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Public Comment 8 www.JazzPharmaceuticals.com May 20, 2021 Priya Shah West Virginia Medicaid 350 Capitol Street, Room 251 Charleston WV 25301 Dear Priya Shah, Thank you for your request for information regarding XYWAV™ (calcium, magnesium, potassium, and sodium oxybates) oral solution. If you did not specifically request the enclosed information, please contact Jazz Medical Information at 1-800-520-5568. XYWAV is indicated for the treatment of cataplexy or excessive daytime sleepiness (EDS) in patients 7 years of age and older with narcolepsy. Below is the information you requested. • XYWAV (calcium, magnesium, potassium, and sodium oxybates) Oral Solution Written Comments for Medicaid • XYWAV Prescribing Information Please refer to the accompanying XYWAV™ full Prescribing Information including the Boxed Warning. This information is provided to you as a professional courtesy and may include content that has not been approved by the United States Food and Drug Administration (FDA). Statements in this communication are not intended to advocate any indication, dosage, or other claim not set forth in the prescribing information. This response contains information of a general nature and is intended solely to assist you in formulating your own conclusions regarding our product. It is not meant to be a thorough review of the literature and does not represent all professional points of view on this subject. Thank you for your interest in XYWAV™. Please contact Medical Information at 1-800-520-5568 if you have further questions. Sincerely, Jazz Pharmaceuticals Medical Information Department Enclosure(s): • XYWAV (calcium, magnesium, potassium, and sodium oxybates) Oral Solution Written Comments for Medicaid • XYWAV Prescribing Information CASE-0004188 XywavTM (calcium, magnesium, potassium, and sodium oxybates) Oral Solution Written Comments for Medicaid Xywav Overview XywavTM (calcium, magnesium, potassium, and sodium oxybates) oral solution is a central nervous system (CNS) depressant indicated for the treatment of cataplexy or EDS in patients 7 years and older with narcolepsy.1 This oxybate therapy contains the same active moiety as Xyrem® (sodium oxybate), and is a mixture of calcium, magnesium, potassium, and sodium oxybates. At a 9 gram nightly dose (the maximum recommended dosage) of Xywav, sodium intake is reduced by 1509 mg (a 92% reduction; Xywav maximum sodium contribution is 131 mg/night) compared to sodium oxybate,1,2 and exposure to each cation is within the adult recommended daily allowance.3 Distinct from sodium oxybate, Xywav does not have a warning regarding high sodium content or subsequent precautions around monitoring patients with heart failure, hypertension, or impaired renal function.1,2 The mechanism of action of Xywav in the treatment of narcolepsy is unknown; however, it is hypothesized that its therapeutic effects on cataplexy and EDS are mediated through GABAB actions during sleep at noradrenergic and dopaminergic neurons, as well as at thalamocortical neurons.1 The recommended dosage range for Xywav in adults is 6 g to 9 g per night orally.1 Oxybate- naïve adult patients receive an initial nightly dosage of 4.5 g divided into 2 doses.1 Pediatric patients are recommended to follow a calibrated starting dosage, titration regimen, and maximum total nightly dosage based on their body weight.1 For patients transitioning from sodium oxybate, Xywav is initiated at the same gram-for-gram dose and regimen as sodium oxybate with an option for additional titration to balance efficacy and tolerability as needed.1 The prescribing information of both Xywav and sodium oxybate note that some patients may achieve better responses with unequal doses at bedtime and 2.5 to 4 hours later.1,2 Xywav is a Schedule III controlled substance and has a Black Box Warning associated with CNS depression and Abuse and Misuse (see below).1 Xywav is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the Xywav and Xyrem REMS.1 The efficacy and safety of Xywav in patients with idiopathic hypersomnia is being evaluated by an ongoing phase 3 trial (Study 2). Continued on Next Page 2 M-US-XYW-2000006 Narcolepsy Overview Narcolepsy is a chronic neurologic disorder involving dysregulation of the sleep/wake cycle.4 This rare disorder affects both adults and children, with an estimated U.S. prevalence of 50 per 100,000 persons,5 including a pediatric prevalence of 9.97 per 100,000 persons.6 It is characterized by a pentad of symptoms: excessive daytime sleepiness (EDS), cataplexy (sudden transient loss of muscle tone), hypnogogic/hypnopompic hallucinations (hallucinations upon falling asleep/awakening), sleep paralysis, and disrupted nighttime sleep (DNS; associated with fragmented sleep resulting from awakenings/arousals