Summary |
Chemotherapy drugs or toxic chemicals which are detoxified through hepatic glucuronidaiton can be reactivated by eG back to toxic form and thus inducing intestine damage, diarrhea, carcinogenesis, and colon cancer. Therefore, we have successfully developed eG specific inhibitor as a novel drug for chemo-induced damage and colorectal cancer. |
Scientific Breakthrough |
Glucuronidation is a major process for toxin detoxification occurring mainly in the liver. Generally, carcinogens or drugs are conjugated with glucuronic acid to be inactive and facilitate their subsequent elimination from the body. However, when the pharmacologically inactive glucuronides enter the intestine via bile through enterohepatic circulation, they are reactivated by bacterial -glucuronidase (G), releasing the cytotoxic drugs and thus leading to intestinal injury. Repeatedly direct exposure of epithelium to carcinogens in the intestine leads to gene mutation and cell damage that increases the risk for colorectal malignancies. Therefore, we developed bacterial G-specific inhibitor as a novel drug for the following use: 3.Chemoprevention drug or treatment drug: For the patients with high risk of developing colorectal cancer, the inhibitor can be used to prevent reactivating of the carcinogen in the intestine and thus reducing chemo-induced carcinogenesis and colon cancer. Chemotherapy adjuvant: The inhibitor can be combined with chemo drug to prevent chemotherapy -induced intestinal damage and diarrhea, thus improving patients’ quality of life and increasing patient’s drug tolerance to increase therapy efficacy. |