Introduction: Methods: Aqueous extracts were evaluated for endotoxin contamination and cytotoxicity to ensure suitability for in vitro experimentation. PCR analysis was employed to quantify CYP enzyme gene expression. Computational tools, including Protox-II, Swiss ADME, and molecular docking, were used to assess pharmacokinetics, CYP interactions, and biological targets. Competitive binding assays were performed to investigate the involvement of the constitutive androstane receptor (CAR) in CYP induction. Results: The results suggest that several metabolites, particularly ursodeoxycholic acid and beta-sitosterol, show potential interactions with CYP enzymes, with ursodeoxycholic acid demonstrating the highest probability of biological effects on CYP and a strong binding affinity to the Constitutive Androstane Receptor (CAR). Moreover, a receptor competitive binding assay suggested that the primary mechanism of CYP 2B6 and 3A4 induction is through activation of the CAR receptor although additional confirmatory studies are necessary. Discussion: The observed CYP enzyme induction through CAR receptor activation aligns with USFDA guidelines for CYP studies. However, the hepatotoxic potential of ursodeoxycholic acid and the associated toxicity risks of other metabolites underscore the need for caution. The findings highlight the potential for herb-drug interactions, particularly with pharmaceuticals metabolized by CYP enzymes. Conclusion: In conclusion, there is a potential for interactions between