An antidepressant primarily used to treat depression.

Its full effect may take more than four weeks to occur, with some benefit possibly as early as one to two weeks.

Trade name Remeron.

Often it is used in depression complicated by anxiety or trouble sleeping.

Oral agent.

Pregnancy category US: C (Risk not ruled out)

Bioavailability 50%.

Protein binding 85%.

Hepatic metabolism-CYP1A2, CYP2D6, CYP3A4

Metabolite desmethylmirtazapine contributes 3–10% of activity.

Elimination half-life 20–40 hours.

Excretion Urine: 75% and Feces: 15%

Common side effects include: weight gain, sleepiness, and dizziness.

Serious side effects may include an increased suicide among children, mania resulting in the diagnosis of bipolar disorder, and low white blood count.

Withdrawal symptoms may occur with stopping.

Should not be used together with an MAO inhibitor.

Unclear if use during pregnancy is safe.

Mechanism of action may involve blocking certain adrenergic and serotonin receptors.

A tetracyclic antidepressant, and also has strong antihistamine effects.

Primary use is the treatment of major depressive disorder and other mood disorders.

Onset of action appears faster than some SSRIs and similar to tricyclic antidepressants.

Sometimes prescribed for treatment of:

Generalized anxiety disorder.

Social anxiety disorder.

Obsessive–compulsive disorder.

Panic disorder.

Post-traumatic stress disorder.

Low appetite/underweight.


Nausea and vomiting


Headaches and migraine

It is equally effective as other antidepressants. No difference between mirtazapine and other antidepressants on any efficacy measure.

There is strong evidence that patients taking mirtazapine are less likely to leave treatment early because of side effects.

It appears to have a faster onset in people for whom it works, at about 2 weeks.

Its effectiveness is about the same as other antidepressants at 6 weeks.

In many people with sleep disorders caused by depression, it reduces the time it takes to fall asleep and increases the quality of sleep.

However, in some people it can disturb sleep, especially at higher doses.

It causes restless leg syndrome in 8 to 28% of people and in rare cases causes REM sleep behavior disorder.

An analysis of 21 antidepressants found them to be fairly similar overall.

It has an earlier onset of action compared to SSRIs.

It is more likely to cause weight gain and sleepiness than other antidepressants.

It is less likely to cause tremor than tricyclic antidepressants, and less likely to cause nausea and sexual dysfunction than SSRIs.

Very common adverse effects of greater than 10% include constipation, dry mouth, sleepiness, increased appetite and weight gain.

Common adverse effects include weakness, confusion, dizziness, peripheral edema, and elevated transaminases, elevated serum triglycerides, and elevated total cholesterol.

It can paradoxically exacerbate depression or anxiety or cause suicidal ideation, especially for people under the age of 25.

Discontinuation may cause a discontinuation syndrome upon cessation, and a gradual and slow reduction in dose is recommended to minimize discontinuation symptoms.

Sudden cessation of treatment may include: depression, anxiety, tinnitus, panic attacks, vertigo, restlessness, irritability, decreased appetite, insomnia, diarrhea, nausea, vomiting, flu-like symptoms such as allergies and pruritus, headaches and sometimes hypomania or mania.

Considered to be relatively safe in the event of an overdose, although slightly more toxic in overdose than most of the SSRIs.

Has no significant cardiovascular adverse effects.

An overdose with as much as 30 to 50 times the standard dose is relatively nontoxic, compared to tricyclic antidepressants.

Rare reported fatalities have been attributed to overdose, with a fatal toxicity index 3.1 deaths per million prescriptions, similar to that observed with SSRIs.

Concurrent use with inhibitors or inducers of the cytochrome (CYP) P450 isoenzymes CYP1A2, CYP2D6, and/or CYP3A4 can result in altered concentrations of the drug, as these are the main enzymes responsible for its metabolism.

Fluoxetine and paroxetine, inhibitors of these enzymes, are known to modestly increase mirtazapine levels, while carbamazepine, an inducer, considerably decreases them.

Liver impairment decreases the oral clearance of mirtazapine by about 30%;

Renal impairment decreases clearance by 50%.

It should not be utilized with monoamine oxidase inhibitors.

Can be used in combination with an SSRI, SNRI, or TCA as an adjunctive strategy.

The serotonin syndrome has been induced by the combination of mirtazapine with other agents olanzapine, quetiapine, tramadol and venlafaxine.

It has antihistamine, α2-blocker, and antiserotonergic activity.

It does not inhibit the reuptake of serotonin, norepinephrine, or dopamine, nor does it inhibit monoamine oxidase.

Has as weak or no activity as an anticholinergic or blocker of sodium or calcium channels, in contrast to most tricyclic antidepressants.

It has better tolerability and low toxicity in overdose than tricyclic antidepressants.

Mirtazapine increases dopamine release in the prefrontal cortex.

Its antagonism of 5-HT2A receptors has beneficial effects on anxiety, sleep and appetite, as well as sexual function.

Lowers drug seeking behaviour in various studies.

It shares antagonism of the 5-HT3 receptor, and significantly improves pre-existing symptoms of nausea, vomiting, diarrhea, and irritable bowel syndrome in afflicted individuals.

May be used as an inexpensive antiemetic alternative to ondansetron.

Mirtazapine is a tetracyclic antidepressant with 5-HT2 antagonist effects and only very modest 5-HT3 antagonist effects that also possesses strong anti-emetic properties, however it is also very sedating. 

Mirtazapine is as equally effective in treating chemotherapy-related nausea and vomiting as standard treatments; it is also cheaper and has fewer side effects than typical anti-emetics, and its antidepressant qualities may be an added benefit for cancer patientd..

Inhibition of the 5-HT3 receptors has also shown to improve anxiety and to be effective in the treatment of drug addiction, including methamphetamines.

The SSRIs, SNRIs, MAOIs, and some TCAs increase the general activity of the 5-HT2A, 5-HT2C, and 5-HT3 receptors leading to a host of negative changes and side effects, the most prominent of which including anorexia, insomnia, sexual dysfunction, nausea, and diarrhea, it is often combined with these drugs to reduce their side-effect profile and to produce a stronger antidepressant effect.

Does not have serotonergic activity and does not cause serotonergic side effects or serotonin syndrome.

It is a very strong H1 receptor inverse agonist and, as a result, it can cause powerful sedative and hypnotic effects.

A single 15 mg dose of mirtazapine to healthy volunteers has been found to result in over 80% occupancy of the H1 receptor and to induce intense sleepiness.

After a short period of chronic treatment, the antihistamine effects become more tolerable as the H1 receptor tends to desensitize.

H1 receptor blockade may improve pre-existing allergies, pruritus, nausea, and insomnia in patients.

Has only low affinity for the muscarinic acetylcholine receptors, although anticholinergic side effects like dry mouth, constipation, and mydriasis are still sometimes seen.

Oral bioavailability about 50%.

About 85% bound to plasma proteins.

Metabolized primarily in the liver by demethylation and hydroxylation via cytochrome P450 enzymes.

The overall elimination half-life is 20–40 hours.

About 15% is eliminated in feces and 75% in urine.

Dose 15 mg tablet.

Leave a Reply

Your email address will not be published. Required fields are marked *