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Pharmaceutical drug From Wikipedia, the free encyclopedia
Dextromethorphan/quinidine, sold under the brand name Nuedexta, is a fixed-dose combination medication for the treatment of pseudobulbar affect (PBA).[1][2] It contains dextromethorphan (DXM) and the class I antiarrhythmic agent quinidine.[1]
Combination of | |
---|---|
Dextromethorphan | Sigma-1 receptor agonist, NMDA receptor antagonist, serotonin–norepinephrine reuptake inhibitor |
Quinidine | Antiarrhythmic agent, CYP2D6 inhibitor |
Clinical data | |
Trade names | Nuedexta |
Other names | AVP-923; DXM/quinidine |
AHFS/Drugs.com | Monograph |
MedlinePlus | a611048 |
License data | |
Routes of administration | By mouth |
ATC code |
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Legal status | |
Legal status |
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Pharmacokinetic data | |
Bioavailability | dextromethorphan 11%, quinidine 70-80%. Food has no effect on absorption. |
Metabolism | Liver, extensive. Dextromethorphan is catalyzed by CYP2D6. Quinidine is metabolized by CYP3A4 and competitively inhibits the metabolism of dextromethorphan to increase and prolong plasma concentrations of dextromethorphan |
Elimination half-life | dextromethorphan 13h, quinidine 7h |
Excretion | quinidine 5-20% |
Identifiers | |
CAS Number | |
KEGG |
Dextromethorphan/quinidine was approved for medical use in the United States in October 2010, and is marketed by Avanir Pharmaceuticals.[3]
DXM/quinidine is used in the treatment of PBA. In a 12-week randomized, double-blind trial, amyotrophic lateral sclerosis and multiple sclerosis patients with significant PBA were given either Nuedexta 20/10 mg or placebo. In 326 randomized patients, the PBA-episode daily rate was 46.9% (p < 0.0001) lower for Nuedexta than for placebo.[4] The three deaths in each of the two drug treatment arms and the single death in the placebo arm of the study were believed to be due to the natural course of the disease.[1]
Common risks and side effects include:[1]
Dextromethorphan acts as a σ1 receptor agonist, serotonin–norepinephrine reuptake inhibitor, and NMDA receptor antagonist, while quinidine is an antiarrhythmic agent acting as a CYP2D6 inhibitor.[5] Quinidine prevents the metabolism of dextromethorphan into its active metabolite dextrorphan, which is a much more potent NMDA receptor antagonist but much less potent serotonin reuptake inhibitor than dextromethorphan.[5][2] The mechanism of action of dextromethorphan/quinidine in the treatment of PBA is unknown.[2]
Dextromethorphan/quinidine was investigated for the treatment of agitation associated with dementia, diabetic neuropathy, drug-induced dyskinesia, migraine, and neuropathic pain, but development for these indications was discontinued.[6] Another formulation, deudextromethorphan/quinidine, is still under investigation for various indications.[7] These include agitation, schizophrenia, and major depressive disorder, among others.[7]
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