Pharmacogenetic Optimization of Smoking Cessation Treatment

Chenoweth, Meghan J.; Tyndale, Rachel F.

doi:10.1016/j.tips.2016.09.006

Cited by 39 publications

(47 citation statements)

References 79 publications

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“…CYP2B6*6 has been associated with reduced metabolism of bupropion, a pro-drug which is activated by CYP2B6. The effect of CYP2B6*6 allele on the efficacy of bupropion on smoking cessation has been shown in some, but not all, studies (Chenoweth & Tyndale, 2017;Lee, Jepson, Hoffmann, Epstein, Hawk, Lerman et al, 2007;Zhu, Cox, Nollen, Faseru, Okuyemi, Ahluwalia et al, 2012)). Pharmacokinetics of several other CYP2B6 substrates, such as cyclophosphamide, methadone and nevirapine have been reported to be influenced by CYP2B6…”

Section: Cyp2b6mentioning

confidence: 95%

Cytochrome P450 in Pharmacogenetics: An Update

Tornio

Backman

2018

Advances in Pharmacology

130

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Interindividual variability in drug disposition is a major cause of lack of efficacy and adverse effects of drug therapies. The majority of hepatically cleared drugs are metabolized by cytochrome P450 (CYP) enzymes, mainly in families CYP1, CYP2, and CYP3. Genes encoding these enzymes are highly variable with allele distribution showing considerable differences between populations. Genetic variability of especially CYP2C9, CYP2C19, CYP2D6, and CYP3A5 is known to have clear clinical impact on drugs that are metabolized by these enzymes. CYP1A2, CYP2A6, CYP2B6, CYP2C8, and CYP3A4 all show variability that affects pharmacokinetics of drugs as well, but so far the evidence regarding their clinical implications is not as conclusive. In this review, we provide an up-to-date summary of the pharmacogenetics of the major human drug-metabolizing CYP enzymes, focusing on clinically significant examples.

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Section: Cyp2b6mentioning

confidence: 95%

Cytochrome P450 in Pharmacogenetics: An Update

Tornio

Backman

2018

Advances in Pharmacology

130

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“…The decreased activity or loss of function variants, CYP2A6*2 , *4 , *5 , *7 , *9 , *10 , *12 , *17 and *35 and several others, all reduce the rate of nicotine metabolism, compared to the reference allele ( Figure 5 ) [ 69 , 73 ]. Moreover, CYP2A6 genotype and the NMR have been associated with the efficacy of nicotine replacement therapy [ 74 , 75 , 76 ] and, following the success of a recent randomized clinical trial [ 77 ], have been proposed as biomarkers to guide drug selection for smoking cessation pharmacotherapy [ 78 ].…”

Section: Resultsmentioning

confidence: 99%

P450 Pharmacogenetics in Indigenous North American Populations

Henderson

Claw

Woodahl

et al. 2018

JPM

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Indigenous North American populations, including American Indian and Alaska Native peoples in the United States, the First Nations, Métis and Inuit peoples in Canada and Amerindians in Mexico, are historically under-represented in biomedical research, including genomic research on drug disposition and response. Without adequate representation in pharmacogenetic studies establishing genotype-phenotype relationships, Indigenous populations may not benefit fully from new innovations in precision medicine testing to tailor and improve the safety and efficacy of drug treatment, resulting in health care disparities. The purpose of this review is to summarize and evaluate what is currently known about cytochrome P450 genetic variation in Indigenous populations in North America and to highlight the importance of including these groups in future pharmacogenetic studies for implementation of personalized drug therapy.

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“…Smoking cessation is perhaps the most important therapy to limit the progression of COPD [59]. There has been extensive pharmacogenomics research related to smoking cessation, which has been reviewed elsewhere [60][61][62].…”

Section: Genome-wide Association Studies In Copd Pharmacogenomicsmentioning

confidence: 99%

Pharmacogenomics of chronic obstructive pulmonary disease

Hersh

2019

Expert Review of Respiratory Medicine

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Introduction: Chronic obstructive pulmonary disease (COPD) is a heterogeneous condition, which presents the opportunity for precision therapy based on genetics or other biomarkers. Areas covered: Alpha-1 antitrypsin deficiency, a genetic form of emphysema, provides an example of this precision approach to diagnosis and therapy. To date, research in COPD pharmacogenomics has been limited by small sample sizes, lack of accessible target tissue, failure to consider COPD subtypes, and different outcomes relevant for various medications. There have been several published genome-wide association studies and other omics studies in COPD pharmacogenomics; however, clinical implementation remains far away. There is a growing evidence base for precision prescription of inhaled corticosteroids in COPD, based on clinical phenotypes and blood biomarkers, but not yet based on pharmacogenomics. Expert opinion: At this time, there is insufficient evidence for clinical implementation of COPD pharmacogenomics. Additional genome-wide studies will be required to discover predictors of drug response and to identify genomic biomarkers of COPD subtypes, which could be targeted with subtype-directed therapies.

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Pharmacogenetic Optimization of Smoking Cessation Treatment

Cited by 39 publications

References 79 publications

Cytochrome P450 in Pharmacogenetics: An Update

Cytochrome P450 in Pharmacogenetics: An Update

P450 Pharmacogenetics in Indigenous North American Populations

Pharmacogenomics of chronic obstructive pulmonary disease

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