Pharmacotherapeutic group: drugs used in nicotine dependence, ATC code: N07BA04
Desmoxan facilitates a gradual reduction in nicotine dependence by alleviating withdrawal symptoms.
The active substance of Desmoxan is cytisine, a plant alkaloid (found, among other sources, in the seeds of the laburnum shrub, genus Laburnum) with a chemical structure similar to that of nicotine. It acts on nicotinic acetylcholine receptors. The action of cytisine resembles that of nicotine but is generally weaker. Cytisine competes with nicotine for the same receptors and, owing to its stronger binding affinity, gradually displaces nicotine. It has a lower capacity to stimulate nicotinic receptors, particularly the α4β2 subtype (of which it is a partial agonist), and crosses into the central nervous system to a lesser extent than nicotine. Within the central nervous system, cytisine is thought to act on the mechanism underlying nicotine dependence and neurotransmitter release. It prevents the full, nicotine-dependent activation of the mesolimbic dopamine system and modestly increases brain dopamine levels, thereby mitigating the central symptoms associated with nicotine withdrawal. In the peripheral nervous system, cytisine stimulates and subsequently modulates the autonomic ganglia, producing reflex stimulation of respiration and catecholamine secretion from the adrenal medulla, raising blood pressure, and preventing the peripheral symptoms associated with nicotine withdrawal.
⚠️ Warnings
Desmoxan should only be used by individuals with a serious intention to overcome nicotine dependence. Patients must be aware that concurrent use of the medicinal product with smoking or other nicotine-containing products may exacerbate the adverse effects of nicotine.
Desmoxan should be used with caution in patients with ischaemic heart disease, heart failure, hypertension, phaeochromocytoma, atherosclerosis and other peripheral vascular diseases, gastric and duodenal ulcer, gastro-oesophageal reflux disease, hyperthyroidism, diabetes, and schizophrenia.
Effect of smoking cessation: Polycyclic aromatic hydrocarbons in tobacco smoke induce the metabolism of medicinal products metabolised by CYP1A2 (and possibly CYP1A1). When a smoker stops smoking, this may result in slower metabolism and a consequent rise in the plasma concentrations of such drugs. This is of potential clinical relevance for medicinal products with a narrow therapeutic window, such as theophylline, tacrine, clozapine, and ropinirole.
Plasma concentrations of other medicinal products partially metabolised by CYP1A2, e.g. imipramine, olanzapine, clomipramine, and fluvoxamine, may also increase on smoking cessation, although confirmatory data are lacking and the possible clinical significance of this effect on these drugs is unknown. Limited data suggest that the metabolism of flecainide and pentazocine may likewise be induced by smoking.
Depressed mood, rarely including suicidal ideation and suicide attempts, may be a symptom of nicotine withdrawal. Prescribers must be alert to the possibility of serious neuropsychiatric symptoms in patients attempting to quit smoking, whether with or without pharmacological treatment.
A history of psychiatric disorders during smoking cessation, with or without pharmacotherapy, has been associated with the exacerbation of underlying psychiatric illness (e.g. depression).
Caution is required in patients with a history of psychiatric illness, who should be counselled accordingly.
Women of childbearing potential
Women of childbearing potential must use highly effective contraception during treatment with Desmoxan (see sections 4.5 and 4.6).
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Verified by medical editor
Dr. Ozarchuk, PharmD · April 2026
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