Nucleotide metabolism pathway (null)

The nucleotide metabolism pathway comprises the series of enzymatic reactions responsible for the synthesis (de novo and salvage pathways) and degradation of nucleotides, the fundamental building blocks for DNA, RNA, and cellular energy transfer (ATP, GTP). These pathways are essential for all proliferating cells, particularly cancer cells and viruses, as they supply cellular replication machinery and support rapid cell division and survival[3][5][7][9]. Targeting nucleotide metabolism is a cornerstone of chemotherapy, as many antimetabolite drugs disrupt key enzymes in purine or pyrimidine synthesis, thereby inhibiting DNA/RNA production and inducing cell death in rapidly dividing cells[3][5][6]. Therapeutic agents include nucleotide analogs, antifolates, and specific enzyme inhibitors (e.g., DHODH inhibitors). While these interventions are effective, their lack of selectivity can also compromise immune cell function and increase toxicity in normal proliferative tissues. Recent research shows that modulating nucleotide metabolism can enhance the efficacy of immunotherapies and affect the immunogenicity of tumors, but personalized and combination strategies are being developed to optimize benefits and reduce adverse effects[1][4][8]. Importantly, “nucleotide metabolism pathway” itself is **not a specific molecular target** (such as a receptor, enzyme, or transporter), but an entire class of pathways involving numerous molecular targets—including enzymes like DHODH, IMPDH, and CAD, among others[9]. Thus, it is too broad and not suitable as an individual therapeutic target entry; correct therapeutic target entries would be the specific enzymes or proteins within the pathway (e.g., “Dihydroorotate dehydrogenase”).

Other names

Nucleotide metabolic pathwayNucleotide biosynthesis pathwayNucleotide synthesis pathway

Inhibition of de novo purine or pyrimidine synthesis; Inhibition of nucleotide salvage pathways; Blockade of DNA/RNA polymerization; Interference with cellular replication and survival; Alteration of nucleotide pools affecting immune cell proliferation