdata.fda.gov Initial approved US label — primary source for indications, dosing, contraindications, drug interactions, and incidence figures cited throughout this monograph.
- DailyMed (NIH). DAYVIGO (lemborexant) tablet, film coated — current label. dailymed.nlm.nih.gov Searchable, regularly updated mirror of the FDA-approved labeling, including current PLLR-format Pregnancy and Lactation sections.
- U.S. Drug Enforcement Administration. Schedules of Controlled Substances: Placement of Lemborexant in Schedule IV. Federal Register, April 7, 2020. federalregister.gov Final rule placing lemborexant in DEA Schedule IV, effective April 7, 2020.
- U.S. Food and Drug Administration. FDA Drug Safety Communication: FDA adds Boxed Warning for risk of serious injuries caused by sleepwalking with certain prescription insomnia medicines. April 30, 2019. fda.gov FDA communication clarifying that the 2019 Boxed Warning applies to eszopiclone, zaleplon, and zolpidem; lemborexant is not included.
- Rosenberg R, Murphy P, Zammit G, et al. Comparison of lemborexant with placebo and zolpidem tartrate extended release for the treatment of older adults with insomnia disorder: a phase 3 randomized clinical trial. JAMA Netw Open. 2019;2(12):e1918254. doi: 10.1001/jamanetworkopen.2019.18254 Pivotal SUNRISE 1 trial (Study 304, NCT02783729) in adults ≥55 years with insomnia disorder; 1-month, placebo- and zolpidem-controlled, with polysomnographic latency to persistent sleep as the primary endpoint. Corresponds to FDA Study 2.
- Kärppä M, Yardley J, Pinner K, et al. Long-term efficacy and tolerability of lemborexant compared with placebo in adults with insomnia disorder: results from the phase 3 randomized clinical trial SUNRISE 2. Sleep. 2020;43(9):zsaa123. doi: 10.1093/sleep/zsaa123 SUNRISE 2 trial (Study 303, NCT02952820), 6-month placebo-controlled period in 949 adults ≥18 years; corresponds to FDA Study 1. Patient-reported sleep diary outcomes; supports efficacy and the absence of rebound insomnia or withdrawal.
- Yardley J, Kärppä M, Inoue Y, et al. Long-term effectiveness and safety of lemborexant in adults with insomnia disorder: results from a phase 3 randomized clinical trial. Sleep Med. 2021;80:333–342. doi: 10.1016/j.sleep.2021.01.048 Full 12-month SUNRISE 2 outcomes including the 6-month active-treatment-only extension period; demonstrates sustained patient-reported efficacy across one year of treatment.
- Moline M, Thein S, Bsharat M, et al. Safety and efficacy of lemborexant in patients with irregular sleep–wake rhythm disorder and Alzheimer’s disease dementia: results from a phase 2 randomized clinical trial. J Prev Alzheimers Dis. 2021;8(1):7–18. doi: 10.14283/jpad.2020.69 Exploratory phase 2 dose-finding RCT (62 patients; 2.5/5/10/15 mg vs placebo) using actigraphy and clinical scales over 4 weeks of treatment in mild-to-moderate AD-D — supporting evidence for the off-label use of lemborexant in ISWRD with AD-D.
- Sateia MJ, Buysse DJ, Krystal AD, Neubauer DN, Heald JL. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2):307–349. doi: 10.5664/jcsm.6470 AASM 2017 guideline; pre-dates lemborexant approval (December 2019) and therefore does not include a specific recommendation for lemborexant.
- Qaseem A, Kansagara D, Forciea MA, Cooke M, Denberg TD; Clinical Guidelines Committee of the American College of Physicians. Management of chronic insomnia disorder in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2016;165(2):125–133. doi: 10.7326/M15-2175 ACP guideline emphasising CBT-I as first-line treatment for chronic insomnia, with pharmacotherapy reserved for patients in whom CBT-I is inadequate or unavailable.
- Beuckmann CT, Suzuki M, Ueno T, Nagaoka K, Arai T, Higashiyama H. In vitro and in silico characterization of lemborexant (E2006), a novel dual orexin receptor antagonist. J Pharmacol Exp Ther. 2017;362(2):287–295. doi: 10.1124/jpet.117.241422 Receptor-binding and selectivity profile of lemborexant — establishes the OX1R/OX2R potency at low nanomolar concentrations and selectivity over 88 other receptors, transporters, and ion channels.
- Sakurai T. The neural circuit of orexin (hypocretin): maintaining sleep and wakefulness. Nat Rev Neurosci. 2007;8(3):171–181. Foundational review of orexin signalling and its role in arousal — the conceptual basis for orexin antagonism as a hypnotic strategy.
- Landry I, Aluri J, Hall N, et al. Effect of CYP3A inhibition and induction on the pharmacokinetics of lemborexant. Clin Pharmacokinet. 2021;60(4):539–552. Dedicated PK studies underpinning the CYP3A inhibitor and inducer interaction recommendations in the FDA label.
- Vermeeren A, Jongen S, Murphy P, et al. On-the-road driving performance the morning after bedtime administration of lemborexant in healthy adult and elderly volunteers. Sleep. 2019;42(4):zsy260. doi: 10.1093/sleep/zsy260 On-the-road driving study underpinning the FDA caution about next-morning driving impairment in some subjects taking the 10 mg dose.
- Murphy P, Moline M, Mayleben D, et al. Lemborexant, a dual orexin receptor antagonist (DORA) for the treatment of insomnia disorder: results from a Bayesian, adaptive, randomized, double-blind, placebo-controlled study. J Clin Sleep Med. 2017;13(11):1289–1299. Phase 2b dose-finding study supporting the registrational dosing strategy.