<p><strong>Pharmacodynamics</strong>: The mechanism of action of Mirtazapine as with other drugs effective in the treatment of major depressive disorder is unknown. Evidence gathered in preclinical studies suggests that Mirtazapine enhances central noradrenergic and serotonergic activity. These studies have shown that Mirtazapine acts as an antagonist at central presynaptic &alpha;2-adrenergic inhibitory autoreceptors and heteroreceptors, an action that is postulated to result in an increase in central noradrenergic and serotonergic activity. Mirtazapine is a potent antagonist of 5- HT2&nbsp;and 5-HT3&nbsp;receptors. Mirtazapine has no significant affinity for the 5-HT1A&nbsp;and 5-HT1B&nbsp;receptors. Mirtazapine is a potent antagonist of histamine (H1) receptors, a property that may explain its prominent sedative effects. Mirtazapine is a moderate peripheral &alpha;1-adrenergic antagonist, a property that may explain the occasional orthostatic hypotension reported in association with its use. Mirtazapine is a moderate antagonist at muscarinic receptors, a property that may explain the relatively low incidence of anticholinergic side effects associated with its use.<br />
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<strong>Pharmacokinetics</strong>: After oral administration of Mirtazapine tablets, the active constituent mirtazapine is rapidly and well-absorbed, reaching peak plasma levels after about 2 hours. Binding of mirtazapine to plasma proteins is approximately 85%. The mean half-life of elimination is 20-40 hours; (26 hours in males, 37 hours in females). The half-life of elimination is sufficient to justify once-a-day dosing. Mirtazapine displays linear pharmacokinetics within the recommended dose range. Mirtazapine is extensively metabolized and eliminated via the urine and faeces four days. Major pathways of biotransformation are demethylation and oxidation followed by conjugation.</p>