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Identification
Name Duloxetine
Accession Number DB00476 (APRD00060)
Type small molecule
Groups approved
Description

Duloxetine (brand names Cymbalta, Yentreve, and in parts of Europe, Xeristar or Ariclaim) is a drug which primarily targets major depressive disorder (MDD), generalized anxiety disorder (GAD), pain related to diabetic peripheral neuropathy and in some countries stress urinary incontinence (SUI). It is manufactured and marketed by Eli Lilly and Company.

Duloxetine has not yet been FDA approved for stress urinary incontinence or for fibromyalgia.

Duloxetine is a selective SNRI (selective serotonin-norepinephrine reuptake inhibitor). Duloxetine is a systemic drug therapy which affects the body as a whole. Known also under the code name LY248686, it is a potent dual reuptake inhibitor of serotonin (5-hydroxytryptamine, 5-HT) and norepinephrine (NE), possessing comparable affinities in binding to NE- and 5-HT transporter sites. It is a less potent inhibitor of dopamine reuptake.
Structure Thumb
Download: MOL | SDF | SMILES | InChI
Display: 2D Structure | 3D Structure
Synonyms
Duloxetine HCl
Duloxetine Hydrochloride
Salts Not Available
Brand names
Name Company
Cymbalta
Yentreve
Brand mixtures Not Available
Categories
  • Dopamine Uptake Inhibitors
  • Adrenergic Uptake Inhibitors
  • Antidepressive Agents
  • Serotonin Uptake Inhibitors
CAS number 136434-34-9
Weight Average: 297.415
Monoisotopic: 297.118734925
Chemical Formula C18H19NOS
InChI Key InChIKey=ZEUITGRIYCTCEM-KRWDZBQOSA-N
InChI
InChI=1S/C18H19NOS/c1-19-12-11-17(18-10-5-13-21-18)20-16-9-4-7-14-6-2-3-8-15(14)16/h2-10,13,17,19H,11-12H2,1H3/t17-/m0/s1
Plain Text
IUPAC Name
methyl[(3S)-3-(naphthalen-1-yloxy)-3-(thiophen-2-yl)propyl]amine
SMILES
CNCC[C@H](OC1=CC=CC2=CC=CC=C12)C1=CC=CS1
Plain Text
Mass Spec Not Available
Taxonomy
Kingdom Organic
Classes
  • Naphthalenes
Substructures
  • Naphthalenes
  • Aliphatic and Aryl Amines
  • Phenols and Derivatives
  • Ethers
  • Benzene and Derivatives
  • Heterocyclic compounds
  • Aromatic compounds
  • Anisoles
  • Thiophenes
  • Phenyl Esters
Pharmacology
Indication For the acute and maintenance treatment of major depressive disorder (MDD), as well as acute management of generalized anxiety disorder. Also used for the management of neuropathic pain associated with diabetic peripheral neuropathy, and fibromyalgia. Has been used in the management of moderate to severe stress urinary incontinence (SUI) in women.
Pharmacodynamics Duloxetine is in a class of medications called selective serotonin and norepinephrine reuptake inhibitors (SSNRIs) and primarily targets major depressive disorders (MDD) and stress urinary incontinence (SUI). Duloxetine is also used to treat pain and tingling caused by diabetic neuropathy (damage to nerves that can develop in people who have diabetes). Known also as LY248686, it is a potent dual inhibitor of serotonin (5-hydroxytryptamine, 5-HT) and norepinephrine (NE) reuptake, possessing comparable affinities in binding to NE and 5-HT transport sites. Interestingly, its behavior contrasts to most other dual-reuptake inhibitors. Furthermore, duloxentine lacks affinity for monoamine receptors within the central nervous system.
Mechanism of action Duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake and a less potent inhibitor of dopamine reuptake. Duloxetine has no significant affinity for dopaminergic, adrenergic, cholinergic, histaminergic, opioid, glutamate, and GABA receptors. The antidepressant and pain inhibitory actions of duloxetine are believed to be related to its potentiation of serotonergic and noradrenergic activity in the CNS. The mechanism of action of duloxetine in SUI has not been determined, but is thought to be associated with the potentiation of serotonin and norepinephrine activity in the spinal cord, which increases urethral closure forces and thereby reduces involuntary urine loss.
