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The first and only low-sodium* oxybate
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Product Information:
FDA Findings of Clinical Superiority
According to the FDA, XYWAV is clinically superior to XYREM® (sodium oxybate) oral solution by means of greater safety because XYWAV provides a greatly reduced chronic sodium burden compared to XYREM. The differences in the sodium content of the two products at the recommended doses will be clinically meaningful in reducing cardiovascular morbidity in a substantial proportion of patients for whom the drug is indicated.5
The decision of the FDA Office of Orphan Products Development is based on findings that XYWAV provides a greatly reduced chronic sodium burden compared to XYREM. There are no head-to-head data for XYWAV and XYREM.5
About narcolepsy
What is narcolepsy?
Narcolepsy is a chronic, debilitating neurologic sleep disorder. It is characterized by excessive daytime sleepiness (EDS), which is the inability to stay awake and alert during the day. This results in the irrepressible need to sleep or having unplanned lapses into sleep or drowsiness, and an inability to regulate sleep-wake cycles normally.6
- Daily periods of irrepressible need to sleep or daytime lapses into drowsiness or sleep
- One or both of the following:
- Cataplexy and either:
- Mean sleep latency ≤8 minutes and ≥2 SOREMPs on MSLT
- SOREMP (≤15 min after sleep onset) on nocturnal PSG
- CSF hypocretin-1 concentration, measured by radioimmunoassay, is either ≤110 pg/mL or <1/3 of mean values in normal subjects using the same standardized assay
- Cataplexy and either:
- The signs and symptoms are not better explained by other causes, such as chronic insufficient sleep, delayed sleep phase disorder, mental disorder, or medication/substance use or withdrawal
- Cataplexy is absent‡
- Daily periods of irrepressible need to sleep or daytime lapses into drowsiness or sleep occurring for at least three months
- Mean sleep latency ≤8 minutes and ≥2 SOREMPs on MSLT; SOREMP (≤15 min after sleep onset) on preceding nocturnal PSG may replace one of the SOREMPs on MSLT
- CSF hypocretin-1 concentration measured by radioimmunoassay is either >110 pg/mL or >1/3 of mean values in normal subjects using the same standardized assay‡
- The signs and symptoms are not better explained by other causes, such as chronic insufficient sleep, delayed sleep phase disorder, mental disorder, or medication/substance use or withdrawal
There is no cure for narcolepsy, therefore, EDS is lifelong and may have a substantial negative impact on a person's ability to function psychologically, socially, and professionally.8
Patients with narcolepsy may be at a greater risk for CV events. In a retrospective medical claims analysis, patients had a greater risk for any stroke (1.7x), major adverse cardiovascular events (MACE) (1.5x), heart failure (1.4x) and cardiovascular disease (CVD)‖ (1.3x) compared to patients without narcolepsy.9¶#
‡If cataplexy develops later or low or absent CSF hypocretin-1 levels are discovered, reclassify as narcolepsy type 1.4
§The exact prevalence of narcolepsy in the pediatric population is uncertain.10,11
‖Grouped instances of stroke, atrial fibrillation, heart failure, and myocardial infarction.9
¶Retrospective medical claims analysis including 12,816 adults with narcolepsy and 38,441 matched controls. Controls were matched in 3:1 on cohort entry date, age, sex, region, and insurance type. Evaluated post-narcolepsy diagnosis for CV events. Excluded patients in each analysis with a history of that CV event in the 6 months prior to cohort entry. Patients remained eligible for inclusion in other CV event analyses (eg, a patient with a history of stroke could still be included in the heart failure and MACE analyses).9
#HR: any stroke (95% CI) 1.71 (1.24–2.34); heart failure (95% CI) 1.35 (1.03–1.76); MACE (95% CI) 1.45 (1.20–1.74); CVD (95% CI) 1.30 (1.08–1.56).9
CI = confidence interval; CSF = cerebrospinal fluid; CVD = cardiovascular disease; HR = hazard ratio; ICSD = international classification of sleep disorders; MACE = major adverse cardiovascular event; MSLT = multiple sleep latency test; PSG = polysomnography; SOREMP = sleep-onset REM period.