and frequent sleep stage shifts).7 All patients diagnosed with narcolepsy experience EDS, 73%-81% experience DNS, 35%-69% experience sleep paralysis, 42%-77% experience sleep hallucinations, and the frequency of cataplexy is contingent of narcolepsy subtype.8-11 A subset of 10%-25% of individuals with narcolepsy will experience all 5 symptoms during the course of their illness.12 The International Classification of Sleep Disorders 3rd edition (ICSD-3) separates narcolepsy into two subtypes that reflect their clinical profiles and underlying pathophysiology. Narcolepsy type 1 (NT1) is marked by the presence of cataplexy or documented cerebrospinal fluid (CSF) hypocretin deficiency.8 Narcolepsy type 2 (NT2) is absent cataplexy, and CSF hypocretin levels, if documented, are above the threshold specified for NT1.8 In both cases, diagnosis must be corroborated by objective sleep tests, such as nocturnal polysomnography (PSG), multiple sleep latency test (MSLT), or an immunoreactivity assay (i.e. CSF hypocretin).8 Narcolepsy can have a profound impact on affected patients’ health-related quality of life (HRQoL), social functioning, productivity/performance, and personal safety. Patient’s HRQoL is impacted by persistent sleepiness, unpredictability of narcolepsy symptoms, and negative public perception of narcolepsy.13 Mean HRQoL scores on the 36-Item Short Form Health Survey Version 2 (SF-36v2) are substantially lower in patients with narcolepsy compared to matched non-narcolepsy controls in the U.S., and this is the case for both the physical and mental component scores,14 with similar trends among patients in other parts of the world.15 Patients with narcolepsy are also adversely impacted with regard to mental health and work impairment relative to matched controls.14 Additionally, patients with narcolepsy report 3 M-US-XYW-2000006 significantly more feelings of social rejection, financial insecurity, internalized shame and social isolation than those without narcolepsy.16 Clinical Burden Associated with Narcolepsy Studies have demonstrated a diagnosis of narcolepsy is associated with an increased prevalence of cardiovascular (CV), metabolic, and psychiatric comorbidities.17-21 Specifically, hypertension, obesity, diabetes, and dyslipidemia are generally more prevalent in patients with narcolepsy relative to matched, non-narcolepsy controls.17-21 Furthermore, standardized mortality ratios of the narcolepsy population for each year between 2008-2010 show an approximate 1.5 fold increase in all-cause mortality relative to non-narcolepsy patients (p< 0.001).22 The pathophysiology of narcolepsy may explain the higher prevalence rates of cardiometabolic conditions among narcolepsy patients. Hypocretin, an excitatory neuropeptide responsible for stabilizing sleep and wake regulation, participates in modulating several physiologic functions, including blood pressure (BP) regulation, appetite, energy expenditure, and insulin secretion.23- 27 Autoimmune destruction of hypocretin neurons in the hypothalamus and reduced CSF hypocretin signaling, core characteristics of NT1,8 may therefore be associated with significant dysregulating effects throughout the body. Although the pathophysiology underlying NT2 is less clear, moderate hypocretin neuronal loss or insufficient release of hypocretin may still be present.28-30 The destabilization of the sleep-wake cycle is also disruptive to the natural oscillations in nocturnal patterns of “BP dipping,”25 which is a phenomenon physiologically characterized by BP decreases of >10% to 20% at night.31 “Blunted” or “non-dipping BP” is classified as a decrease of ≤10% during nighttime sleep.31 This blunted BP is more common among narcolepsy patients with cataplexy regardless of baseline hypertension.32 Diminished BP dipping has been shown to carry an increased CV risk independent of hypertension and is one of the strongest predictors among ambulatory heart rate (HR) components for all-cause mortality.33-35 Impact of Sodium on Health In the general population, it has been well-established that excessive sodium consumption is associated with increased risk of hypertension and cardiovascular disease.3,37,39,55,56,69 Furthermore, high sodium intake over a long period of time has the potential to cause renal injury, which can lead to sodium-sensitive BP.45-48,70 The cyclical effect wherein kidney dysfunction can aggravate elevated BP, in turn can increase sodium sensitivity.48,70 Additionally, elevated BP may be on the causal pathway underlying the association between sodium consumption and stroke risk. Excess sodium intake is directly related to increased BP,39,40 and dose-response trials have shown that the BP response to sodium reduction is progressive and nonlinear.49
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