Venlafaxine: Difference between revisions
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| author = Partridge SJ; MacIver DH; Solanki T | | author = Partridge SJ; MacIver DH; Solanki T | ||
| url = http://www.medscape.com/medline/abstract/10930064 | | url = http://www.medscape.com/medline/abstract/10930064 | ||
}}</ref> | }}</ref> | ||
==History== | ==History== | ||
'''Effexor''' brand of venlafaxine was approved by the [[Food and Drug Administration]] in the [[United States]] with a [http://www.fda.gov/Drugs/DevelopmentApprovalProcess/HowDrugsareDevelopedandApproved/ApprovalApplications/NewDrugApplicationNDA/ New Drug Application] (NDA) in 1993.<ref>{{FDA-Drug_Details|020151}}</ref> A generic version was approved with a NDA in 2008.<ref>{{FDA-Drug_Details|022104}}</ref> | '''Effexor''' brand of venlafaxine was approved by the [[Food and Drug Administration]] in the [[United States of America|United States]] with a [http://www.fda.gov/Drugs/DevelopmentApprovalProcess/HowDrugsareDevelopedandApproved/ApprovalApplications/NewDrugApplicationNDA/ New Drug Application] (NDA) in 1993.<ref>{{FDA-Drug_Details|020151}}</ref> A generic version was approved with a NDA in 2008.<ref>{{FDA-Drug_Details|022104}}</ref> | ||
Generic versions of the time-release form are also available. | Generic versions of the time-release form are also available. | ||
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===Excretion=== | ===Excretion=== | ||
===Toxicity=== | ===Toxicity=== | ||
==Clinical uses== | |||
===Depression=== | |||
In a meta-analysis of eight trials of venflaxine versus the pure SSRIs [[fluoxetine]], [[fluvoxamine]] and [[paroxetine]], it had a superior rate of remission of depression. This improvement was evident versus placebo in week 2 of treatment, while the other drugs were superior to placebo only after 4 weeks.<ref>{{citation | journal = Br. J. Psychiatry | year = 2001 | url = http://www.hawaii.edu/hivandaids /Remission%20Rates%20During%20Treatment%20With%20Venlafaxine%20Or%20Selective%20Serotonin%20Reuptake%20Inhibitors.pdf | |||
| author = Thase ME; Entsuah R; Rudolph RL | title = Remission rates during treatment with venlafaxine or selective serotonin reuptake inhibitors }}</ref> When extended-release venlafaxine was compared to extended-release [[bupropion]], efficacy was comparable but bupropion had a better side effect profile.<ref>{{citation | (Abstract) A double-blind comparison between bupropion XL and venlafaxine XR: sexual functioning, antidepressant efficacy, and tolerability. | journal = J Clin Psychopharmacol | year = 2006 | volume = 26 | issue =5 | pages = 482-8 | author = Thase ME; Clayton AH; Haight BR; Thompson AH; Modell JG; Johnston JA }}</ref> | |||
===Neuropathic pain=== | |||
"TCAs and venlafaxine have NNTs of approximately three."<ref name="pmid17943857">{{cite journal| author=Saarto T, Wiffen PJ| title=Antidepressants for neuropathic pain. | journal=Cochrane Database Syst Rev | year= 2007 | volume= | issue= 4 | pages= CD005454 | pmid=17943857 | doi=10.1002/14651858.CD005454.pub2 | pmc= | url= }} </ref> | |||
==External links== | ==External links== |
Latest revision as of 13:34, 2 February 2023
In medicine and neuropharmacology, venlafaxine is a second generation antidepressant that has unusual chemistry: it inhibits the reuptake of several neurotransmitters depending on dose. In other words, it is an atypical second-generation drug that is neither a pure selective serotonin reuptake inhibitor (SSRI), a pure selective norepinephrine reuptake inhibitor (SNRI), or an equal inhibitor of both. To a lesser extent, it inhibits dopamine reuptake. [1]
History
Effexor brand of venlafaxine was approved by the Food and Drug Administration in the United States with a New Drug Application (NDA) in 1993.[2] A generic version was approved with a NDA in 2008.[3]
Generic versions of the time-release form are also available.
Pharmacology
Administration
Distribution
Metabolism
At the basic dosage level, it increases serotonin levels in synaptic gaps, by inhibiting presynaptic reuptake. With this
Excretion
Toxicity
Clinical uses
Depression
In a meta-analysis of eight trials of venflaxine versus the pure SSRIs fluoxetine, fluvoxamine and paroxetine, it had a superior rate of remission of depression. This improvement was evident versus placebo in week 2 of treatment, while the other drugs were superior to placebo only after 4 weeks.[4] When extended-release venlafaxine was compared to extended-release bupropion, efficacy was comparable but bupropion had a better side effect profile.[5]
Neuropathic pain
"TCAs and venlafaxine have NNTs of approximately three."[6]
External links
The most up-to-date information about Venlafaxine and other drugs can be found at the following sites.
- Venlafaxine - FDA approved drug information (drug label) from DailyMed (U.S. National Library of Medicine).
- Venlafaxine - Drug information for consumers from MedlinePlus (U.S. National Library of Medicine).
- Venlafaxine - Detailed information from DrugBank.
References
- ↑ Partridge SJ; MacIver DH; Solanki T (2000), "(Abstract) A depressed myocardium.", J Toxicol Clin Toxicol 38 (4): 453-5
- ↑ Anonymous. Drugs@FDA for FDA Application No. 020151. U S Food and Drug Administration
- ↑ Anonymous. Drugs@FDA for FDA Application No. 022104. U S Food and Drug Administration
- ↑ Thase ME; Entsuah R; Rudolph RL (2001), "/Remission%20Rates%20During%20Treatment%20With%20Venlafaxine%20Or%20Selective%20Serotonin%20Reuptake%20Inhibitors.pdf Remission rates during treatment with venlafaxine or selective serotonin reuptake inhibitors", Br. J. Psychiatry
- ↑ Thase ME; Clayton AH; Haight BR; Thompson AH; Modell JG; Johnston JA (2006), J Clin Psychopharmacol 26 (5): 482-8
- ↑ Saarto T, Wiffen PJ (2007). "Antidepressants for neuropathic pain.". Cochrane Database Syst Rev (4): CD005454. DOI:10.1002/14651858.CD005454.pub2. PMID 17943857. Research Blogging.