Pharmacogenetic Optimization of Smoking Cessation Treatment

被引:30
作者
Chenoweth, Meghan J. [1 ,2 ]
Tyndale, Rachel F. [1 ,2 ,3 ]
机构
[1] Ctr Addict & Mental Hlth, Campbell Family Mental Hlth Res Inst, Toronto, ON, Canada
[2] Univ Toronto, Dept Pharmacol & Toxicol, Toronto, ON, Canada
[3] Univ Toronto, Dept Psychiat, Toronto, ON, Canada
基金
美国国家卫生研究院; 加拿大健康研究院; 加拿大创新基金会;
关键词
NICOTINE METABOLITE RATIO; SUSTAINED-RELEASE BUPROPION; RECEPTOR PARTIAL AGONIST; TRANSDERMAL NICOTINE; GENETIC-VARIATION; IN-VIVO; CLINICAL-TRIAL; CYP2A6; VARENICLINE; THERAPY;
D O I
10.1016/j.tips.2016.09.006
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Worldwide, approximately one billion people smoke cigarettes. Cigarette smoking persists in part because long-term smoking cessation rates are modest on existing treatments. Smoking cessation outcomes are influenced by genetic factors, including genetic variation in enzymes that metabolize nicotine and smoking cessation medications, as well as in receptor targets for nicotine and treatment medications. For example, smokers with genetically slow nicotine metabolism have higher cessation success on behavioural counseling and nicotine patches compared with smokers with genetically fast nicotine metabolism. In this review, we highlight new progress in our understanding of how genetic variation in the pharmacological targets of nicotine and smoking cessation medications could be used to tailor smoking cessation therapy, increase quit rates, and reduce tobacco-related harm.
引用
收藏
页码:55 / 66
页数:12
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