Each tablet contains 20 mg citalopram (as 24.98 mg citalopram hydrobromide).
The tablets can be divided into equal halves.
Excipients/Inactive Ingredients: Tablet core: Maize starch, Lactose monohydrate, Microcrystalline cellulose, Copovidone, Glycerol 85%, Croscarmellose sodium, Magnesium stearate.
Coating: Hypromellose 5, Macrogol 400, Titanium dioxide (E 171).
Pharmacotherapeutic group: antidepressants, selective serotonin reuptake inhibitor. ATC code: N 06 AB 04.
Pharmacology: Pharmacodynamics: Mechanism of action: Biochemical and behavioural studies have been shown that citalopram is a potent inhibitor of the serotonin (5-HT)-uptake. Tolerance to the inhibition of 5-HT-uptake is not induced by long-term treatment with citalopram.
Citalopram is a very Selective Serotonin Reuptake Inhibitor (SSRI) with no, or minimal, effect on noradrenaline (NA), dopamine (DA) and gamma aminobutyric acid (GABA) uptake.
In contrast to many tricyclic antidepressants and some of the newer SSRIs, citalopram has no or very low affinity for a series of receptors including 5-HT1A, 5-HT2, DA D1 and D2 receptors, α1-, α2-, β-adrenoceptors, histamine H1, muscarine cholinergic, benzodiazepine, and opioid receptors. A series of functional in vitro tests in isolated organs as well as functional in vivo tests have confirmed the lack of receptor affinity. This absence of effects on receptors could explain why citalopram produces fewer of the traditional side effects such as dry mouth, bladder and gut disturbance, blurred vision, somnolence, cardiotoxicity and orthostatic hypotension.
The main metabolites of citalopram are all SSRIs although their potency and selectivity ratios are lower than those of citalopram. However, the selectivity ratios of the metabolites are higher than those of many of the newer SSRIs. The metabolites do not contribute to the overall antidepressant effect.
Pharmacodynamic effects: Suppression of rapid eye movement (REM) sleep is considered a predictor of antidepressant activity. Like tricyclic antidepressants, other SSRIs and MAO inhibitors, citalopram suppresses REM-sleep and increases deep slow-wave sleep.
Although citalopram does not bind to opioid receptors, it potentiates the antinociceptive effect of commonly used opioid analgesics.
In humans, citalopram does not impair cognitive (intellectual function) and psychomotor performance and has no or minimal sedative properties, either alone or in combination with alcohol.
Citalopram did not reduce saliva flow in a single dose study in human volunteers and in none of the studies in healthy volunteers did citalopram have significant influence on cardiovascular parameters. Citalopram has no effect on the serum levels of growth hormone. Citalopram like other SSRIs may increase plasma prolactin, an effect secondary to the prolactin-stimulating role of serotonin and of no clinical importance.
In a double-blind, placebo-controlled ECG study in healthy subjects, the change from baseline to QTc (Fridericia-correction) was 7.5 (90% CI 5.9 - 9.1) ms at the 20 mg/day dose and 16.7 (90% CI 15.0 - 18.4) ms at the 60 mg/day dose (see Contraindications, Precautions, Interactions, Adverse Reactions, and Overdosage).
Pharmacokinetics: Absorption: Absorption is almost complete and independent of food intake (Tmax mean 3 hours). Oral bioavailability is about 80%.
Distribution: The apparent volume of distribution (Vd) is about 12-17 L/kg. The plasma protein binding is below 80% for citalopram and its main metabolites.
Biotransformation: Citalopram is metabolised to the active demethylcitalopram, didemethylcitalopram, citalopram-N-oxide and an inactive deaminated propionic acid derivative. All the active metabolites are also SSRIs, although weaker than the parent compound. Unchanged citalopram is the predominant compound in plasma. The concentrations of demethylcitalopram and didemethylcitalopram are usually 30-50% and 5-10% of the citalopram concentration, respectively. The biotransformation of citalopram to demethylcitalopram is mediated by CYP2C19 (approx. 38%), CYP3A4 (approx. 31%) and CYP2D6 (approx. 31%).
Elimination: The elimination half-life (T½β) is about 1½ days, and the systemic citalopram plasma clearance (Cls) is about 0.3-0.4 L/min, and oral plasma clearance (Cloral) is about 0.4 L/min.
