The 1st VMAT2 inhibitor approved for both TD and HD chorea1,2

For adults with TD or HD chorea1

Make a move that matters With ONE PILL, ONCE-DAILY AUSTEDO XR

Real-World Results AUSTEDO XR

Significant response at Week 12 in pivotal
studies.
Increasing improvement observed
over
3 years in open-label extension study3-5*†

only with austedo xr

Flexibility for effective and tolerable control, including for patients taking medications metabolized by CYP3A4/5 or CYP2D6, or
P-gp substrates1,2,6

only with austedo xr

Patients can start AUSTEDO XR for free with the 4-week Titration Kit6

​

*Patients in the pivotal and long-term studies received the AUSTEDO BID formulation.1,5

†71% of patients at Week 145 saw improvement relative to Week 15.6

Mechanism of Action:

VMAT2 inhibition can help regulate dopamine function.7

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Voiceover:

Maintaining a balance in the level of dopamine is essential for controlled movement.


Dopamine signaling is facilitated by vesicular monoamine transporter 2, or VMAT2, which transports monoamines, including dopamine, from the cytosol into synaptic vesicles, keeping them ready for subsequent release in response to an action potential.


When an action potential reaches the nerve terminal of the presynaptic neuron, dopamine is released from the synaptic vesicles into the synaptic cleft.


This dopamine binds to receptors on the postsynaptic neuron, thereby signaling movement.


Excess dopamine signaling manifests as abnormal involuntary movements.


AUSTEDO® (deutetrabenazine) is a VMAT2 inhibitor.


Deutetrabenazine contains deuterium, a naturally occurring heavy version of hydrogen. Deuterium forms stronger molecular bonds with carbon atoms, thereby extending the half-life of therapeutic metabolites.


The precise mechanism by which deutetrabenazine exerts its effects on abnormal involuntary movements is unknown. It is believed to be related to its effect as a reversible depleter of monoamines, including dopamine, from nerve terminals.


Deutetrabenazine binds to VMAT2 on the vesicle in the presynaptic neuron and inhibits the uptake of dopamine into synaptic vesicles.


Dopamine molecules collect outside the blocked VMAT2 and are degraded by monoamine oxidase.


Reducing dopamine levels in the presynaptic neuron results in less dopamine signaling to the postsynaptic neuron.


Limiting dopamine signaling is believed to lead to fewer abnormal involuntary movements.

HD, Huntington’s disease; TD, tardive dyskinesia; VMAT2, vesicular monoamine transporter 2.

REFERENCES: 1. AUSTEDO XR® (deutetrabenazine) extended-release tablets and AUSTEDO® current Prescribing Information. Parsippany, NJ: Teva Neuroscience, Inc. 2. Ingrezza® (valbenazine) capsules. Prescribing Information. San Diego, CA: Neurocrine Biosciences, Inc. 3. Anderson KE, Stamler D, Davis MD, et al. Deutetrabenazine for treatment of involuntary movements in patients with tardive dyskinesia (AIM-TD): a double-blind, randomised, placebo-controlled, phase 3 trial. Lancet Psychiatry. 2017;4(8):595-604. 4. Fernandez HH, Factor SA, Hauser RA, et al. Randomized controlled trial of deutetrabenazine for tardive dyskinesia: the ARM-TD study. Neurology. 2017;88(21):2003-2010. 5. Hauser RA, Barkay H, Fernandez HH, et al. Long-term deutetrabenazine treatment for tardive dyskinesia is associated with sustained benefits and safety: a 3-year, open-label extension study. Front Neurol. 2022;13:773999. 6. Data on file. Parsippany, NJ: Teva Neuroscience, Inc. 7. Solmi M, Pigato G, Kane JM, Correll CU. Treatment of tardive dyskinesia with VMAT-2 inhibitors: a systematic review and meta-analysis of randomized controlled trials. Drug Des Devel Ther. 2018;12:1215-1238.