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As a prodrug, gemcitabine hydrochloride is a good substrate for phosphorylation of deoxythymidine kinase in the cell and is converted into the following metabolites under the action of enzymes: gemcitabine monophosphate (dFdCMP), gemcitabine diphosphate (dFdCDP) and gemcitabine Phosphate (dFdCTP) dFdCDP and dFdCTP are active products. dFdCDP inhibits ribonucleotide reductase, thereby reducing the amount of deoxynucleotides required for repair of DNA synthesis (especially dCTP). Low levels of dCTP reverse the normal negative feedback inhibition of deoxyglycoside kinase, resulting in more dFdCTP Accumulation. At the same time, dFdCDP inhibits the deamination effect of dCTP-induced deoxycytidine on dFdCMP, and dFdCTP directly inhibits deoxycytidine deaminase, thereby converting more dFdCMP into the active metabolite dFdCMP deamination, and dFdCTP directly inhibits deoxygenation Cytidine deaminase, which converts more dFdCMP into the active metabolite dFdCDP, dFd-CTP and dFdCTP competes with dCTP for binding into the DNA strand, inserting it into the deoxycytidine site in the DNA strand, and allowing guanosine to interact with it After pairing, the gemcitabine molecule is "masked" by this guanosine to prevent it from being removed and repaired by exonuclease, and then DNA strand synthesis stops, and DNA breaks and the cell dies.