This product is a formyl derivative of tetrahydrofolate, mainly used for the rescue of high-dose methotrexate and other folic acid antagonists. It can be converted into tetrahydrofolate by tetrahydrofolate reductase, which can limit the damage of methotrexate to normal cells and reverse the reaction of methotrexate to bone marrow and gastrointestinal mucosa, but it has no obvious effect on the neurotoxicity caused by methotrexate.

This product is a formyl derivative of tetrahydrofolate, mainly used for the rescue of high-dose methotrexate and other folic acid antagonists. It can be converted into tetrahydrofolate by tetrahydrofolate reductase, which can limit the damage of methotrexate to normal cells and reverse the reaction of methotrexate to bone marrow and gastrointestinal mucosa, but it has no obvious effect on the neurotoxicity caused by methotrexate.

This product is a formyl derivative of tetrahydrofolate, mainly used for the rescue of high-dose methotrexate and other folic acid antagonists. It can be converted into tetrahydrofolate by tetrahydrofolate reductase, which can limit the damage of methotrexate to normal cells and reverse the reaction of methotrexate to bone marrow and gastrointestinal mucosa, but it has no obvious effect on the neurotoxicity caused by methotrexate.

Cell cycle specific antimetabolites mainly act on tumor cells in the DNA synthesis phase (S phase), preventing the progression from the G1 phase to the S phase; they are converted into active metabolites gemcitabine monophosphate (dFdCMP), gemcitabine diphosphate (dFdCDP) and gemcitabine triphosphate (dFdCTP) by enzymes in the cell. dFdCDP inhibits ribonucleotide reductase to reduce the amount of deoxynucleotides, and dFdCTP competes with dCTP to bind to the DNA chain, resulting in cessation of DNA synthesis, breakage and cell death.

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