About idiopathic hypersomnia (IH)
What is idiopathic hypersomnia?
Patients with idiopathic hypersomnia may experience additional challenges including impairments in social, educational, and occupational functioning.15
The actual prevalence may be higher due to the many difficulties in identifying and diagnosing idiopathic hypersomnia, as well as distinguishing it from other similar sleep disorders. It is estimated that far fewer patients are currently receiving pharmacological treatment for their idiopathic hypersomnia.17,18
Increased odds of cardiovascular disease
(2.26, 2.14-2.38)
Increased odds of major adverse cardiovascular event (MACE)
(2.08, 1.89-2.30)
Increased odds of stroke
(2.07, 1.87-2.29)
**Based on a retrospective analysis of US healthcare claims from Symphony Healthcare Services Integrated Dataverse database (October 2014–September 2019). Patients with ≥1 medical claim with an IH diagnosis were initially identified. This estimate was calculated using the number of patients with ≥2 IH diagnostic claims within a 5-year period. Eligibility criteria to determine total patients at risk were not applied.16
††Based on a retrospective cohort study using U.S. administrative claims data from the Merative™ MarketScan® Research Databases covering the period from December 31, 2013, to February 29, 2020. Adults aged 18 years or older with at least one inpatient or outpatient claim with a diagnosis of idiopathic hypersomnia were included. Each individual with idiopathic hypersomnia was matched with up to 5 non–idiopathic hypersomnia controls based on age, sex, region, insurance type, and calendar month and year of cohort entry. In total, 11,412 individuals in the idiopathic hypersomnia cohort and 57,058 individuals in the matched non-idiopathic hypersomnia cohort were eligible. All participants were followed over a two-year assessment period, comprising the 365 days before and after the cohort entry date.19,20
Impact and relevance of sodium intake
Sodium intake is a modifiable risk factor for CV disease.21 In adults with or without hypertension, reduction of dietary sodium intake is recommended to <2300 mg/day, moving toward an ideal limit of <1500 mg/day to prevent or treat elevated blood pressure and hypertension.22
A meta-analysis by Ma et al. revealed that each 1000 mg increase in urinary sodium excretion was associated with an 18% increase in CV risk.23‡‡ The study assessed urinary sodium excretion using multiple 24-hour urine samples in 10,709 participants with a median follow-up of 8.8 years.23§§
CV comorbidity prevalence is an important consideration in managing people living with narcolepsy. A growing body of evidence indicates that people living with narcolepsy have an increased risk of CVD and events—including higher risk of stroke, heart failure, and MACE.9,24-26
CV comorbidity prevalence is an important consideration in managing people living with IH. According to a retrospective claims analysis, adults with IH have a greater prevalence of CV comorbidities compared to matched controls without IH.19††
‡‡Adjusted hazard ratio (95% CI): 1.18 (1.08-1.29).23
§§A meta-analysis of 10,709 participants from 6 studies showed that higher 24-hour sodium excretion was associated with higher cardiovascular risk in analyses that controlled for confounding factors. Multiple 24-hour urine samples, the most accurate method for assessing sodium intake, were obtained for each participant. Primary outcome was a cardiovascular event, defined as a composite of coronary revascularization (coronary-artery bypass grafting or percutaneous coronary intervention), fatal or nonfatal myocardial infarction, or fatal or nonfatal stroke.23
††Based on a retrospective cohort study using U.S. administrative claims data from the Merative™ MarketScan® Research Databases covering the period from December 31, 2013, to February 29, 2020. Adults aged 18 years or older with at least one inpatient or outpatient claim with a diagnosis of idiopathic hypersomnia were included. Each individual with idiopathic hypersomnia was matched with up to 5 non–idiopathic hypersomnia controls based on age, sex, region, insurance type, and calendar month and year of cohort entry. In total, 11,412 individuals in the idiopathic hypersomnia cohort and 57,058 individuals in the matched non-idiopathic hypersomnia cohort were eligible. All participants were followed over a two-year assessment period, comprising the 365 days before and after the cohort entry date.19
Your members could benefit from XYWAV
Proven Efficacy
XYWAV is indicated for the treatment of cataplexy or excessive daytime sleepiness (EDS) in patients 7 years of age and older with narcolepsy, and for the treatment of idiopathic hypersomnia (IH) in adults.1
At the 9-g nightly dose, XYWAV contains 131 mg of sodium.3
For narcolepsy patients, choosing XYWAV over a high-sodium oxybate can make a difference of up to ~1509 mg of sodium a day. High-sodium oxybates, including XYREM® (sodium oxybate) oral solution and LUMRYZ™ (sodium oxybate) for extended-release oral suspension, have ~1640 mg of sodium in a 9-g dose.3,27,28
Dosing Information1
XYWAV’s dosing options can be individualized for patients across both indications.
