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An Intestine/Liver Microphysiological System for Drug Pharmacokinetic and Toxicological Assessment

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Metabolomic profiling reveals ADB-BUTINACA-induced long-term hepatotoxicity.

Siyue Zheng¹, Yi Zhou², Xiaoran Song³

¹College of Chemical Engineering, Zhejiang University of Technology, Hangzhou, 310014, China.

Chemico-Biological Interactions

|September 25, 2025

Summary

ADB-BUTINACA, a synthetic cannabinoid, causes liver damage and disrupts lipid metabolism. This study reveals its toxic effects on fatty acid and TCA cycle pathways, highlighting risks associated with this emerging contaminant.

Keywords:

ADB-BUTINACA Hepatotoxicity Inflammation Molecular docking Non-targeted metabolomics

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Area of Science:

Toxicology
Metabolomics
Pharmacology

Background:

ADB-BUTINACA is a synthetic cannabinoid with high abuse potential and known multi-organ toxicity.
Long-term toxicological effects and metabolic mechanisms of ADB-BUTINACA are not well understood.
Understanding these effects is crucial for public health risk assessment.

Purpose of the Study:

To investigate the hepatotoxic potential of ADB-BUTINACA.
To elucidate the metabolic disruption induced by ADB-BUTINACA.
To explore the molecular mechanisms underlying ADB-BUTINACA-induced liver injury.

Main Methods:

A 30-day oral exposure model in mice using ADB-BUTINACA at varying doses (0.1, 1, 10 mg/kg).
Serum biochemical analysis, histopathology, non-targeted metabolomics, RT-qPCR, and molecular docking.
Analysis of key metabolic pathways and enzyme interactions.

Main Results:

ADB-BUTINACA induced dose-dependent liver injury, systemic inflammation, and lipid dysregulation (elevated TNF-α, IL-6, cholesterol, triglycerides, LDL-C).
Metabolomic profiling identified 60 altered metabolites and 12 perturbed pathways, including unsaturated fatty acid biosynthesis and the TCA cycle.
Reduced levels of EPA, DHA, and taurine were observed, with evidence of ADB-BUTINACA inhibiting TCA cycle and fatty acid synthesis enzymes (FADS2, ELOVL2).

Conclusions:

ADB-BUTINACA causes significant hepatotoxicity through metabolic disruption, particularly affecting lipid metabolism and the TCA cycle.
The compound interferes with endogenous lipid regulation by binding to key enzymes like FADS2 and ELOVL2.
These findings highlight the potential health risks posed by ADB-BUTINACA as an emerging synthetic cannabinoid contaminant.