Citalopram is excreted mainly via the liver (85%) and the remainder (15%) via the kidneys; 12-23% of the daily dose is excreted in urine as unchanged citalopram. Hepatic (residual) clearance is about 0.3 L/min and renal clearance about 0.05-0.08 L/min.
Linearity: The kinetics is linear. Steady sate plasma levels are achieved in 1-2 weeks. Average concentrations of 300 nmol/L (165-405 nmol/L) are achieved at a daily dose of 40 mg.
Elderly patients (>65 years): Longer half-lives (1.5-3.75 days) and decreased clearance values (0.08-0.3 L/min) due to a reduced rate of metabolism have been demonstrated in elderly patients. Steady state values were about twice as high in the elderly as in younger patients treated with the same dose.
Reduced hepatic function: Citalopram is eliminated more slowly in patients with reduced hepatic function. The half-life of citalopram is about twice as long and steady state citalopram concentrations at a given dose will be about twice as high as in patients with normal liver function.
Reduced renal function: Citalopram is eliminated more slowly in patients with mild to moderate reduction of renal function, without any major impact on the pharmacokinetics of citalopram. At present, no information is available for treatment of patients with severely reduced renal function (creatinine clearance <20 mL/min).
Polymorphism: In vivo investigations have shown that the metabolism of citalopram exhibits no clinically important polymorphism of the sparteine/debrisoquine oxidation (CYP2D6). For CYP2C19, as a precaution, an initial dose of 10 mg should be considered for known poor metabolisers (see Dosage & Administration and Precautions).
Pharmacokinetic / pharmacodynamic relationship: There is no clear relationship between citalopram plasma levels and therapeutic response or side effects.
The metabolites do not contribute to the overall antidepressant effect.
Toxicology: Preclinical safety data: Acute toxicity: Citalopram has low acute toxicity.
Chronic toxicity: In chronic toxicity studies, there were no findings of concern for the therapeutic use of citalopram.
Reproduction studies: Based on data from reproduction toxicity studies (segment I, II and III), there is no reason to have special concern for the use of citalopram in women of childbearing potential.
Citalopram appears in milk in low concentrations.
Embryotoxicity studies in rats with doses of 56 mg/kg/day, which cause maternal toxicity, showed bone anomalies in the region of the vertebral column and ribs. The maternal plasma level was then 2-3 times the therapeutic concentration in man. In rats, citalopram did not have any effect on fertility, pregnancy and postnatal development, but diminished the birth weight of the pups. Citalopram and its metabolites reach foetal concentrations, which are 10-15 times the maternal plasma level. Clinical experience of use in pregnant women and during lactation is limited.
Animal data have shown that citalopram induces a reduction of fertility index and pregnancy index, reduction in number in implantation and abnormal sperm at exposure well in excess of human exposure.
Mutagenic and carcinogenic potential: Citalopram has no mutagenic or carcinogenic potential.
Treatment of depression and prevention of relapse/recurrence.
Panic disorder with or without agoraphobia.
Obsessive-compulsive disorder (OCD).
Adults: Treating depression: Citalopram should be administered as a single oral dose of 20 mg daily. Dependent on individual patient response and severity of depression, the dose may be increased to a maximum of 40 mg daily.
Treating panic disorder: A single oral dose of 10 mg is recommended for the first week before increasing the dose to 20 mg daily. The dose may be further increased, up to a maximum of 40 mg daily, dependent on individual patient response.
Treating OCD: An initial dose of 20 mg daily is recommended. The dose can be increased in increments of 20 mg to 40 mg daily if necessary, based on clinical judgement.
Elderly patients (>65 years of age): In elderly patients, the dose may be increased to a maximum of 40 mg daily.
Children and adolescents (<18 years): Cipram should not be used in the treatment of children and adolescents under the age of 18 years (see Precautions).
Reduced renal function: Dosage adjustment is not necessary in patients with mild or moderate renal impairment. No information is available on treatment of patients with severely reduced renal function (creatinine clearance <20 mL/min).
Reduced hepatic function: Patients with reduced hepatic function should receive dosages of no more than 30 mg/day.
Poor metabolisers of CYP2C19: An initial dose of 10 mg daily during the first two weeks of treatment is recommended for patients who are known to be poor metabolisers with respect to CYP2C19. The dose may be increased to a maximum of 20 mg daily depending on individual patient response (see Pharmacology: Pharmacokinetics under Actions).
Duration of treatment: The antidepressant effect usually sets in after 2 to 4 weeks. Treatment with antidepressants is symptomatic and must therefore be continued for an appropriate length of time, usually up to 6 months after recovery in order to prevent relapse.
