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Last Updated: 3 years ago

Possible Interaction: Ethanol and Fenofibrate



Research Papers that Mention the Interaction

Moreover, a phase 2 clinical trial led by Barbara Mason (The Scripps Research Institute) was started to test the hypothesis that alcohol-dependent subjects treated with fenofibrate will report decreased craving for alcohol following cue-exposure and will report less drinking post treatment (
Alcohol and alcoholism  •  2015  |  View Paper
It has been reported that administering fenofibrate to high-drinking rats increases hepatic catalase levels and blood acetaldehyde after administering ethanol and a 60-70% inhibition of voluntary alcohol intake.
The studies show that treatment with fenofibrate not only increased the activity of catalase in the liver of alcohol-drinking rats, as reported earlier, but also increased the levels and enzymatic activity of ADH1, while ALDH2 remained unchanged.
Adicciones  •  2019  |  View Paper
Results showed fenofibrate dose‐dependently decreased EtOH self‐administration under both schedules of reinforcement with the greatest effects seen after four to five days of treatment.
Studies have shown the PPAR&agr; agonist fenofibrate decreases voluntary EtOH consumption however its impact on the reinforcing and motivational effects of EtOH is unknown.
The effects of fenofibrate on EtOH self‐administration were dose‐dependent.
Neuropharmacology  •  2017  |  View Paper
EtOH clearance was increased by both fenofibrate and tesaglitazar.
Alcoholism, clinical and experimental research  •  2016  |  View Paper
We determined whether animals chronically allowed access to ethanol and subsequently treated with fenofibrate , would a) increase liver catalase activity, and b) increase blood acetaldehyde levels after a 24-h ethanol deprivation and the subsequent administration of 1 g ethanol/kg.
Alcohol  •  2014  |  View Paper
Fenofibrate reduced ethanol voluntary intake by 60%, in chronically drinking rats, at the three doses tested.
In summary, reduction of ethanol intake by fenofibrate appears to be a consequence of a combination of catalase induction in the liver and central pharmacological effects.
Front. Behav. Neurosci.  •  2017  |  View Paper