Abstract
A nicotine-degrading enzyme termed NicA2 was altered (NicA2-J1) through fusion of an albumin binding domain to increase its half-life. Examination of NicA2-J1 in vivo demonstrated a complete blockade of brain nicotine access, which in turn blunted nicotine's psychoactive effects. These data further support development of pharmacokinetic nicotine cessation therapeutics.