Absorption Orally administered duloxetine hydrochloride is well absorbed.
Volume of distribution
  • 1640 L
Protein binding Protein binding is greater than 90%.
Metabolism The major biotransformation pathways for duloxetine involve oxidation of the naphthyl ring followed by conjugation and further oxidation. Both CYP2D6 and CYP1A2 catalyze the oxidation of the naphthyl ring in vitro. Metabolites found in plasma include 4-hydroxy duloxetine glucuronide and 5-hydroxy, 6-methoxy duloxetine sulfate. The major circulating metabolites have not been shown to contribute significantly to the pharmacologic activity of duloxetine.
Route of elimination Many additional metabolites have been identified in urine, some representing only minor pathways of elimination. Most (about 70%) of the duloxetine dose appears in the urine as metabolites of duloxetine; about 20% is excreted in the feces.
Half life 12 hours (range 8-17 hours)
Clearance Not Available
Toxicity Oral, rat LD50: 491 mg/kg for males and 279 mg/kg for females. Symptoms of overdose include tremors, convulsions, reduced activity, slow pupillary response, intermittent tremors, and rigidity.
Affected organisms
  • Humans and other mammals
Pathways Not Available
Pharmacoeconomics
Manufacturers
  • Eli lilly and co
Packagers
Dosage forms
Form Route Strength
Capsule, coated pellets Oral
Prices
Unit description Cost Unit
Cymbalta 30 mg Enteric Coated Capsule 5.38 USD capsule
Cymbalta 60 mg Enteric Coated Capsule 5.38 USD capsule
Cymbalta 30 mg capsule 5.18 USD capsule
Cymbalta 60 mg capsule 5.18 USD capsule
Cymbalta 20 mg Enteric Coated Capsule 4.64 USD capsule
Cymbalta 20 mg capsule 4.62 USD capsule
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Country Patent Number Approved Expires (estimated)
United States 6596756 1999-09-10 2019-09-10
United States 5023269 1993-06-11 2013-06-11
Canada 2344057 2008-11-18 2019-09-10
Canada 2153856 2005-05-10 2015-07-13
Properties
State solid
Experimental Properties
Property Value Source
logP 4 Not Available
Predicted Properties
Property Value Source
water solubility 2.96e-03 g/l ALOGPS
logP 4.72 ALOGPS
logP 4.2 ChemAxon
logS -5 ALOGPS
pKa (strongest basic) 9.7 ChemAxon
physiological charge 1 ChemAxon
hydrogen acceptor count 2 ChemAxon
hydrogen donor count 1 ChemAxon
polar surface area 21.26 ChemAxon
rotatable bond count 6 ChemAxon
refractivity 87.73 ChemAxon
polarizability 33.15 ChemAxon
References
Synthesis Reference Not Available
General Reference
  1. Turcotte JE, Debonnel G, de Montigny C, Hebert C, Blier P: Assessment of the serotonin and norepinephrine reuptake blocking properties of duloxetine in healthy subjects. Neuropsychopharmacology. 2001 May;24(5):511-21. Pubmed
  2. Anttila S, Leinonen E: Duloxetine Eli Lilly. Curr Opin Investig Drugs. 2002 Aug;3(8):1217-21. Pubmed
  3. Karpa KD, Cavanaugh JE, Lakoski JM: Duloxetine pharmacology: profile of a dual monoamine modulator. CNS Drug Rev. 2002 Winter;8(4):361-76. Pubmed
  4. van Groeningen CJ, Peters GJ, Pinedo HM: Lack of effectiveness of combined 5-fluorouracil and leucovorin in patients with 5-fluorouracil-resistant advanced colorectal cancer. Eur J Cancer Clin Oncol. 1989 Jan;25(1):45-9. Pubmed
  5. Jost W, Marsalek P: Duloxetine: mechanism of action at the lower urinary tract and Onuf’s nucleus. Clin Auton Res. 2004 Aug;14(4):220-7. Pubmed