The onset of action in treating OCD is 2-4 weeks with further improvement over time.
When stopping therapy, the drug should be gradually withdrawn during a couple of weeks.
Method of administration: Citalopram tablets are administered as a single daily dose.
Citalopram tablets can be taken at any time of the day without regard to food intake.
Citalopram is given to patients at potential risk of suicide and some reports of attempted suicide have been received. Detail is often lacking regarding precise dose or combination with other drugs and/or alcohol.
Symptoms: Experience from cases considered to be due to citalopram alone showed the following pattern. At doses below 600 mg, mild symptoms of nausea, dizziness, tachycardia, tremor, drowsiness and somnolence may occur. At doses above 600 mg, convulsions may occur within few hours after ingestion. ECG changes may occur and rarely rhabdomyolysis. Very few fatalities have been reported.
Treatment: There is no specific antidote. Treatment is symptomatic and supportive. Gastric lavage should be carried out as soon as possible after oral ingestion. ECG monitoring is recommended when more than 600 mg have been ingested. Convulsions may be treated with diazepam.
An adult patient has survived intoxication with 5,200 mg citalopram.
ECG monitoring is advisable in cases of overdose in patients with congestive heart failure/bradyarrhythmias, in patients using concomitant medications that prolong the QT interval, or in patients with altered metabolism e.g. liver impairment.
Hypersensitivity to citalopram or to any of the excipients.
Citalopram is contraindicated in patients with known QT interval prolongation or congenital long QT syndrome.
MAOIs (monoamine oxidase inhibitors): Cases of serious and sometimes fatal reactions have been reported in patients receiving an SSRI in combination with a monoamine oxidase inhibitor (MAOI), including the selective MAO-B inhibitor selegiline and the reversible MAOI (RIMA) moclobemide, and in patients who have recently discontinued an SSRI and have been started on a MAOI.
Some cases presented with features resembling serotonin syndrome.
Citalopram must not be used in combination with a MAOI, including selegiline, in doses above 10 mg daily.
Treatment with citalopram may be instituted 14 days after discontinuation of non-selective MAOIs and minimum one day after discontinuation of moclobemide. Treatment with MAOIs may be introduced 7 days after discontinuation of citalopram (see Interactions).
Paradoxical anxiety: Some patients with panic disorder may experience intensified anxiety symptoms at the start of treatment with antidepressants. This paradoxical reaction usually subsides within the first two weeks of starting treatment. A low starting dose is advised to reduce the likelihood of a paradoxical anxiogenic effect (see Dosage & Administration).
Hyponatraemia: Hyponatraemia, probably due to inappropriate antidiuretic hormone secretion (SIADH), has been reported as a rare adverse reaction with the use of SSRIs. Especially elderly female patients seem to be a risk group.
Suicide: The possibility of suicide attempt is inherent in depression and may persist until significant improvement occurs, either spontaneously or following treatment.
Patients being treated with antidepressants should be monitored carefully, especially at the beginning of treatment, for clinical worsening and/or the emergence of suicidality (suicidal ideation and behaviour).
This precaution should also be observed when treating other psychiatric disorders because of the possibility of co-morbidity with major depressive disorder.
Mania: In patients with manic-depressive illness, a change towards the manic phase may occur. Should the patient enter a manic phase, citalopram should be discontinued.
Seizures: Although animal experiments have shown that citalopram has no epileptogenic potential, it should, like other antidepressants, be used with caution in patients with a history of seizures.
Diabetes: As described for other psychotropics, citalopram may modify insulin and glucose responses calling for adjustment of the antidiabetic therapy in diabetic patients; in addition, the depressive illness itself may affect patients' glucose balance.
Serotonin syndrome: Rarely, the occurrence of "serotonin syndrome" has been reported in patients receiving SSRIs. A combination of symptoms, possibly including agitation, confusion, tremor, myoclonus and hyperthermia, may indicate the development of this condition.
Haemorrhage: There have been reports of cutaneous bleeding abnormalities, such as ecchymoses and purpura, with SSRIs. Caution is advised in patients taking SSRIs, particularly with concomitant use of oral anticoagulants; drugs known to affect platelet function (e.g. atypical antipsychotics and phenothiazines, most tricyclic antidepressants, acetylsalicylic acid and non-steroidal anti-inflammatory drugs (NSAIDs), ticlopidine and dipyridamole) as well as in patients with a history of bleeding disorders (see Interactions).
