Effect of severe renal impairment on pharmacokinetics, safety, and tolerability of lemborexant

The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects w...

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Published inPharmacology research & perspectives Vol. 9; no. 2; pp. e00734 - n/a
Main Authors Landry, Ishani, Aluri, Jagadeesh, Hall, Nancy, Filippov, Gleb, Dayal, Satish, Moline, Margaret, Reyderman, Larisa
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.04.2021
John Wiley and Sons Inc
Wiley
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ISSN2052-1707
2052-1707
DOI10.1002/prp2.734

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Abstract The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15–29 ml/min/1.73 m2; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10‐mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (Cmax) was similar, whereas area under the plasma concentration–time curve from zero to time of last quantifiable concentration (AUC(0‐t)) and AUC from zero to infinity (AUC(0‐inf)) were about 1.5‐fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4–142.0), 150.5 (113.2–200.3), and 149.8 (113.1–198.6) for Cmax, AUC(0‐t), and AUC(0‐inf), respectively. In both groups, the median lemborexant time to Cmax (tmax) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, Cmax was reduced ~20% and exposure (AUC(0‐t) and AUC(0‐inf)) was ~1.4‐ to 1.5‐fold higher in subjects with SRI versus healthy subjects; tmax was delayed ~1.5–2 h for M4 and M10. All treatment‐emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment. Lemborexant is a dual orexin receptor antagonist approved for the treatment of adults with insomnia. Lemborexant tmax and Cmax were not altered in subjects with severe renal impairment compared with healthy subjects, but exposure (AUC) was increased approximately 1.5‐fold. Lemborexant has a favorable safety profile and dosing is initiated at 5 mg, which can be increased based on efficacy and tolerability. Thus, these results support the use of lemborexant in subjects with mild to severe renal impairment without dosing adjustment.
AbstractList The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15–29 ml/min/1.73 m2; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10‐mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (Cmax) was similar, whereas area under the plasma concentration–time curve from zero to time of last quantifiable concentration (AUC(0‐t)) and AUC from zero to infinity (AUC(0‐inf)) were about 1.5‐fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4–142.0), 150.5 (113.2–200.3), and 149.8 (113.1–198.6) for Cmax, AUC(0‐t), and AUC(0‐inf), respectively. In both groups, the median lemborexant time to Cmax (tmax) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, Cmax was reduced ~20% and exposure (AUC(0‐t) and AUC(0‐inf)) was ~1.4‐ to 1.5‐fold higher in subjects with SRI versus healthy subjects; tmax was delayed ~1.5–2 h for M4 and M10. All treatment‐emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment.
The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15–29 ml/min/1.73 m2; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10‐mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (Cmax) was similar, whereas area under the plasma concentration–time curve from zero to time of last quantifiable concentration (AUC(0‐t)) and AUC from zero to infinity (AUC(0‐inf)) were about 1.5‐fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4–142.0), 150.5 (113.2–200.3), and 149.8 (113.1–198.6) for Cmax, AUC(0‐t), and AUC(0‐inf), respectively. In both groups, the median lemborexant time to Cmax (tmax) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, Cmax was reduced ~20% and exposure (AUC(0‐t) and AUC(0‐inf)) was ~1.4‐ to 1.5‐fold higher in subjects with SRI versus healthy subjects; tmax was delayed ~1.5–2 h for M4 and M10. All treatment‐emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment. Lemborexant is a dual orexin receptor antagonist approved for the treatment of adults with insomnia. Lemborexant tmax and Cmax were not altered in subjects with severe renal impairment compared with healthy subjects, but exposure (AUC) was increased approximately 1.5‐fold. Lemborexant has a favorable safety profile and dosing is initiated at 5 mg, which can be increased based on efficacy and tolerability. Thus, these results support the use of lemborexant in subjects with mild to severe renal impairment without dosing adjustment.
