- Advanced search
- Immuno Portal
- Malaria Portal
Abbreviated name: TBZ
Synonyms: Nitoman® | Revocon® | Ro-19569
tetrabenazine is an approved drug (FDA (2008))
Compound class: Synthetic organic
Comment: Tetrabenazine is an inhibitor of the vesicular monoamine transporter type 2 (VMAT2; SLC18A2). Tetrabenazine was the first dopamine-depleting drug approved in the US for the treatment of Huntington's disease. The potential for using dopamine-depleters to manage hyperkinetic movement disorders is reviewed in . Since the approval of tetrabenazine, the deuterated analogue deutetrabenazine has been a granted marketing authorisation by the FDA (April 2107), and valbenazine is in clinical trial for tardive dyskinesia and Tourette syndrome
Ligand Activity Visualisation Charts
These are box plot that provide a unique visualisation, summarising all the activity data for a ligand taken from ChEMBL and GtoPdb across multiple targets and species. Click on a plot to see the median, interquartile range, low and high data points. A value of zero indicates that no data are available. A separate chart is created for each target, and where possible the algorithm tries to merge ChEMBL and GtoPdb targets by matching them on name and UniProt accession, for each available species. However, please note that inconsistency in naming of targets may lead to data for the same target being reported across multiple charts.✖
|No information available.
|Summary of Clinical Use
|Tetrabenazine has been used in the past as an antipsychotic, but is now used primarily in the symptomatic treatment of hyperkinetic disorders including chorea in Huntington's disease, Tourette syndrome and tardive dyskinesia.
|Mechanism Of Action and Pharmacodynamic Effects
|Reversibly inhibits the vesicular monoamine transporter 2 (SLC18A2). This decreases the amount of the monoamine neurotransmitters serotonin, norepinephrine, and dopamine stored in presynaptic vesicles, and results in increased metabolism of the extra-vesicular neurotransmitters by monoamine oxidase. This leads to an net reduction in catecholamine-driven neuro-activity. The principal action is believed to be depletion of presynaptic dopamine levels.
For extended ADME data see the following:
Electronic Medicines Compendium (eMC)