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QuickView for Citalopram (compound)

Summary
General Info

PubChem

PubChem Compound 10832572

Name:	Citalopram
PubChem Compound ID:	10832572
Description:	A furancarbonitrile that is one of the SEROTONIN UPTAKE INHIBITORS used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from tardive dyskinesia in preference to tricyclic antidepressants, which aggravate this condition.
Molecular formula:	C₁₇H₁₈BrNO₃
Molecular weight:	364.234 g/mol

DrugBank

Identification

Name:	Citalopram
Name (isomeric):	DB00215
Drug Type:	small molecule
Description:	A furancarbonitrile that is one of the SEROTONIN UPTAKE INHIBITORS used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from tardive dyskinesia in preference to tricyclic antidepressants, which aggravate this condition.
Synonyms:	Citalopramum [INN-Latin]; Citalopram Hydrobromide
Brand:	Celius, Talam, Zentius, Talohexal, Citabax, Celexa, Dalsan, Citol, Zetalo, Humorup, Citalec, Cipram, Cilift, Cimal, Citrol, Seropram, Ciprapine, Citox, Elopram, Oropram, Nitalapram, Recital, Celapram, Cipramil, Akarin, Ciazil, Citopam, Pramcit, Vodelax, Temperax
Category:	Antidepressants, Antidepressive Agents, Second-Generation, Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin Uptake Inhibitors
CAS number:	59729-33-8

Pharmacology

Indication:	For the treatment of depression. Unlabeled indications include: treatment of mild dementia-associated agitation in nonpsychotic patients, smoking cessation, ethanol abuse, obsessive-compulsive disorder (OCD) in children, and diabetic neuropathy.
Pharmacology:	Citalopram is one of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). It is used to treat the depression associated with mood disorders. It is also used on occassion in the treatment of body dysmorphic disorder and anxiety. The antidepressant, antiobsessive-compulsive, and antibulimic actions of citalopram are pr... show more » Citalopram is one of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). It is used to treat the depression associated with mood disorders. It is also used on occassion in the treatment of body dysmorphic disorder and anxiety. The antidepressant, antiobsessive-compulsive, and antibulimic actions of citalopram are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. In vitro studies show that citalopram is a potent and selective inhibitor of neuronal serotonin reuptake and has only very weak effects on norepinephrine and dopamine neuronal reuptake. Citalopram has no significant affinity for adrenergic (α₁, α₂, β), cholinergic, GABA, dopaminergic, histaminergic, serotonergic (5HT_1A, 5HT_1B, 5HT₂), or benzodiazepine receptors; antagonism of such receptors has been hypothesized to be associated with various anticholinergic, sedative, and cardiovascular effects for other psychotropic drugs. The chronic administration of citalopram was found to downregulate brain norepinephrine receptors, as has been observed with other drugs effective in the treatment of major depressive disorder. Citalopram does not inhibit monoamine oxidase. show less «
Mechanism of Action:	The antidepressant, antiobsessive-compulsive, and antibulimic actions of citalopram are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. Citalopram blocks the reuptake of serotonin at the serotonin reuptake pump of the neuronal membrane, enhancing the actions of serotonin on 5HT_1A autoreceptors. SSRIs bind wit... show more » The antidepressant, antiobsessive-compulsive, and antibulimic actions of citalopram are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. Citalopram blocks the reuptake of serotonin at the serotonin reuptake pump of the neuronal membrane, enhancing the actions of serotonin on 5HT_1A autoreceptors. SSRIs bind with significantly less affinity to histamine, acetylcholine, and norepinephrine receptors than tricyclic antidepressant drugs. show less «
Absorption:	Rapidly and well absorbed from the GI tract. Peak plasma concentrations occur within 4 hours of a single orally administered dose. Bioavailability is 80% following oral administration. Food does not affect absorption.
Protein binding:	80% based on in vitro studies.
Biotransformation:	Citalopram is metabolized mainly in the liver via N-demethylation to its principle metabolite, demethylcitalopram. Other metabolites include didemethylcitalopram, citalopram N-oxide, and a deaminated propionic acid derivative. Cytochrome P450 (CYP) 3A4 and 2C19 isozymes appear to be principally involved in producing demethylcitalopram. Demethylcitalopram appears to be further N-demethylated by CYP2D6 to didemethylcitalopram. Citalopram metabolites possess little pharmacologic activity in comparison to their parent compound and do not likely contribute to the clinical effect of the drug.
Route of elimination:	The systemic clearance of citalopram was 330 mL/min, with approximately 20% of that due to renal clearance. Citalopram is metabolized to demethylcitalopram (DCT), didemethylcitalopram (DDCT), citalopram-N-oxide, and a deaminated propionic acid derivative.
Half Life:	35 hours
Toxicity:	Symptoms most often accompanying citalopram overdose, alone or in combination with other drugs and/or alcohol, included dizziness, sweating, nausea, vomiting, tremor, somnolence, and sinus tachycardia. In more rare cases, observed symptoms included amnesia, confusion, coma, convulsions, hyperventilation, cyanosis, rhabdomyolysis, and ECG changes (including QTc prolongation, nodal rhythm, ventricular arrhythmia, and very rare cases of torsade de pointes). Acute renal failure has been very rarely reported accompanying overdose. Withdrawal symptoms include flu-like symptoms, insomnia, nausea, imbalance, sensory changes and hyperactivity.
Affected organisms:	Humans and other mammals

