In the body, aspirin is metabolized into salicylic acid and absorbed in the intestine. Similarly, in our study, both aspirin and the aspirin-cysteine conjugate will break down into salicylic acid in SIF. We used SIF as a simulated environment to mimic the conditions of the intestine in the body. Additionally, we employed the FeCl 3 assay to detect the hydrolysis of aspirin into salicylic acid. This assay is similar to the metabolic process that occurs in the body, where the ester bond in aspirin is hydrolyzed to salicylic acid. Therefore, the use of SIF and the FeCl 3 assay allowed us to model and monitor the metabolism of aspirin and the aspirin-cysteine conjugate in a manner that is relevant to the body. As expected, aspirin showed a relatively linear release profile over time, while the aspirin-cysteine conjugate exhibited an exponential release pattern. This can be attributed to the prodrug nature of the conjugate, which requires hydrolysis to release the active aspirin moiety. The initial slower release rate of the conjugate may be attributed to the time required for the hydrolysis reaction to occur. However, once the hydrolysis process is initiated, the release of aspirin from the conjugate increases rapidly, resulting in an exponential release profile. These results suggest that the aspirin-cysteine conjugate has the potential to provide a prolonged and sustained release of aspirin in the body.