All patients should take the first nightly dose of XYWAV in bed at night and at least 2 hours after eating.
Twice-nightly dosing for adults with narcolepsy with cataplexy and/or EDS or adults with idiopathic hypersomnia (IH)
- For patients new to oxybates, the recommended starting dose is 4.5 g per night orally, divided into 2 doses:
- 2.25 g taken at bedtime and 2.25 g taken 2.5 to 4 hours later
- Increase the dosage by up to 1.5 g per night per week to the recommended dosage range of 6 g to 9 g per night
- Doses higher than 9 g per night have not been studied and ordinarily should not be administered
- Some patients may achieve better responses with unequal doses at bedtime and 2.5 to 4 hours later
- For pediatric patients ≥7 years of age with narcolepsy, the starting dosage, titration regimen and maximum nightly dose are based on weight
Once-nightly dosing option for adults with IH
- For patients new to oxybates, the recommended starting dose is 3 g per night
- Increase the dosage by up to 1.5 g per night per week to the recommended dosage range of 6 g per night
- Single doses >6 g per night have not been studied and ordinarily should not be administered
The medicine is distributed exclusively through the XYWAV and XYREM Risk Evaluation and Mitigation Strategy (REMS) program due to risks associated with CNS depression and abuse and misuse.
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INDICATIONS AND USAGE
XYWAV® (calcium, magnesium, potassium, and sodium oxybates) oral solution, 0.5 g/mL total salts (equivalent to 0.413 g/mL of oxybate) is indicated for the treatment of cataplexy or excessive daytime sleepiness (EDS) in patients 7 years of age and older with narcolepsy, and for the treatment of idiopathic hypersomnia (IH) in adults.
IMPORTANT SAFETY INFORMATION
WARNING: CENTRAL NERVOUS SYSTEM DEPRESSION and ABUSE AND MISUSE.
Central Nervous System Depression
XYWAV is a CNS depressant. Clinically significant respiratory depression and obtundation may occur in patients treated with XYWAV at recommended doses. Many patients who received XYWAV during clinical trials in narcolepsy and idiopathic hypersomnia were receiving CNS stimulants.
Abuse and Misuse
The active moiety of XYWAV is oxybate or gamma-hydroxybutyrate (GHB). Abuse or misuse of illicit GHB, either alone or in combination with other CNS depressants, is associated with CNS adverse reactions, including seizure, respiratory depression, decreases in the level of consciousness, coma, and death.
Because of the risks of CNS depression and abuse and misuse, XYWAV is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the XYWAV and XYREM REMS.
Contraindications
XYWAV is contraindicated
- in combination with sedative hypnotics or alcohol and
- in patients with succinic semialdehyde dehydrogenase deficiency.
Warnings and Precautions
Central Nervous System Depression
The concurrent use of XYWAV with other CNS depressants, including but not limited to opioid analgesics, benzodiazepines, sedating antidepressants or antipsychotics, sedating anti-epileptic drugs, general anesthetics, muscle relaxants, and/or illicit CNS depressants, may increase the risk of respiratory depression, hypotension, profound sedation, syncope, and death. If use of these CNS depressants in combination with XYWAV is required, dose reduction or discontinuation of one or more CNS depressants (including XYWAV) should be considered. In addition, if short-term use of an opioid (eg, post- or perioperative) is required, interruption of treatment with XYWAV should be considered.
After first initiating treatment and until certain that XYWAV does not affect them adversely (eg, impair judgment, thinking, or motor skills), caution patients against hazardous activities requiring complete mental alertness or motor coordination such as operating hazardous machinery, including automobiles or airplanes. Also caution patients against these hazardous activities for at least 6 hours after taking XYWAV. Patients should be queried about CNS depression-related events upon initiation of XYWAV therapy and periodically thereafter.