The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15–29 ml/min/1.73 m 2 ; n  = 8) compared with demographically matched healthy subjects with normal renal function ( n  = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10‐mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration ( C max ) was similar, whereas area under the plasma concentration–time curve from zero to time of last quantifiable concentration (AUC (0‐ t ) ) and AUC from zero to infinity (AUC (0‐inf) ) were about 1.5‐fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4–142.0), 150.5 (113.2–200.3), and 149.8 (113.1–198.6) for C max , AUC (0‐ t ) , and AUC (0‐inf) , respectively. In both groups, the median lemborexant time to C max ( t max ) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, C max was reduced ~20% and exposure (AUC (0‐ t ) and AUC (0‐inf) ) was ~1.4‐ to 1.5‐fold higher in subjects with SRI versus healthy subjects; t max was delayed ~1.5–2 h for M4 and M10. All treatment‐emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment.
The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15–29 ml/min/1.73 m2; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10‐mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (C max) was similar, whereas area under the plasma concentration–time curve from zero to time of last quantifiable concentration (AUC(0‐ t )) and AUC from zero to infinity (AUC(0‐inf)) were about 1.5‐fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4–142.0), 150.5 (113.2–200.3), and 149.8 (113.1–198.6) for C max, AUC(0‐ t ), and AUC(0‐inf), respectively. In both groups, the median lemborexant time to C max (t max) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, C max was reduced ~20% and exposure (AUC(0‐ t ) and AUC(0‐inf)) was ~1.4‐ to 1.5‐fold higher in subjects with SRI versus healthy subjects; t max was delayed ~1.5–2 h for M4 and M10. All treatment‐emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment. Lemborexant is a dual orexin receptor antagonist approved for the treatment of adults with insomnia. Lemborexant t max and C max were not altered in subjects with severe renal impairment compared with healthy subjects, but exposure (AUC) was increased approximately 1.5‐fold. Lemborexant has a favorable safety profile and dosing is initiated at 5 mg, which can be increased based on efficacy and tolerability. Thus, these results support the use of lemborexant in subjects with mild to severe renal impairment without dosing adjustment.
The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single-dose, open-label, parallel-group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15-29 ml/min/1.73 m ; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10-mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (C ) was similar, whereas area under the plasma concentration-time curve from zero to time of last quantifiable concentration (AUC ) and AUC from zero to infinity (AUC ) were about 1.5-fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4-142.0), 150.5 (113.2-200.3), and 149.8 (113.1-198.6) for C , AUC , and AUC , respectively. In both groups, the median lemborexant time to C (t ) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, C was reduced ~20% and exposure (AUC and AUC ) was ~1.4- to 1.5-fold higher in subjects with SRI versus healthy subjects; t was delayed ~1.5-2 h for M4 and M10. All treatment-emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment.
The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single-dose, open-label, parallel-group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15-29 ml/min/1.73 m2 ; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10-mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (Cmax ) was similar, whereas area under the plasma concentration-time curve from zero to time of last quantifiable concentration (AUC(0-t) ) and AUC from zero to infinity (AUC(0-inf) ) were about 1.5-fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4-142.0), 150.5 (113.2-200.3), and 149.8 (113.1-198.6) for Cmax , AUC(0-t) , and AUC(0-inf) , respectively. In both groups, the median lemborexant time to Cmax (tmax ) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, Cmax was reduced ~20% and exposure (AUC(0-t) and AUC(0-inf) ) was ~1.4- to 1.5-fold higher in subjects with SRI versus healthy subjects; tmax was delayed ~1.5-2 h for M4 and M10. All treatment-emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment.The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single-dose, open-label, parallel-group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15-29 ml/min/1.73 m2 ; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10-mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (Cmax ) was similar, whereas area under the plasma concentration-time curve from zero to time of last quantifiable concentration (AUC(0-t) ) and AUC from zero to infinity (AUC(0-inf) ) were about 1.5-fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4-142.0), 150.5 (113.2-200.3), and 149.8 (113.1-198.6) for Cmax , AUC(0-t) , and AUC(0-inf) , respectively. In both groups, the median lemborexant time to Cmax (tmax ) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, Cmax was reduced ~20% and exposure (AUC(0-t) and AUC(0-inf) ) was ~1.4- to 1.5-fold higher in subjects with SRI versus healthy subjects; tmax was delayed ~1.5-2 h for M4 and M10. All treatment-emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment.
