• Metabolism: Metabolism is limited (<10%). Most of the active compound is excreted renally (81%). A small proportion is glucuronidated, oxidated, N-formylated or conjugated to a hexose. Varenicline undergoes minimal metabolism with 92% excreted unchanged in the urine. Renal elimination of varenicline is primarily through glomerular filtration along with active tubular secretion possibly via the organic cation transporter, OCT2 (MSDS, A308). Route of Elimination: Varenicline undergoes minimal metabolism, with 92% excreted unchanged in the urine. Renal elimination of varenicline is primarily through glomerular filtration along with active tubular secretion possibly via the organic cation transporter, OCT2. Half Life: The elimination half-life of varenicline is approximately 24 hours
• Uses/Sources: For use as an aid in smoking cessation (A308).
• Health Effects: Some disorders may include anemia, lymphadenopathy, angina pectoris, arrhythmia, bradycardia, ventricular extrasystoles, myocardial infarction, palpitations, tachycardia, deafness, meniere's disease, dhyroid gland disorders, conjunctivitis, acquired night blindness, blindness transient, cataract subcapsular, gastric ulcer, intestinal obstruction, pancreatitis acute, chest pain, influenza like illness, edema, diabetes mellitus, facial palsy, mental impairment, multiple sclerosis, polyuria, and menstrual disorder.(A308).
• Symptoms: Nausea, sleep disturbance, constipation, flatulence, and vomiting.
• Treatment: In case of overdose, standard supportive measures should be instituted as required. (L1712)
• Route of Exposure: Ingestion (A308)

Varenicline is an alpha-4 beta-2 neuronal nicotinic acetylcholine receptor partial agonist. The drug shows high selectiviyty for this receptor subclass, relative to other nicotinic receptors (>500-fold alpha-3 beta-4, >3500-fold alpha-7, >20,000-fold alpha-1 beta gamma delta) or non-nicotinic receptors and transporters (>2000-fold). The drug competitively inhibits the ability of nicotine to bind to and activate the alpha-4 beta-2 receptor. The drug exerts mild agonistic activity at this site, though at a level much lower than nicotine; it is presumed that this activation eases withdrawal symptoms.