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The degradation rate and half-life (t1/2) of the drugs were determined by measuring the decrease in area under the curve (AUC) at their retention times [1]

Nevertheless, conflicting views persist regarding the precise mechanistic pathways driving liver injury, with earlier reports emphasizing apoptosis, caspase-independent cell death, the ubiquitin-proteasome system, or ROS involvement [54]

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[] Although most of them are metabolized in the liver and intestines, a small amount can persist in the bloodstream and organs such as the kidneys, lungs, heart, and brain

Pre-clinical data suggests upregulation of nerve growth factor and vascular endothelial growth factor in injury models [9]