Abstract The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor antagonist indicated for the treatment of insomnia. A phase 1 multicenter, single‐dose, open‐label, parallel‐group study was conducted in subjects with SRI not requiring dialysis (estimated glomerular filtration rate 15–29 ml/min/1.73 m2; n = 8) compared with demographically matched healthy subjects with normal renal function (n = 8). Plasma levels of lemborexant and its metabolites were measured over 240 h following a single oral 10‐mg dose administered in the morning. Relative to subjects with normal renal function, lemborexant maximum plasma concentration (Cmax) was similar, whereas area under the plasma concentration–time curve from zero to time of last quantifiable concentration (AUC(0‐t)) and AUC from zero to infinity (AUC(0‐inf)) were about 1.5‐fold higher in subjects with SRI. The geometric mean ratios (90% confidence interval) were 104.8 (77.4–142.0), 150.5 (113.2–200.3), and 149.8 (113.1–198.6) for Cmax, AUC(0‐t), and AUC(0‐inf), respectively. In both groups, the median lemborexant time to Cmax (tmax) was 1 h, and the mean unbound fraction of lemborexant was ~7%. For the M4, M9, and M10 metabolites, Cmax was reduced ~20% and exposure (AUC(0‐t) and AUC(0‐inf)) was ~1.4‐ to 1.5‐fold higher in subjects with SRI versus healthy subjects; tmax was delayed ~1.5–2 h for M4 and M10. All treatment‐emergent adverse events were mild or moderate. Lemborexant pharmacokinetics were not sufficiently altered to warrant a dose adjustment for subjects with renal impairment.
Author Dayal, Satish
Filippov, Gleb
Landry, Ishani
Reyderman, Larisa
Moline, Margaret
Hall, Nancy
Aluri, Jagadeesh
AuthorAffiliation 1 Eisai Inc. Woodcliff Lake NJ USA
2 Eisai Ltd. Hatfield United Kingdom
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CitedBy_id crossref_primary_10_1016_j_sleepx_2023_100070
crossref_primary_10_7759_cureus_71049
crossref_primary_10_1177_02698811221080459
crossref_primary_10_1007_s11920_022_01357_w
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Issue 2
Keywords chronic kidney disease
phase 1
drug safety
pharmacokinetics
clinical pharmacology
lemborexant
renal impairment
Language English
License Attribution-NonCommercial-NoDerivs
2021 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics.
This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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Notes Funding information
This study was financially supported by Eisai Inc., Woodcliff Lake, New Jersey, USA. Eisai Inc. is the owner and manufacturer of lemborexant. The investigators retained full independence in the conduct of this research.
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Snippet The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin receptor...
Abstract The primary aim of this study was to examine the effect of severe renal impairment (SRI) on the pharmacokinetics of lemborexant, a dual orexin...
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SubjectTerms Adolescent
Adult
Aged
Area Under Curve
Body mass index
Chromatography
chronic kidney disease
clinical pharmacology
Drug dosages
drug safety
Female
Glomerular Filtration Rate - physiology
Glycoproteins
Half-Life
Humans
Insomnia
lemborexant
Male
Metabolism
Metabolites
Middle Aged
Orexin Receptor Antagonists - administration & dosage
Orexin Receptor Antagonists - adverse effects
Orexin Receptor Antagonists - pharmacokinetics
Original
Pharmacokinetics
Pharmacology
phase 1
Plasma
Proteins
Pyridines - administration & dosage
Pyridines - adverse effects
Pyridines - pharmacokinetics
Pyrimidines - administration & dosage
Pyrimidines - adverse effects
Pyrimidines - pharmacokinetics
Renal Elimination - physiology
renal impairment
Renal Insufficiency - diagnosis
Renal Insufficiency - metabolism
Renal Insufficiency - physiopathology
Severity of Illness Index
Sleep
Sleep Initiation and Maintenance Disorders - drug therapy
Urine
Young Adult
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Title Effect of severe renal impairment on pharmacokinetics, safety, and tolerability of lemborexant
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