  6. Carter NJ, McCormack PL: Duloxetine: a review of its use in the treatment of generalized anxiety disorder. CNS Drugs. 2009;23(6):523-41. doi: 10.2165/00023210-200923060-00006. Pubmed
External Links
Resource Link
KEGG Drug D01179 Link_out
PubChem Compound 60835 Link_out
PubChem Substance 46507937 Link_out
ChemSpider 54822 Link_out
ChEBI 36795 Link_out
ChEMBL 36795 Link_out
Therapeutic Targets Database DAP000494 Link_out
PharmGKB PA10066 Link_out
IUPHAR 202 Link_out
Guide to Pharmacology 202 Link_out
RxList http://www.rxlist.com/cgi/generic/cymbalta.htm Link_out
Drugs.com http://www.drugs.com/cdi/duloxetine-delayed-release-capsules.html Link_out
Wikipedia http://en.wikipedia.org/wiki/Duloxetine Link_out
ATC Codes
  • N06AX21
AHFS Codes Not Available
PDB Entries Not Available
FDA label show (104 KB)
MSDS show (76.3 KB)
Interactions
Drug Interactions
Drug Interaction
Amitriptyline Possible increase in the levels of this agent when used with duloxetine
Ciprofloxacin Ciprofloxacin, a strong CYP1A2 inhibitor, may decrease the metabolism of duloxetine. Monitor for changes in the therapeutic and adverse effects of duloxetine if ciprofloxacin is initiated or discontinued.
Desipramine Possible increase in the levels of this agent when used with duloxetine
Desvenlafaxine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Flecainide Possible increase in the levels of this agent when used with duloxetine
Fluvoxamine Fluvoxamine increases the effect and toxicity of duloxetine
Imipramine Possible increase in the levels of this agent when used with duloxetine
Isocarboxazid Possible severe adverse reaction with this combination
Nortriptyline Possible increase in the levels of this agent when used with duloxetine
Phenelzine Possible severe adverse reaction with this combination
Propafenone Possible increase in the levels of this agent when used with duloxetine
Rasagiline Possible severe adverse reaction with this combination
Tamoxifen Duloxetine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy.
Tamsulosin Duloxetine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Duloxetine is initiated, discontinued, or dose changed.
Terbinafine Terbinafine may reduce the metabolism and clearance of Duloxetine. Consider alternate therapy or monitor for therapeutic/adverse effects of Duloxetine if Terbinafine is initiated, discontinued or dose changed.
Thiabendazole The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Duloxetine by decreasing Duloxetine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Duloxetine if Thiabendazole is initiated, discontinued or dose changed.
Thioridazine Increased risk of cardiotoxicity and arrhythmias
Tramadol Duloxetine may decrease the effect of Tramadol by decreasing active metabolite production. Increased risk of serotonin syndrome. Monitor for Tramadol efficacy and symptoms of serotonin syndrome.
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.
Trazodone Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Trimipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Triprolidine The CNS depressants, Triprolidine and Duloxetine, may increase adverse/toxic effects due to additivity. Monitor for increased CNS depressant effects during concomitant therapy.
Venlafaxine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome.
Zolmitriptan Use of two serotonin modulators, such as zolmitriptan and duloxetine, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy.
Food Interactions
  • Food does not affect maximum levels reached, but delays it (from 6 to 10 hours) and total product exposure appears to be reduced by only 10%.
  • People taking this product who drink large amounts of alcohol are exposed to a higher risk of liver toxicity.
  • Take without regard to meals.
Targets

