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In this study, we performed a ChaC1-activity-directed pharmacological screening from FDA-approved drug library to identify GSH-sensitive agents, and found that ChaC1 overexpression mediated glutathione depletion largely enhanced auranofin (AUR)-induced cell death in hepatocellular carcinoma (HCC) cells

Methods This open-label, pre-post study was performed on FM patients whose diagnoses were confirmed by a rheumatologist based on the 2016 American College of Rheumatology (ACR)

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We also assess enabling technologies such as spatial transcriptomics, proteomics, and patient-derived organoids, and discuss their translational relevance in stratifying metabolic vulnerabilities and informing individualized therapies