Abuse and Misuse
XYWAV is a Schedule III controlled substance. The active moiety of XYWAV is oxybate, also known as gamma-hydroxybutyrate (GHB), a Schedule I controlled substance. Abuse of illicit GHB, either alone or in combination with other CNS depressants, is associated with CNS adverse reactions, including seizure, respiratory depression, decreases in the level of consciousness, coma, and death. The rapid onset of sedation, coupled with the amnestic features of GHB particularly when combined with alcohol, has proven to be dangerous for the voluntary and involuntary user (eg, assault victim). Physicians should carefully evaluate patients for a history of drug abuse and follow such patients closely.
XYWAV and XYREM REMS
- Because of the risks of central nervous system depression and abuse and misuse, XYWAV is available only through a restricted distribution program called the XYWAV and XYREM REMS.
Notable requirements of the XYWAV and XYREM REMS include the following:
- Healthcare Providers who prescribe XYWAV are specially certified
- XYWAV will be dispensed only by the central pharmacy that is specially certified
- XYWAV will be dispensed and shipped only to patients who are enrolled in the XYWAV and XYREM REMS with documentation of safe use
Further information is available at www.XYWAVXYREMREMS.com or 1-866-997-3688.
Respiratory Depression and Sleep‑Disordered Breathing
XYWAV may impair respiratory drive, especially in patients with compromised respiratory function. In overdoses of oxybate and with illicit use of GHB, life-threatening respiratory depression has been reported. Increased apnea and reduced oxygenation may occur with XYWAV administration in adult and pediatric patients. A significant increase in the number of central apneas and clinically significant oxygen desaturation may occur in patients with obstructive sleep apnea treated with XYWAV. Prescribers should be aware that sleep-related breathing disorders tend to be more prevalent in obese patients, in men, in postmenopausal women not on hormone replacement therapy, and among patients with narcolepsy.
Depression and Suicidality
In Study 1, the randomized-withdrawal clinical trial in adult patients with narcolepsy (n=201), depression and depressed mood were reported in 3% and 4%, respectively, of patients treated with XYWAV. Two patients (1%) discontinued XYWAV because of depression. In most cases, no change in XYWAV treatment was required.
In Study 2, the randomized-withdrawal clinical trial in adult patients with idiopathic hypersomnia (n=154), depression and depressed mood were reported in 1% and 3%, respectively, of patients treated with XYWAV. All patients continued XYWAV treatment.
Two suicides and two attempted suicides occurred in adult clinical trials with oxybate (same active moiety as XYWAV). One patient experienced suicidal ideation and two patients reported depression in a pediatric clinical trial with oxybate. These events occurred in patients with and without previous histories of depressive disorders. The emergence of depression in patients treated with XYWAV requires careful and immediate evaluation. Monitor patients for the emergence of increased depressive symptoms and/or suicidality while taking XYWAV.
Other Behavioral or Psychiatric Adverse Reactions
In Study 1, confusion and anxiety occurred in 1% and 5% of patients with narcolepsy treated with XYWAV, respectively. One patient experienced visual hallucinations and confusion after ingesting approximately 9 grams of XYWAV.
In Study 2, confusion and anxiety occurred in 3% and 16% of patients with idiopathic hypersomnia, respectively. One patient experienced visual hallucinations, which led to discontinuation of XYWAV.
Other neuropsychiatric reactions reported with oxybate (same active moiety as XYWAV) in adult or pediatric clinical trials and in the postmarketing setting include hallucinations, paranoia, psychosis, aggression, agitation, confusion and anxiety. The emergence or increase in the occurrence of behavioral or psychiatric events in patients taking XYWAV should be carefully monitored.
Parasomnias
Parasomnias can occur in patients taking XYWAV.
In Study 1 and Study 2, parasomnias, including sleepwalking, were reported in 6% and 5% of adult patients treated with XYWAV, respectively.