Interactions

Food interaction:

Avoid St.John's Wort.

Avoid alcohol.

Take without regard to meals.

Drug interaction:

Propranolol	The SSRI, citalopram, may increase the bradycardic effect of the beta-blocker, propranolol.
Tramadol	The use of two serotonin modulators, such as citalopram and tramadol, may increase the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy.
Telithromycin	Telithromycin may reduce clearance of Citalopram. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Citalopram if Telithromycin is initiated, discontinued or dose changed.
Phenelzine	Possible severe adverse reaction with this combination
Triprolidine	The CNS depressants, Triprolidine and Citalopram, may increase adverse/toxic effects due to additivity. Monitor for increased CNS depressant effects during concomitant therapy.

Propranolol	The SSRI, citalopram, may increase the bradycardic effect of the beta-blocker, propranolol.
Tramadol	The use of two serotonin modulators, such as citalopram and tramadol, may increase the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy.
Telithromycin	Telithromycin may reduce clearance of Citalopram. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Citalopram if Telithromycin is initiated, discontinued or dose changed.
Phenelzine	Possible severe adverse reaction with this combination
Triprolidine	The CNS depressants, Triprolidine and Citalopram, may increase adverse/toxic effects due to additivity. Monitor for increased CNS depressant effects during concomitant therapy.
Almotriptan	Increased risk of CNS adverse effects
Selegiline	Possible severe adverse reaction with this combination
Linezolid	Combination associated with possible serotoninergic syndrome
Trimipramine	The SSRI, Citalopram, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Citalopram is initiated, discontinued or dose changed.
Dicumarol	The SSRI, citalopram, increases the effect of anticoagulant, dicumarol.
Tranylcypromine	Increased risk of serotonin syndrome. Concomitant therapy should be avoided. A significant washout period, dependent on the half-lives of the agents, should be employed between therapies.
St. John's Wort	St. John's Wort increases the effect and toxicity of the SSRI, citalopram.
Venlafaxine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Isocarboxazid	Possible severe adverse reaction with this combination
Lumefantrine	Additive QTc-prolongation may occur. Concomitant therapy should be avoided.
Pimozide	The SSRI, citalopram, may increase the effect and toxicity of pimozide.
Ziprasidone	Additive QTc-prolongation may occur increasing the risk of life-threatening ventricular arrhythmias and torsade de pointes. Concomitant therapy should be avoided.
Troleandomycin	Possible serotoninergic syndrome with this combination
Zuclopenthixol	Additive QTc prolongation may occur. Consider alternate therapy or use caution and monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP).
Treprostinil	The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Citalopram. Monitor for increased bleeding during concomitant thearpy.
Tiaprofenic acid	Additive antiplatelet effects increase the risk of bleeding. Consider alternate therapy or monitor for increased bleeding.
Anisindione	The SSRI, citalopram, increases the effect of anticoagulant, anisindione.
Rasagiline	Possible severe adverse reaction with this combination
Tolmetin	Increased antiplatelet effects may enhance the risk of bleeding. Alternate therapy may be considered or monitor for inreased bleeding during concomitant therapy.
Carvedilol	The SSRI, citalopram, may increase the bradycardic effect of the beta-blocker, carvedilol.
Trazodone	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Naratriptan	Increased risk of CNS adverse effects
Voriconazole	Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of citalopram by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of citalopram if voriconazole is initiated, discontinued or dose changed.
Desvenlafaxine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Moclobemide	Possible serotoninergic syndrome
Metoprolol	The SSRI, citalopram, may increase the bradycardic effect of the beta-blocker, metoprolol.
Oxycodone	Increased risk of serotonin syndrome
Frovatriptan	Increased risk of CNS adverse effects
Warfarin	The SSRI, citalopram, increases the effect of anticoagulant, warfarin.
Ticlopidine	Ticlopidine may decrease the metabolism and clearance of Citalopram. Consider alternate therapy or monitor for adverse/toxic effects of Citalopram if Ticlopidine is initiated, discontinued or dose changed.
Erythromycin	Possible serotoninergic syndrome with this combination
Josamycin	Possible serotoninergic sydrome with this combination
Acenocoumarol	The SSRI, citalopram, increases the effect of anticoagulant, acenocoumarol.
Clarithromycin	Possible serotoninergic syndrome with this combination
Sibutramine	Risk of serotoninergic syndrome
Artemether	Additive QTc-prolongation may occur. Concomitant therapy should be avoided.
Eletriptan	Increased risk of CNS adverse effects
Sumatriptan	Increased risk of CNS adverse effects
Zolmitriptan	The use of two serotonin modulators, such as zolmitriptan and citalopram, may increase the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy.
Rizatriptan	Increased risk of CNS adverse effects
Ginkgo biloba	Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided.
Ketoprofen	Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy.
Clozapine	The antidepressant increases the effect of clozapine