1. Sodium-dependent serotonin transporter

Pharmacological action: yes
Actions: inhibitor

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

Organism class: human
UniProt ID: P31645 Link_out
Gene: SLC6A4 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Chen F, Larsen MB, Sanchez C, Wiborg O: The S-enantiomer of R,S-citalopram, increases inhibitor binding to the human serotonin transporter by an allosteric mechanism. Comparison with other serotonin transporter inhibitors. Eur Neuropsychopharmacol. 2005 Mar;15(2):193-8. Pubmed
  2. Troelsen KB, Nielsen EO, Mirza NR: Chronic treatment with duloxetine is necessary for an anxiolytic-like response in the mouse zero maze: the role of the serotonin transporter. Psychopharmacology (Berl). 2005 Oct;181(4):741-50. Epub 2005 Sep 29. Pubmed
  3. Gould GG, Javors MA, Frazer A: Effect of chronic administration of duloxetine on serotonin and norepinephrine transporter binding sites in rat brain. Biol Psychiatry. 2007 Jan 15;61(2):210-5. Epub 2006 May 2. Pubmed
  4. Mirza NR, Nielsen EO, Troelsen KB: Serotonin transporter density and anxiolytic-like effects of antidepressants in mice. Prog Neuropsychopharmacol Biol Psychiatry. 2007 May 9;31(4):858-66. Epub 2007 Jan 30. Pubmed
  5. Vaishnavi SN, Nemeroff CB, Plott SJ, Rao SG, Kranzler J, Owens MJ: Milnacipran: a comparative analysis of human monoamine uptake and transporter binding affinity. Biol Psychiatry. 2004 Feb 1;55(3):320-2. Pubmed
  6. Beique JC, Lavoie N, de Montigny C, Debonnel G: Affinities of venlafaxine and various reuptake inhibitors for the serotonin and norepinephrine transporters. Eur J Pharmacol. 1998 May 15;349(1):129-32. Pubmed
  7. Karpa KD, Cavanaugh JE, Lakoski JM: Duloxetine pharmacology: profile of a dual monoamine modulator. CNS Drug Rev. 2002 Winter;8(4):361-76. Pubmed
  8. van Groeningen CJ, Peters GJ, Pinedo HM: Lack of effectiveness of combined 5-fluorouracil and leucovorin in patients with 5-fluorouracil-resistant advanced colorectal cancer. Eur J Cancer Clin Oncol. 1989 Jan;25(1):45-9. Pubmed
  9. Jost W, Marsalek P: Duloxetine: mechanism of action at the lower urinary tract and Onuf’s nucleus. Clin Auton Res. 2004 Aug;14(4):220-7. Pubmed
  10. Trivedi MH, Desaiah D, Ossanna MJ, Pritchett YL, Brannan SK, Detke MJ: Clinical evidence for serotonin and norepinephrine reuptake inhibition of duloxetine. Int Clin Psychopharmacol. 2008 May;23(3):161-9. Pubmed
  11. Bymaster FP, Lee TC, Knadler MP, Detke MJ, Iyengar S: The dual transporter inhibitor duloxetine: a review of its preclinical pharmacology, pharmacokinetic profile, and clinical results in depression. Curr Pharm Des. 2005;11(12):1475-93. Pubmed
  12. Khullar V, Cardozo L, Dmochowski R: Mixed incontinence: current evidence and future perspectives. Neurourol Urodyn. 2010 Apr;29(4):618-22. Pubmed
  13. Carter NJ, McCormack PL: Duloxetine: a review of its use in the treatment of generalized anxiety disorder. CNS Drugs. 2009;23(6):523-41. Pubmed
  14. Hunziker ME, Suehs BT, Bettinger TL, Crismon ML: Duloxetine hydrochloride: a new dual-acting medication for the treatment of major depressive disorder. Clin Ther. 2005 Aug;27(8):1126-43. Pubmed

2. Sodium-dependent noradrenaline transporter

Pharmacological action: yes
Actions: inhibitor

Amine transporter. Terminates the action of noradrenaline by its high affinity sodium-dependent reuptake into presynaptic terminals