In a clinical trial of XYREM (same active moiety as XYWAV) in adult patients with narcolepsy, five instances of sleepwalking with potential injury or significant injury were reported. Parasomnias, including sleepwalking, have been reported in a pediatric clinical trial with sodium oxybate (same active moiety as XYWAV) and in postmarketing experience with sodium oxybate.
Episodes of sleepwalking should be fully evaluated and appropriate interventions considered.
Most Common Adverse Reactions
The most common adverse reactions (occurring in ≥5% of XYWAV-treated patients in adult clinical trials in either narcolepsy or IH) were nausea, headache, dizziness, anxiety, insomnia, decreased appetite, hyperhidrosis, vomiting, diarrhea, dry mouth, parasomnia, somnolence, fatigue, and tremor.
In the pediatric clinical trial with XYREM (same active moiety as XYWAV) that included pediatric patients 7 to 17 years of age with narcolepsy, the most common adverse reactions (≥5%) were nausea (20%), enuresis (19%), vomiting (18%), headache (17%), weight decreased (13%), decreased appetite (9%), dizziness (8%), and sleepwalking (6%). The overall adverse reaction profile of XYREM in the pediatric clinical trial was similar to that seen in the adult clinical trial program. The safety profile in pediatric patients with XYWAV is expected to be similar to that of adult patients treated with XYWAV and to that of pediatric patients treated with XYREM.
Additional Adverse Reactions
Adverse reactions that occurred in 2-<5% of adult patients treated with XYWAV in the Open-Label Titration and Stable Dose Periods of the randomized-withdrawal study in adult patients with narcolepsy with cataplexy (Study 1) were fatigue, dry mouth, depressed mood, enuresis, irritability, paresthesia, depression, tremor, somnolence, and muscle spasms. Adverse reactions occurring in 2-<5% of patients treated with XYWAV in the IH study include balance disorder, muscle spasms, fall, paresthesia, snoring, weight decreased, bruxism, confusional state, depressed mood, feeling drunk, and irritability.
Adverse reactions that occurred in ≥2% of patients in clinical studies with oxybate (but not in Study 1) and which may be relevant for XYWAV, were pain, feeling drunk, pain in extremity, cataplexy, disturbance in attention, sleep paralysis, and disorientation.
Discontinuation: In Study 1, 9 of 201 patients (4%) reported adverse reactions that led to withdrawal from the study (anxiety, decreased appetite, depressed mood, depression, fatigue, headache, irritability, nausea, pain in extremity, parasomnia, somnolence, and vomiting). The most common adverse reaction leading to discontinuation was nausea (1.5%). In Study 2, 17 of 154 (11%) patients across all study periods (excluding placebo during the DB RWP) (up to 42 weeks) reported adverse reactions that led to withdrawal from the study (anxiety, nausea, insomnia, vomiting, fatigue, feeling abnormal, fall, decreased appetite, dizziness, paresthesia, tremor, parasomnia, confusional state, hallucination visual, and irritability). The most common adverse reaction leading to discontinuation was anxiety (3.2%). In Study 1 and Study 2, the majority of adverse reactions leading to discontinuation began during the first few weeks of treatment.
In the pediatric clinical trial with XYREM (same active moiety as XYWAV), 7 of 104 patients reported adverse reactions that led to withdrawal from the study (hallucination, tactile; suicidal ideation; weight decreased; sleep apnea syndrome; affect lability; anger, anxiety, depression; and headache).
Drug Interactions
XYWAV is contraindicated in combination with alcohol or sedative hypnotics. Use of other CNS depressants may potentiate the CNS-depressant effects of XYWAV.
Concomitant use of sodium oxybate with divalproex sodium results in an increase in systemic exposure to GHB, which was shown to cause a greater impairment on some tests of attention and working memory in a clinical study. A similar increase in exposure is expected with concomitant use of XYWAV and divalproex sodium; therefore, an initial dose reduction of XYWAV is recommended when used concomitantly with divalproex sodium. Prescribers are advised to monitor patient response closely and adjust dose accordingly if concomitant use of XYWAV and divalproex sodium is warranted.
