Research and Development

Background

Dopamine is a brain neurotransmitter and several dopamine neuronal systems reach through many brain regions. One of these is the ’Reward pathway’ which is central to the brain reward system. Dopamine release in this system is involved in feelings of euphoria in response to natural rewards. Addictive drugs cause a powerful dopamine release, resulting in intense euphoric feelings. With long-term use, the dopamine system is exhausted, creating a dopamine deficit.

Human studies indicate that both pre- and postsynaptic aspects of basal dopamine neurotransmission are reduced in AUD. Further, reduced dopamine transmission has been associated with increased alcohol intake as well as increased craving and alcohol-cue reactivity in animal and human studies, respectively. These data suggest that by normalizing dopamine levels alcohol intake may be reduced.

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Clinical phase II study

A clinical phase II randomized, double-blind, placebo-controlled trial was initiated in 2019, examining the effects of the combination therapy  in 380 patients with moderate to severe AUD. The study is a multicenter study in Sweden. The study reports heavy drinking days as outcome measurement as well as an objective alcohol blood marker for alcohol intake; Phosphatidylethanol (PEth) is uniquely specific to alcohol and measures intake over the last two weeks, which enables a close monitoring of alcohol intake both in research and clinical setting.

Early research

Recent pre clinical data show that the combination of varenicline and burporpione produce an effect on dopamin release in the rat ventral striatum and that the combination abolishes the alcohol deprivation effect in alcohol high-consuming rats. The latter measure is considered to have high predictive value for effect in humans.
The concept of using varenicline in AUD has been studied in preclinical and clinical studies and has shown to have effect in reducing alcohol intake.

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Publications

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