QT interval prolongation: Citalopram has been found to cause a dose-dependent prolongation of the QT interval. Cases of QT interval prolongation and ventricular arrhythmia including torsade de pointes have been reported during the post-marketing period, predominantly in patients of the female gender, with hypokalaemia, or with pre-existing QT prolongation or other cardiac diseases. Dose escalations over 20 mg/day in CYP2C19 poor metabolisers or patients taking concomitant cimetidine or another CYP2C19 inhibitor are not recommended (see Contraindications, Interactions, Adverse Reactions, Overdosage, and Pharmacology: Pharmacodynamics under Actions).
Caution is advised in patients with significant bradycardia or in patients with recent acute myocardial infarction or uncompensated heart failure.
Electrolyte disturbances, such as hypokalaemia and hypomagnesaemia, increase the risk for malignant arrhythmias and should be corrected before treatment with citalopram is started. Caution is advised in treating patients with diseases or conditions that causes hypokalaemia or hypomagnesaemia.
If patients with stable cardiac diseases are treated, an ECG review should be considered before treatment is started.
If signs of cardiac arrhythmia occur during treatment with citalopram, the treatment should be withdrawn and an ECG should be performed.
Clinical experience with citalopram in patients with certain concomitant systemic illnesses is limited.
Withdrawal symptoms: After prolonged administration, abrupt cessation of SSRIs may produce withdrawal symptoms such as dizziness, paraesthesia, tremor, anxiety, nausea and palpitation in some patients. It is recommended that withdrawal of treatment should proceed by tapering off the dosage over one to two weeks to avoid occurrence of discontinuation symptoms. These symptoms are not indicative of addiction.
Angle-closure glaucoma: SSRIs including citalopram may have an effect on pupil size resulting in mydriasis. This mydriatic effect has the potential to narrow the eye angle resulting in increased intraocular pressure and angle-closure glaucoma, especially in patients pre-disposed. Citalopram should therefore be used with caution in patients with angle-closure glaucoma or history of glaucoma.
Excipients: The tablets contain lactose monohydrate. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not receive this medicine.
Treatment of patients with reduced kidney and liver function: See Dosage & Administration.
Effects on ability to drive and use machines: Citalopram does not impair intellectual function and psychomotor performance. However, patients who are prescribed psychotropic medication may be expected to have some impairment of general attention and concentration and should be cautioned about their ability to drive a car and operate machinery.
Use in the Elderly: See Dosage & Administration.
Use in Children: Antidepressants should not be used in the treatment of children and adolescents under the age of 18 years. Suicide-related behaviours (suicide attempt and suicidal thoughts) and hostility (predominately aggression, oppositional behaviour and anger) were more frequently observed in clinical trials among children and adolescents treated with antidepressants compared to those treated with placebo. If, based on clinical need, a decision to treat is nevertheless taken, the patient should be carefully monitored for the appearance of suicidal symptoms.
Pregnancy: Published data on pregnant women (more than 2500 exposed outcomes) indicate no malformative feto/neonatal toxicity. However, citalopram should not be used during pregnancy unless clearly necessary and only after careful consideration of risk/benefit.
Based on data from reproduction toxicity studies (segment I, II and III), there is no reason to have special concern for the use of citalopram in women of childbearing potential.
Using SSRIs in the third trimester may result in effects, including neurobehavioral disturbances, in the newborn infant.
The following effects were reported in neonates with SSRIs administered to pregnant women until date of birth: irritability, tremor, hypertonia, increased muscle tone, constant crying, difficulty in suckling or in sleeping. They may either indicate serotonergic effects or withdrawal syndrome. If used during pregnancy, SSRIs should never be stopped abruptly.
Infants exposed to SSRIs in late pregnancy may have an increased risk for persistent pulmonary hypertension of the newborn (PPHN). PPHN occurs in 1-2 per 1000 live births in the general population and is associated with substantial neonatal morbidity and mortality. In a retrospective case-control study of 377 women whose infants were born with PPHN and 836 women whose infants were born healthy, the risk for developing PPHN was approximately six-fold higher for infants exposed to SSRIs after the 20th week of gestation compared to infants who has not been exposed to antidepressants during pregnancy. There is currently no corroborative evidence regarding the risk for PPHN following exposure to SSRIs in pregnancy; this is the first study that has investigated the potential risk. The study did not include enough cases with exposure to individual SSRIs to determine if all SSRIs posed similar levels of PPHN risk.
