We investigated the efficacy of standard (8-week nicotine, 16-week placebo) vs extended (24-week nicotine) patch therapy for smoking cessation, and the effect of slow nicotine metabolism, indicated by CYP2A6 reduced metabolizer (RM) genotype or low 3-hydroxycotinine/cotinine ratio (3HC/COT), on abstinence. RM versus normal genotype predicted lower 3HC/COT. Extended vs standard treatment produced higher abstinence at 24 weeks (32% vs 20%), but not at 52 weeks (both 14%). Low 3HC/COT and RM genotype predicted higher abstinence on extended versus standard treatment at 24 (47% vs 25%, 38% vs 17%) and 28 weeks (34% vs 19%, 23% vs 11%), while high 3HC/COT or normal genotype did not. Within extended treatment, low versus high 3HC/COT predicted higher abstinence at 8 (48% vs 29%), 24 (47% vs 25%), and 28 weeks (34% vs 16%), with similar trends for the genotype effect. Overall, extending nicotine treatment increased abstinence during therapy, particularly for slow metabolizers.

We investigated the efficacy of standard (8-week nicotine, 16-week placebo) vs extended (24-week nicotine) patch therapy for smoking cessation, and the effect of slow nicotine metabolism, indicated by CYP2A6 reduced metabolizer (RM) genotype or low 3-hydroxycotinine/cotinine ratio (3HC/COT), on abstinence. RM versus normal genotype predicted lower 3HC/COT. Extended vs standard treatment produced higher abstinence at 24 weeks (32% vs 20%), but not at 52 weeks (both 14%). Low 3HC/COT and RM genotype predicted higher abstinence on extended versus standard treatment at 24 (47% vs 25%, 38% vs 17%) and 28 weeks (34% vs 19%, 23% vs 11%), while high 3HC/COT or normal genotype did not. Within extended treatment, low versus high 3HC/COT predicted higher abstinence at 8 (48% vs 29%), 24 (47% vs 25%), and 28 weeks (34% vs 16%), with similar trends for the genotype effect. Overall, extending nicotine treatment increased abstinence during therapy, particularly for slow metabolizers.