Pregnancy and Lactation
There are no adequate data on the developmental risk associated with the use of XYWAV or sodium oxybate in pregnant women. XYWAV should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. GHB is excreted in human milk after oral administration of sodium oxybate. There is insufficient information on the risk to a breastfed infant, and there is insufficient information on milk production in nursing mothers. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for XYWAV and any potential adverse effects on the breastfed infant from XYWAV or from the underlying maternal condition.
Pediatric Use
The safety and effectiveness of XYWAV for the treatment of cataplexy or excessive daytime sleepiness in pediatric patients 7 years of age and older with narcolepsy have been established. XYWAV has not been studied in a pediatric clinical trial for narcolepsy or IH. Use of XYWAV in pediatric patients 7 years of age and older with narcolepsy is supported by evidence from an adequate and well-controlled study of sodium oxybate in pediatric patients 7 to 17 years of age, a study in adults showing a treatment effect of XYWAV similar to that observed with sodium oxybate, pharmacokinetic data of sodium oxybate from adult and pediatric patients, and pharmacokinetic data of XYWAV from healthy adult volunteers.
Safety and effectiveness of XYWAV in pediatric patients below the age of 7 years with narcolepsy have not been established.
Safety and effectiveness of XYWAV for the treatment of idiopathic hypersomnia in pediatric patients have not been established.
Geriatric Use
In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
Hepatic Impairment
The starting dose of XYWAV should be reduced in patients with liver impairment.
Dosage Modification in Patients with Hepatic Impairment: The recommended starting dosage in patients with hepatic impairment is one-half of the original dosage per night, administered orally, divided into two doses.
Dependence and Tolerance
There have been case reports of withdrawal, ranging from mild to severe, following discontinuation of illicit use of GHB at frequent repeated doses (18 g to 250 g per day) in excess of the recommended dosage range. Signs and symptoms of GHB withdrawal following abrupt discontinuation included insomnia, restlessness, anxiety, psychosis, lethargy, nausea, tremor, sweating, muscle cramps, tachycardia, headache, dizziness, rebound fatigue and sleepiness, confusion, and, particularly in the case of severe withdrawal, visual hallucinations, agitation, and delirium. These symptoms generally abated in 3 to 14 days. In cases of severe withdrawal, hospitalization may be required.
In the clinical trial experience with XYREM in narcolepsy/cataplexy patients at recommended doses, two patients reported anxiety and one reported insomnia following abrupt discontinuation at the termination of the clinical trial; in the two patients with anxiety, the frequency of cataplexy had increased markedly at the same time. In the XYWAV clinical trial in adult narcolepsy/cataplexy patients at recommended doses, one patient reported insomnia following abrupt discontinuation of XYWAV. In the XYWAV clinical trial in adult idiopathic hypersomnia patients at recommended doses, six patients reported insomnia, two patients reported early insomnia, and one patient reported visual and auditory hallucinations following abrupt discontinuation of XYWAV.
Tolerance to XYWAV has not been systematically studied in controlled clinical trials. There have been some case reports of symptoms of tolerance developing after illicit use at dosages far in excess of the recommended XYWAV dosage regimen.
Please see full Prescribing Information, including BOXED Warning.
1. XYWAV® (calcium, magnesium, potassium, and sodium oxybates). Prescribing Information. Palo Alto, CA: Jazz Pharmaceuticals, Inc.
2. FDA grants first of its kind indication for chronic sleep disorder treatment. News release. U.S. Food and Drug Administration; August 12, 2021. Accessed February 12, 2025. https://www.fda.gov/news-events/press-announcements/fda-grants-first-its-kind-indication-chronic-sleep-disorder-treatment
3. Chen C, Jenkins J, Zomorodi K, Skowronski R. Pharmacokinetics, bioavailability, and bioequivalence of lower-sodium oxybate in healthy participants in two open-label, randomized, crossover studies. Clin Transl Sci. 2021;14(6):2278-2287.
4. American Academy of Sleep Medicine. The International Classification of Sleep Disorders. Third Edition (ICSD-3). 2014.