When treating a pregnant woman with Cipram during the third trimester, the physician should carefully consider both the potential risks and benefits of treatment.
Lactation: Citalopram is excreted into breast milk. It is estimated that the suckling infant will receive about 5% of the weight-related maternal daily dose (in mg/kg). No or only minor events have been observed in the infants. However, the existing information is insufficient for assessment of the risk to the child. Caution is recommended.
Fertility: Animal data have shown that citalopram may affect sperm quality (see Pharmacology: Toxicology: Preclinical safety data under Actions). Human case reports with some SSRIs have shown that an effect on sperm quality is reversible. Impact on human fertility has not been observed so far.
Adverse effects observed with citalopram are in general mild and transient. They are most frequent during the first one or two weeks of treatment and usually attenuate subsequently. The adverse reactions are presented at the MedDRA Preferred Term Level.
Clinical trials: The most commonly observed adverse reactions associated with the use of citalopram (N=1346) in double-blind, placebo-controlled trials and not seen at an equal incidence among placebo-treated patients (N=545) were: Sweating increased, dry mouth, agitation, appetite decreased, impotence, libido decreased, somnolence, yawning, nausea, ejaculation disorder, ejaculation failure, and abnormal orgasm (female). The incidence of each in excess over placebo is low (<10%). For the following reactions, a dose-response was discovered: Sweating increased, dry mouth, insomnia, somnolence, diarrhea, nausea, and fatigue.
The table shows the percentage of adverse drug reactions associated with citalopram seen in ≥1% of patients in double-blind placebo-controlled trials. (See table.)
Click on icon to see table/diagram/image
In comparative double-blind clinical trials with tri- and tetracyclic antidepressants (TTCAs), the incidence of 10 adverse reactions was statistically significantly higher on TTCAs (N=389) (dry mouth, sweating increased, constipation, tremor, dizziness, somnolence, accommodation abnormal, postural hypotension, palpitation, dysgeusia) compared to citalopram (N=682). For two reactions (nausea, ejaculation disorder), the incidence was statistically significantly higher on citalopram compared to TTCAs.
In the comparative trials versus other SSRIs, no statistically significant differences between the groups were found.
Post-marketing reports: In addition to the adverse drug reactions seen in the clinical trials, the following have been observed during post-marketing surveillance.
Very rare (<1/10,000): Hyponatraemia, inappropriate ADH secretion (both in especially elderly women), hypersensitivity NOS, convulsions NOS, grand mal convulsion, serotonin syndrome, drug withdrawal syndrome (dizziness (exc. vertigo), nausea and paraesthesia NEC), ecchymosis, purpura NOS, extrapyramidal disorder NEC.
Bone fractures: Epidemiological studies, mainly conducted in patients 50 years of age and older, show an increased risk of bone fractures in patients receiving SSRIs and TCAs. The mechanism leading to this risk is unknown.
QT interval prolongation: Cases of QT prolongation and ventricular arrhythmia including torsade de pointes have been reported during post-marketing period, predominantly in patients of female gender, with hypokalaemia or with pre-existing QT interval prolongation or other cardiac diseases (see Contraindications, Precautions, Interactions, Overdosage, and Pharmacology: Pharmacodynamics under Actions).
Citalopram is neither the source nor the cause of clinically important drug-drug interactions.
Pharmacodynamic interactions: At the pharmacodynamics level, there have only been few documented cases of serotonin syndrome with citalopram and moclobemide and buspirone.
Contraindicated combinations: MAOIs (non-selective as well as selective A (moclobemide)): Risk of "serotonin syndrome" (see Contraindications).
Combinations requiring precaution for use: Selegiline (selective MAO-B inhibitor): A pharmacokinetic / pharmacodynamic interaction study with concomitantly administered citalopram (20 mg daily) and selegiline (10 mg daily) (a selective MAO-B inhibitor) demonstrated no clinically relevant interactions. Patients tolerated the selegiline-citalopram combination well. The concomitant use of citalopram and selegiline (in doses above 10 mg daily) is contraindicated (see Contraindications).
Serotonergic drugs: Co-administration with serotonergic drugs (e.g. tramadol, sumatriptan) may lead to enhancement of 5-HT-associated effects.
Dynamic interactions between SSRIs and herbal remedy St. John's wort (Hypericum perforatum) can occur, resulting in an increase in undesirable effects.