Organism class: human
UniProt ID: P23975 Link_out
Gene: SLC6A2 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. Pubmed
  2. Gould GG, Javors MA, Frazer A: Effect of chronic administration of duloxetine on serotonin and norepinephrine transporter binding sites in rat brain. Biol Psychiatry. 2007 Jan 15;61(2):210-5. Epub 2006 May 2. Pubmed
  3. Vaishnavi SN, Nemeroff CB, Plott SJ, Rao SG, Kranzler J, Owens MJ: Milnacipran: a comparative analysis of human monoamine uptake and transporter binding affinity. Biol Psychiatry. 2004 Feb 1;55(3):320-2. Pubmed
  4. Beique JC, Lavoie N, de Montigny C, Debonnel G: Affinities of venlafaxine and various reuptake inhibitors for the serotonin and norepinephrine transporters. Eur J Pharmacol. 1998 May 15;349(1):129-32. Pubmed
  5. Vincent S, Bieck PR, Garland EM, Loghin C, Bymaster FP, Black BK, Gonzales C, Potter WZ, Robertson D: Clinical assessment of norepinephrine transporter blockade through biochemical and pharmacological profiles. Circulation. 2004 Jun 29;109(25):3202-7. Epub 2004 Jun 7. Pubmed
  6. Schou M, Halldin C, Pike VW, Mozley PD, Dobson D, Innis RB, Farde L, Hall H: Post-mortem human brain autoradiography of the norepinephrine transporter using (S,S)-[18F]FMeNER-D2. Eur Neuropsychopharmacol. 2005 Oct;15(5):517-20. Epub 2005 Apr 7. Pubmed
  7. Mirza NR, Nielsen EO, Troelsen KB: Serotonin transporter density and anxiolytic-like effects of antidepressants in mice. Prog Neuropsychopharmacol Biol Psychiatry. 2007 May 9;31(4):858-66. Epub 2007 Jan 30. Pubmed
  8. Karpa KD, Cavanaugh JE, Lakoski JM: Duloxetine pharmacology: profile of a dual monoamine modulator. CNS Drug Rev. 2002 Winter;8(4):361-76. Pubmed
  9. van Groeningen CJ, Peters GJ, Pinedo HM: Lack of effectiveness of combined 5-fluorouracil and leucovorin in patients with 5-fluorouracil-resistant advanced colorectal cancer. Eur J Cancer Clin Oncol. 1989 Jan;25(1):45-9. Pubmed
  10. Jost W, Marsalek P: Duloxetine: mechanism of action at the lower urinary tract and Onuf’s nucleus. Clin Auton Res. 2004 Aug;14(4):220-7. Pubmed
  11. Trivedi MH, Desaiah D, Ossanna MJ, Pritchett YL, Brannan SK, Detke MJ: Clinical evidence for serotonin and norepinephrine reuptake inhibition of duloxetine. Int Clin Psychopharmacol. 2008 May;23(3):161-9. Pubmed
  12. Bymaster FP, Lee TC, Knadler MP, Detke MJ, Iyengar S: The dual transporter inhibitor duloxetine: a review of its preclinical pharmacology, pharmacokinetic profile, and clinical results in depression. Curr Pharm Des. 2005;11(12):1475-93. Pubmed
  13. Khullar V, Cardozo L, Dmochowski R: Mixed incontinence: current evidence and future perspectives. Neurourol Urodyn. 2010 Apr;29(4):618-22. Pubmed
  14. Carter NJ, McCormack PL: Duloxetine: a review of its use in the treatment of generalized anxiety disorder. CNS Drugs. 2009;23(6):523-41. Pubmed
  15. Hunziker ME, Suehs BT, Bettinger TL, Crismon ML: Duloxetine hydrochloride: a new dual-acting medication for the treatment of major depressive disorder. Clin Ther. 2005 Aug;27(8):1126-43. Pubmed

3. Sodium-dependent dopamine transporter

Pharmacological action: unknown
Actions: inhibitor

Amine transporter. Terminates the action of dopamine by its high affinity sodium-dependent reuptake into presynaptic terminals

