Relationship between plasma exposure of zolpidem and CYP2D6 genotype in healthy Korean subjects

Jung, Eui Hyun; Lee, Choong-Min; Byeon, J.Y.; Shin, Hyo-Bin; Oh, Kyung-Yul; Cho, Chang‐Keun; Lim, Chang Woo; Jang, Choon‐Gon; Lee, Seok‐Yong; Lee, Yun Jeong

doi:10.1007/s12272-020-01250-1

Cited by 11 publications

(1 citation statement)

References 31 publications

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“…In another study, participants received zolpidem and clarithromycin, a CYP3A4 inhibitor, in order to eliminate the contribution of CYP3A4 to zolpidem metabolism. However, no differences in zolpidem plasma concentrations were found when subjects were divided according to CYP2D6 genotype [312]. Similarly, a lack of association between CYP2C9 genotype and zolpidem metabolism was also reported [313] Pharmacogenomic research resulted in various findings contributing to the improvement in establishing the anxiety treatment and predicting its outcome (Table 5).…”

Section: Pharmacogenomics Of Non-cognitive Symptoms: Anxiolytic Hypno...mentioning

confidence: 92%

Pharmacogenomics of Dementia: Personalizing the Treatment of Cognitive and Neuropsychiatric Symptoms

Vuic,

Milos,

Tudor

et al. 2023

Genes

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Dementia is a syndrome of global and progressive deterioration of cognitive skills, especially memory, learning, abstract thinking, and orientation, usually affecting the elderly. The most common forms are Alzheimer’s disease, vascular dementia, and other (frontotemporal, Lewy body disease) dementias. The etiology of these multifactorial disorders involves complex interactions of various environmental and (epi)genetic factors and requires multiple forms of pharmacological intervention, including anti-dementia drugs for cognitive impairment, antidepressants, antipsychotics, anxiolytics and sedatives for behavioral and psychological symptoms of dementia, and other drugs for comorbid disorders. The pharmacotherapy of dementia patients has been characterized by a significant interindividual variability in drug response and the development of adverse drug effects. The therapeutic response to currently available drugs is partially effective in only some individuals, with side effects, drug interactions, intolerance, and non-compliance occurring in the majority of dementia patients. Therefore, understanding the genetic basis of a patient’s response to pharmacotherapy might help clinicians select the most effective treatment for dementia while minimizing the likelihood of adverse reactions and drug interactions. Recent advances in pharmacogenomics may contribute to the individualization and optimization of dementia pharmacotherapy by increasing its efficacy and safety via a prediction of clinical outcomes. Thus, it can significantly improve the quality of life in dementia patients.

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Section: Pharmacogenomics Of Non-cognitive Symptoms: Anxiolytic Hypno...mentioning

confidence: 92%

Pharmacogenomics of Dementia: Personalizing the Treatment of Cognitive and Neuropsychiatric Symptoms

Vuic,

Milos,

Tudor

et al. 2023

Genes

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show abstract

Physiologically based pharmacokinetic (PBPK) modeling for prediction of celecoxib pharmacokinetics according to CYP2C9 genetic polymorphism

et al. 2021

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Physiologically based pharmacokinetic (PBPK) modelling of tamsulosin related to CYP2D6*10 allele

et al. 2021

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Relationship between plasma exposure of zolpidem and CYP2D6 genotype in healthy Korean subjects

Cited by 11 publications

References 31 publications

Pharmacogenomics of Dementia: Personalizing the Treatment of Cognitive and Neuropsychiatric Symptoms

Pharmacogenomics of Dementia: Personalizing the Treatment of Cognitive and Neuropsychiatric Symptoms

Physiologically based pharmacokinetic (PBPK) modeling for prediction of celecoxib pharmacokinetics according to CYP2C9 genetic polymorphism

Physiologically based pharmacokinetic (PBPK) modelling of tamsulosin related to CYP2D6*10 allele

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