Qilu Pharmaceutical Co., Ltd.

As a folate reductase inhibitor, it mainly inhibits dihydrofolate reductase and prevents dihydrofolate from being reduced to physiologically active tetrahydrofolate, thereby hindering the transfer of one-carbon groups in the biosynthesis of purine nucleotides and pyrimidine nucleotides, resulting in the inhibition of DNA biosynthesis. In addition, it also has an inhibitory effect on thymic nucleotide synthetase, but the effect of inhibiting RNA and protein synthesis is weak. It mainly acts on the S phase of the cell cycle and is a cell cycle-specific drug. It also has a delaying effect on cells in the G1/S phase, but has a weaker effect on cells in the G1 phase.

As a folate reductase inhibitor, this product mainly inhibits dihydrofolate reductase and prevents dihydrofolate from being reduced to physiologically active tetrahydrofolate, thereby hindering the transfer of one-carbon groups in the biosynthesis of purine nucleotides and pyrimidine nucleotides, resulting in the inhibition of DNA biosynthesis. In addition, this product also has an inhibitory effect on thymic nucleotide synthetase, but its effect on inhibiting RNA and protein synthesis is weaker. This product mainly acts on the S phase of the cell cycle and is a cell cycle-specific drug. It also has a delaying effect on cells in the G1/S phase, but its effect on cells in the G1 phase is weaker.

Tetrahydrofolate is an important coenzyme for synthesizing purine nucleotides and pyrimidine deoxynucleotides in the body. As a folate reductase inhibitor, this product mainly inhibits dihydrofolate reductase and prevents dihydrofolate from being reduced to physiologically active tetrahydrofolate, thereby hindering the transfer of one-carbon groups in the biosynthesis of purine nucleotides and pyrimidine nucleotides, resulting in the inhibition of DNA biosynthesis. In addition, this product also has an inhibitory effect on thymic nucleotide synthetase, but its effect on inhibiting RNA and protein synthesis is weaker. This product mainly acts on the S phase of the cell cycle and is a cell cycle-specific drug. It also has a delaying effect on cells in the G1/S phase, but its effect on G1 phase cells is weaker.

A selective histamine H1 receptor antagonist with no obvious anticholinergic and anti-5-hydroxytryptamine effects. It is not easy to pass through the blood-cerebrospinal fluid barrier to act on central H1 receptors. Its central inhibitory effect is relatively mild when used clinically.

Folinic acid is directly involved in biological reactions that use folic acid as a carrier for transferring "one-carbon groups" in the body without the need for reduction by dihydrofolate reductase. L-folinic acid (L-5-formyltetrahydrofolate) is rapidly metabolized to 5,10-methyltetrahydrofolate, 5,10-folinic tetrahydrofolate, and ultimately to L-5-methyltetrahydrofolate. L-5-methyltetrahydrofolate can be metabolized by other pathways to 5,10-methylenetetrahydrofolate, which is irreversibly converted to 5-methyltetrahydrofolate by catalytic reduction by PDAH2 and NADPH coenzymes. Folinic acid can counteract the therapeutic effects and toxicity of hydrochloride antagonists (such as methotrexate) that inhibit dihydrofolate reductase. Folinic acid can enhance the efficacy and toxicity of fluoropyrimidines (such as 5-fluorouracil) in tumor treatment. Folinic acid is easily converted into 5,10-methylenetetrahydrofolate in the body, which can stabilize the binding of deoxyfluorouracil nucleotide to thymidylate synthase, thereby enhancing the inhibitory effect on the enzyme.