Smoking cessation pharmacogenetics: analysis of varenicline and bupropion in placebo-controlled clinical trials.
paper
Cited
Public
- Authors
- King, David P; Paciga, Sara; Pickering, Eve; Benowitz, Neal L; Bierut, Laura J; Conti, David V; Kaprio, Jaakko; Lerman, Caryn; Park, Peter W
- Year
- 2012
- Journal
- Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
- PMID
- 22048466
- DOI
- 10.1038/npp.2011.232
- PMCID
- PMC3260990
Despite effective therapies for smoking cessation, most smokers find quitting difficult and most successful quitters relapse. Considerable evidence supports a genetic risk for nicotine dependence; however, less is known about the pharmacogenetics of smoking cessation. In the first pharmacogenetic investigation of the efficacy of varenicline and bupropion, we examined whether genes important in the pharmacodynamics and pharmacokinetics of these drugs and nicotine predict medication efficacy and adverse events. Subjects participated in randomized, double-blind, placebo-controlled smoking cessation clinical trials, comparing varenicline, a nicotinic acetylcholine receptor (nAChR) partial agonist, with bupropion, a norepinephrine/dopamine reuptake inhibitor, and placebo. Primary analysis included 1175 smokers of European ancestry, and 785 single nucleotide polymorphisms from 24 genes, representing 254 linkage disequilibrium (LD) bins (genes included nAChR subunits, additional varenicline-specific genes, and genes involved in nicotine or bupropion metabolism). For varenicline, continuous abstinence (weeks 9-12) was associated with multiple nAChR subunit genes (including CHRNB2, CHRNA5, and CHRNA4) (OR=1.76; 95% CI: 1.23-2.52) (p<0.005); for bupropion, abstinence was associated with CYP2B6 (OR=1.78; 95% CI: 1.27-2.50) (p<0.001). Incidence of nausea was associated with several nAChR subunit genes (OR=0.50; 95% CI: 0.36-0.70) (p<0.0001) and time to relapse after quitting was associated with HTR3B (HR=1.97; 95% CI: 1.45-2.68) (p<0.0001). These data provide evidence for multiple genetic loci contributing to smoking cessation and therapeutic response. Different loci are associated with varenicline vs bupropion response, suggesting that additional research may identify clinically useful markers to guide treatment decisions.
Genetic markers most significantly associated with continuous abstinence: (a) varenicline, (b) bupropion.
LLM interpretation
This figure consists of two sets of bar charts (a and b) showing the "Percent Quitting" across three treatment groups (Varenicline, Bupropion, and Placebo) based on the number of copies of a minor allele (0, 1, or 2). In panel (a) for *rs7164594*, a positive trend in quitting percentage is visible as the number of minor alleles increases specifically in the Varenicline group. Panel (b) for *rs8109525* compares quitting rates at two time intervals (Weeks 9β12 in dark grey and Weeks 9β52 in light grey), showing a general increase in quitting percentages with more minor alleles in the Bupropion and Varenicline groups.
Time to relapse among those who had successfully quit at weeks 9β12, all groups combined: (a) rs11606194, (b) rs3758987.
LLM interpretation
This figure consists of two Kaplan-Meier survival curves (a and b) showing the proportion of participants surviving (remaining relapse-free) over 50 weeks for two different genetic variants of *HTR3B* (rs11606194 and rs3758987). The x-axis represents "Time to Relapse (weeks)" and the y-axis represents "Proportion Surviving." In both plots, participants with zero copies of the minor allele (dashed line) show a higher proportion of survival compared to those with one (grey line) or two (black line) copies of the minor allele.
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