5. US Department of Health and Human Services, US Food and Drug Administration website. Clinical superiority findings. Updated December 18, 2024. Accessed June 9, 2025. https://www.fda.gov/industry/designating-orphan-product-drugs-and-biological-products/clinical-superiority-findings
6. National Institute of Neurological Disorders and Stroke. Narcolepsy. Accessed October 2024. https://www.ninds.nih.gov/health-information/disorders/narcolepsy?search-term=narcolepsy#toc-what-is-narcolepsy
7. Ahmed I, Thorpy M. Clinical features, diagnosis and treatment of narcolepsy. Clin Chest Med. 2010;31(2):371-381.
8. National Institute of Neurological Disorders and Stroke. Narcolepsy Fact Sheet. NIH Publication No. 17-1637. Updated November 15, 2021. Accessed August 1, 2025. https://www.ninds.nih.gov/disorders/patient-caregiver-education/fact-sheets/narcolepsy-fact-sheet
9. Ben-Joseph RH, Saad R, Black J, et al. Cardiovascular burden of narcolepsy disease (CV-BOND): a real-world evidence study. Sleep. 2023:46(10):zsad161.
10. Babiker MOE, Prasad M. Narcolepsy in children: A diagnostic and management approach. Pediatr Neurol. 2015;52(6):557-565.
11. Nevsimalova S. The diagnosis and treatment of pediatric narcolepsy. Curr Neurol Neurosci Rep. 2014;14(8):469.
12. Trotti LM. Idiopathic hypersomnia. Sleep Med Clin. 2017;12(3):331-344.
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14. Dauvilliers Y, Bogan RK, Arnulf I, Scammell TE, St Louis EK, Thorpy MJ. Clinical considerations for the diagnosis of idiopathic hypersomnia. Sleep Med Rev. 2022;66:101709.
15. Stevens J, Schneider LD, Husain AM, et al. Impairment in functioning and quality of life in patients with idiopathic hypersomnia: the Real World Idiopathic Hypersomnia Outcomes Study (ARISE). Nat Sci Sleep. 2023;15:593-606.
16. Data on File (XYW-2021-025). Palo Alto, CA: Jazz Pharmaceuticals, Inc.
17. Masri TJ, Gonzales CG, Kushida CA. Idiopathic Hypersomnia. Sleep Med Clin. 2012;7(2):283-289.
18. Anderson KN, Pilsworth S, Sharples LD, Smith IE, Shneerson JM. Idiopathic hypersomnia: a study of 77 cases. Sleep. 2007;30(10):1274-1281.
19. Saad R, Lillaney P, Profant DA, et al. Cardiovascular burden of individuals diagnosed with idiopathic hypersomnia: Real-World Idiopathic Hypersomnia Total Health Model (CV-RHYTHM). Sleep Med. 2025;133:106587.
20. Saad R, Markt SC, Lillaney P, et al. The clinical and economic burden of idiopathic hypersomnia: results from the Real-World Idiopathic Hypersomnia Total Health Model (RHYTHM) study. Nat Sci Sleep. 2025;17:1743-1755.
21. Jackson SL, King SM, Zhao L, Cogswell ME. Prevalence of excess sodium intake in the United States—NHANES, 2009-2012. MMWR Morb Mortal Wkly Rep. 2016:64(52):1393-1397.
22. Jones DW, Ferdinand KC, Taler SJ, et al. 2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2025;86(18):1567-1678.
23. Ma Y, He FJ, Sun Q, et al. 24-hour urinary sodium and potassium excretion and cardiovascular risk. N Engl J Med. 2022;386(3):252-263.
24. Black J, Reaven NL, Funk SE, et al. Medical comorbidity in narcolepsy: findings from the Burden of Narcolepsy Disease (BOND) study. Sleep Med. 2017;33:13-18.
25. Ohayon MM. Narcolepsy is complicated by high medical and psychiatric comorbidities: a comparison with the general population. Sleep Med. 2013;14(6):488-492.
26. Riaz M, Bhattacharjee R, Lo-Ciganic W, et al. Narcolepsy and risk of cardiovascular outcomes beyond stimulant use. Sleep. 2025;zsaf197.
27. XYREM® (sodium oxybate) oral solution. Prescribing information. Palo Alto, CA: Jazz Pharmaceuticals, Inc.
28. LUMRYZ™ (sodium oxybate) for extended-release oral suspension. Prescribing information. Dublin, Ireland: Avadel Pharmaceuticals (USA), Inc.