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Targets

Sodium-dependent serotonin transporter

Terminates the action of serotonine by its high affinity sodium-dependent reuptake into presynaptic terminals

UniProt ID:

P31645

Gene:

SLC6A4

Actions:

inhibitor

References:

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Maines LW, Keck BJ, Smith JE, Lakoski JM: Corticosterone regulation of serotonin transporter and 5-HT1A receptor expression in the aging brain. Synapse. 1999 Apr;32(1):58-66.
View Article

Vicentic A, Battaglia G, Carroll FI, Kuhar MJ: Serotonin transporter production and degradation rates: studies with RTI-76. Brain Res. 1999 Sep 11;841(1-2):1-10.
View Article

Dugar A, Keck BJ, Maines LW, Miller S, Njai R, Lakoski JM: Compensatory responses in the aging hippocampal serotonergic system following neurodegenerative injury with 5,7-dihydroxytryptamine. Synapse. 2001 Feb;39(2):109-21.
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Dutta AK, Fei XS, Beardsley PM, Newman JL, Reith ME: Structure-activity relationship studies of 4-[2-(diphenylmethoxy)ethyl]-1-benzylpiperidine derivatives and their N-analogues: evaluation of O-and N-analogues and their binding to monoamine transporters. J Med Chem. 2001 Mar 15;44(6):937-48.
View Article

Plenge P, Wiborg O: High- and low-affinity binding of S-citalopram to the human serotonin transporter mutated at 20 putatively important amino acid positions. Neurosci Lett. 2005 Aug 5;383(3):203-8. Epub 2005 Apr 25.
View Article

Schloss P, Betz H: Heterogeneity of antidepressant binding sites on the recombinant rat serotonin transporter SERT1. Biochemistry. 1995 Oct 3;34(39):12590-5.
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Tatsumi M, Groshan K, Blakely RD, Richelson E: Pharmacological profile of antidepressants and related compounds at human monoamine transporters. Eur J Pharmacol. 1997 Dec 11;340(2-3):249-58.
View Article

Zhong H, Hansen KB, Boyle NJ, Han K, Muske G, Huang X, Egebjerg J, Sanchez C: An allosteric binding site at the human serotonin transporter mediates the inhibition of escitalopram by R-citalopram: kinetic binding studies with the ALI/VFL-SI/TT mutant. Neurosci Lett. 2009 Oct 25;462(3):207-12. Epub 2009 Jul 16.
View Article

Rasmussen TN, Plenge P, Bay T, Egebjerg J, Gether U: A single nucleotide polymorphism in the human serotonin transporter introduces a new site for N-linked glycosylation. Neuropharmacology. 2009 Sep;57(3):287-94. Epub 2009 Jun 3.
View Article

Enzymes

Transporters

Multidrug resistance protein 1