Lithium and tryptophan: No pharmacodynamic interactions have been found in clinical studies in which citalopram has been given concomitantly with lithium. However, there have been reports of enhanced effects when SSRIs have been given with lithium or tryptophan and therefore the concomitant use of citalopram with these drugs should be undertaken with caution.
Haemorrhage: There have been reports of cutaneous bleeding abnormalities, such as ecchymoses and purpura, with SSRIs. Caution is advised in patients taking SSRIs, particularly with concomitant use of oral anticoagulants; drugs known to affect platelet function (e.g. atypical antipsychotics and phenothiazines, most tricyclic antidepressants, acetylsalicylic acid and non-steroidal anti-inflammatory drugs (NSAIDs), ticlopidine and dipyridamole) as well as in patients with a history of bleeding disorders (see Precautions).
ECT (electroconvulsive therapy): There are no clinical studies establishing the risks or benefits of the combined use of electroconvulsive therapy (ECT) and citalopram.
Alcohol: The combination of SSRIs and alcohol is not advisable. However, clinical studies have revealed no adverse pharmacodynamic interactions between citalopram and alcohol.
Linezolid: Serotonergic psychiatric drug should not be started in a patient receiving linezolid. Wait until 24 hours after the last dose of linezolid before starting the serotonergic psychiatric drugs.
QT interval prolongation: Pharmacokinetic and pharmacodynamic studies between citalopram and other medicinal products that prolong the QT interval have not been performed. An additive effect of citalopram and these medicinal products cannot be excluded. Therefore, co-administration of citalopram with medicinal products that prolong the QT interval, such as Class IA and III antiarrhythmics, antipsychotics (e.g. phenothiazine derivatives, pimozide, haloperidol), tricyclic antidepressants, certain antimicrobial agents (e.g. sparfloxacin, moxifloxacin, erythromycin IV, pentamidine, anti-malarial treatment particularly halofantrine), certain antihistamines (astemizole, mizolastine) etc., should only be prescribed after careful consideration.
Pharmacokinetic interactions: Biotransformation of citalopram to demethylcitalopram is mediated by CYP2C19 (approx. 38%), CYP3A4 (approx. 31%) and CYP2D6 (approx. 31%) isozymes of the cytochrome P450 system. The fact that citalopram is metabolised by more than one CYP means that inhibition of its biotransformation is less likely and co-administration of citalopram with other drugs in clinical practice has very low likelihood of producing pharmacokinetic drug interactions (see Dosage & Administration and Precautions).
Influence of other medicinal products on the pharmacokinetics of citalopram: Co-administration with ketoconazole (potent CYP3A4 inhibitor) did not change the pharmacokinetics of citalopram.
A pharmacokinetic interaction study of lithium and citalopram did not reveal any pharmacokinetic interactions.
Cimetidine (potent CYP2D6, 3A4 and 1A2 inhibitor) caused a moderate increase in the average steady state levels of citalopram. Caution is advised when administering citalopram in combination with cimetidine. Dose adjustment may be warranted (see Dosage & Administration and Precautions).
Effects of citalopram on other medicinal products: A pharmacokinetic / pharmacodynamic interaction study with concomitant administration of citalopram and metoprolol (a CYP2D6 substrate) showed a two-fold increase in metoprolol concentrations, but no statistically significant increase in the effect of metoprolol on blood pressure and heart rate in healthy volunteers.
Citalopram and demethylcitalopram are negligible inhibitors of CYP2C9, CYP2E1 and CYP3A4, and only weak inhibitors of CYP1A2, CYP2C19 and CYP2D6 as compared to other SSRIs established as significant inhibitors.
Thus, no change in pharmacokinetics or only very small changes of no clinical importance were observed when citalopram was given with CYP1A2 substrates (clozapine and theophylline), CYP2C9 (warfarin), CYP2C19 (imipramine and mephenytoin), CYP2D6 (sparteine, imipramine, amitriptyline, risperidone) and CYP4A4 (warfarin, carbamazepine and triazolam).
In a pharmacokinetic interaction study, citalopram did not cause any changes in the pharmacokinetics of digoxin meaning that citalopram neither induces nor inhibits P-glycoprotein.
Special precautions of container: Any unused product or waste material should be disposed of in accordance with local requirements.
Dispensing: On prescription only.
Incompatibilities: Not applicable.
Do not store above 25°C.
Shelf life: 5 years.
N06AB04 - citalopram ; Belongs to the class of selective serotonin reuptake inhibitors. Used in the management of depression.
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