Organism class: human
UniProt ID: Q01959 Link_out
Gene: SLC6A3 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Overington JP, Al-Lazikani B, Hopkins AL: How many drug targets are there? Nat Rev Drug Discov. 2006 Dec;5(12):993-6. Pubmed
  2. Imming P, Sinning C, Meyer A: Drugs, their targets and the nature and number of drug targets. Nat Rev Drug Discov. 2006 Oct;5(10):821-34. Pubmed
  3. Carter NJ, McCormack PL: Duloxetine: a review of its use in the treatment of generalized anxiety disorder. CNS Drugs. 2009;23(6):523-41. Pubmed
  4. Pereira P, Gianesini J, da Silva Barbosa C, Cassol GF, Von Borowski RG, Kahl VF, Cappelari SE, Picada JN: Neurobehavioral and genotoxic parameters of duloxetine in mice using the inhibitory avoidance task and comet assay as experimental models. Pharmacol Res. 2009 Jan;59(1):57-61. Epub 2008 Oct 5. Pubmed
  5. Hunziker ME, Suehs BT, Bettinger TL, Crismon ML: Duloxetine hydrochloride: a new dual-acting medication for the treatment of major depressive disorder. Clin Ther. 2005 Aug;27(8):1126-43. Pubmed
Enzymes

1. Cytochrome P450 1A2

Actions: substrate

Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics. Most active in catalyzing 2-hydroxylation. Caffeine is metabolized primarily by cytochrome CYP1A2 in the liver through an initial N3-demethylation. Also acts in the metabolism of aflatoxin B1 and acetaminophen

UniProt ID: P05177 Link_out
Gene: CYP1A2
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Knadler MP, Lobo E, Chappell J, Bergstrom R: Duloxetine: clinical pharmacokinetics and drug interactions. Clin Pharmacokinet. 2011 May 1;50(5):281-94. doi: 10.2165/11539240-000000000-00000. Pubmed
  2. Lobo ED, Bergstrom RF, Reddy S, Quinlan T, Chappell J, Hong Q, Ring B, Knadler MP: In vitro and in vivo evaluations of cytochrome P450 1A2 interactions with duloxetine. Clin Pharmacokinet. 2008;47(3):191-202. Pubmed
  3. Duloxetine: new indication. Depression and diabetic neuropathy: too many adverse effects. Prescrire Int. 2006 Oct;15(85):168-72. Pubmed
  4. Carter NJ, McCormack PL: Duloxetine: a review of its use in the treatment of generalized anxiety disorder. CNS Drugs. 2009;23(6):523-41. doi: 10.2165/00023210-200923060-00006. Pubmed

2. Cytochrome P450 2D6

Actions: substrate, inhibitor

Responsible for the metabolism of many drugs and environmental chemicals that it oxidizes. It is involved in the metabolism of drugs such as antiarrhythmics, adrenoceptor antagonists, and tricyclic antidepressants

UniProt ID: P10635 Link_out
Gene: CYP2D6 Link_out
Protein Sequence: FASTA
Gene Sequence: FASTA
SNPs: SNPJam Report Link_out

References:
  1. Flockhart DA. Drug Interactions: Cytochrome P450 Drug Interaction Table. Indiana University School of Medicine (2007). Accessed May 28, 2010.
  2. Knadler MP, Lobo E, Chappell J, Bergstrom R: Duloxetine: clinical pharmacokinetics and drug interactions. Clin Pharmacokinet. 2011 May 1;50(5):281-94. doi: 10.2165/11539240-000000000-00000. Pubmed
  3. Preskorn SH, Nichols AI, Paul J, Patroneva AL, Helzner EC, Guico-Pabia CJ: Effect of desvenlafaxine on the cytochrome P450 2D6 enzyme system. J Psychiatr Pract. 2008 Nov;14(6):368-78. Pubmed
  4. Duloxetine: new indication. Depression and diabetic neuropathy: too many adverse effects. Prescrire Int. 2006 Oct;15(85):168-72. Pubmed
  5. Carter NJ, McCormack PL: Duloxetine: a review of its use in the treatment of generalized anxiety disorder. CNS Drugs. 2009;23(6):523-41. doi: 10.2165/00023210-200923060-00006. Pubmed
Comments
Drug created on June 13, 2005 07:24 / Updated on February 08, 2013 16:19