Tianeptine sodium salt is a salt of Tianeptine. Tianeptine, a tricyclic compound, is a selective facilitator of 5-HT (serotonin; sc-201146) uptake in vitro and in vivo. Additionally, Tianeptine is reported to act as a selective inhibitor of dopamine uptake . Tianeptine does not have a noted effect on monoamine uptake. In a study utilizing purified synaptosomes from rat brain, Tianeptine was reported to enhance serotonin uptake in selective brain regions. Purified synaptosomes were obtained from rats and incubated with tritium-labeled 5-HT and Tianeptine in vitro . The synaptosomes were then analyzed for uptake and release of 5-HT via a liquid scintillation.

Tianeptine is a drug used for treating major depressive episodes (mild, moderate, or severe). It has structural similarities to the tricyclic antidepressants, but it has different pharmacological properties. Tianeptine is a selective serotonin reuptake enhancer (SSRE), opposite to the action of SSRIs. One review points to the cancellative effects of tianeptine and fluoxetine coadministration on serotonin reuptake. Another suggests that long-term administration of tianeptine has no effect on serotonin pathways. Tianeptine enhances the extracellular concentration of dopamine in the nucleus accumbens and modulates the D2 and D3 dopamine receptors. There is also action on the NMDA and AMPA receptors. Recent reviews point to this pathway as a hypothesized mechanism of action, based on tianeptine's effect of reversing impaired neuroplasticity associated with stress.

Tianeptine reduces the effects of serotonin in the limbic system and the pre-frontal cortex, giving rise to a mood elevation, unlike the mood blunting associated with SSRIs. Like SSRIs, however, tianeptine's onset-of-action delay is approximately 2-6 weeks with improvements sometimes noticeable in as soon as one week. Its short-lived, but pleasant, stimulant effect experienced by some patients is shared with its predecessor, amineptine, whose side effects related to dopamine reuptake inhibition resulted in Servier's research into tianeptine. Suggested dosage is two or three times daily, due to its short duration of action.

Tianeptine has strong antidepressant and anxiolytic properties with a relative lack of sedative, anticholinergic and cardiovascular adverse effects, thus suggesting it is particularly suitable for use in elderly patients and in those following alcohol withdrawal; such patients can be more sensitive to the adverse effects of psychotropic drugs. Recent interesting results indicate anticonvulsant and analgesic activity of tianeptine and its possible interaction with adenosine A1 receptors.

Some indication of tianeptine's potential range of application can be gleaned from its various patents. Thus patent US6599896 proposes "…use of tianeptine in the production of medicaments to treat neurodegenerative pathologies…cerebral ischaemia, cerebral traumatism, cerebral aging, Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, demyelating pathologies, encephalopathies, chronic fatigue syndrome, myalgic encephalomyelitis post-viral fatigue syndrome, the state of fatigue following a bacterial or viral infection, and the dementia syndrome of AIDS". A prospective, double-blind, randomised, placebo-controlled trial of tianeptine for fibromyalgia is currently under way in Spain. Regular tianeptine use may even be good for one's teeth, though it's unlikely to become a staple of orthodox dentistry. Despite this cornucopia of possibilities, tianeptine is not well known in Anglo-American psychiatry or among the English-speaking lay public.

Tianeptine is neuroprotective via multiple neurochemical and cellular mechanisms. In theory, tianeptine's neuroprotective action makes it a potential life-extension drug. When an organism is under stress, or perceives itself under stress, the hypothalamus secretes corticotropin-releasing hormone/factor (CRH/CRF). CRH/CRF in turn increases secretion of adrenocorticotrophic hormone (ACTH) from the anterior pituitary. ACTH in turn stimulates the release of glucocorticoids from the adrenal cortex. Persistent, uncontrolled physical and psychosocial stress causes excess cortisol secretion from the adrenal glands. Excess cortisol causes dendritic shrinkage in the hippocampus and a contrasting growth of dendrites in the lateral amygdala. These stress-induced changes tend to lower mood; they can cause clinical depression in the genetically vulnerable. Current evidence suggests that tianeptine acts to prevent and even reverse stress-induced neural damage, promoting both neuronal survival and synaptic plasticity.

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