Irinotecan is a semi-synthetic water-soluble camptothecin derivative. This product and its metabolite SN38 are inhibitors of DNA topoisomerase I. The complex formed with topoisomerase I and DNA can cause DNA single-strand breaks, prevent DNA replication and inhibit RNA synthesis, which is the S phase of the cell cycle. Specificity.
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Irinotecan is a semisynthetic derivative of camptothecin. It is an inactive prodrug whose main site of metabolism is the liver.
After irinotecan enters the human body through the blood, most of it is converted by carboxylesterase (CES) into the active metabolite SN-38 (7-ethyl-10-hydroxycamptothecin), which has 100 times the anti-tumor ability. Sexually combined with topoisomerase I (TOP-1), thereby achieving anti-tumor effects; the other part is converted into APC and NPC by CYP3A enzyme in liver cells, and then converted into SN-38 by CES to achieve anti-tumor effects.
Topoisomerase I induces reversible DNA single-strand breaks, thereby unwinding the DNA double-stranded structure; irinotecan and its active metabolite SN-38 can bind to topoisomerase I-DNA complexes, thereby preventing the break Single chain reconnection.
During DNA synthesis, replicase interacts with the topoisomerase I-DNA-CPT-11 triplet complex and exerts a cytotoxic effect by causing DNA double-strand breaks. Normally, mammalian cells cannot effectively repair such DNA double-strand breaks.
Common side effects of irinotecan include: delayed diarrhea (occurring within 24 hours after taking the drug), neutropenia, nausea and vomiting, and acute cholinergic syndrome (including early-onset diarrhea, occurring within 24 hours of taking the drug);
A few minor reactions include: anorexia, abdominal pain, mucositis, fatigue, and thrombocytopenia. About 20% of these patients develop severe neutropenia and/or diarrhea when receiving irinotecan-based combination chemotherapy.
The research results suggest that the toxicity of irinotecan is mainly caused by its active metabolite SN-38. SN-38 mainly binds to plasma proteins (binding rate 95%). After exerting its anti-tumor effect, active SN-38 is mainly catalyzed by UGT1A1 (uridine diphosphate glucuronosyltransferase 1A1) located in the liver. It is converted into inactive SN-38G (the activity is about 1/50~1/100 of SN-38), which is then excreted through urine and bile; at the same time, UGT1A1 can also participate in the glycosylation conversion of bilirubin. This in turn produces more soluble conjugated bilirubin.
Be sure to follow your doctor’s advice when using this product
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