TIANEPTINE was introduced to the market as an antidepressant drug. This drug enhances the uptake of serotonin (5-HT) by serotonergic axons. Clearing of 5-HT from the synaptic cleft interferes with central serotonergic activity. At the peripheral level, tianeptine enhances the uptake of plasma free serotonin (f-5HT) by platelets.

Studies have shown the levels of f-5HT in plasma are increased in symptomatic patients with asthma. In addition, the concentration of f-5HT in symptomatic asthmatic patients correlates positively with clinical status and negatively with pulmonary function (FEV1) (Figure). Tianeptine provoked a dramatic and sudden decrease of both clinical rating and f-5HT plasma levels and an increase in pulmonary function (Figure). (References: Lechin et al., Ann Allergy Asthma & Immunol 1996, 77:245-253; Lechin et al., Clin Pharmacol Ther 1998,64:223-232; Lechin et al., J Clin Pharmacol 1998, 38:918-925).

Although adrenal catecholamines (adrenaline and noradrenaline) were found to be raised in symptomatic asthmatic patients, no correlations were found between these neurotransmitters when plotted against clinical rating and pulmonary function (FEV1). However, raised levels of plasma adrenaline are able to trigger platelet aggregation which in turn are responsible for the increase of plasma f-5HT. The pathophysiologic mechanisms involved in the etiopathogenic role displayed by f-5HT on asthma attacks include the release of acetylcholine by parasympathetic nerves as well as mast cell degranulation. Serotonin released at central medullary level provokes exciting of both respiratory and vagal nuclei.