DNA guanine base (N7 position)

The phrase "Alkylating of guanine bases in DNA via phosphoramide mustard metabolite formation from cyclophosphamide" does not refer to a single canonical therapeutic target such as a receptor or enzyme. Instead, it describes a chemical reaction mechanism, where the active metabolite phosphoramide mustard—formed from the prodrug cyclophosphamide—alkylates the N7 position of guanine bases within cellular DNA. This alkylation leads to both interstrand and intrastrand crosslinks that disrupt normal processes like replication and transcription, ultimately causing cell death through apoptosis. This is the primary cytotoxic mechanism underlying cyclophosphamide’s antineoplastic effects[1][4][8]. The actual "target" is not a protein but rather the nucleobase guanine within double-stranded DNA, which is not considered a conventional drug target. Notes on correctness: This entry is not itself an accepted therapeutic target name, but rather describes an important pharmacological process. For structured databases or ontologies focused on drug targets, this would be flagged as incorrect or non-canonical because it refers to an event/mechanism rather than a discrete molecular entity such as "Estrogen receptor" or "Tyrosine-protein kinase ABL". The correct way to represent this would be either under “DNA” as substrate/target for alkylation by certain drugs, or more specifically “Guanine base at N7 position”. Phosphoramide mustard forms DNA crosslinks both between and within strands at guanine N‐7 positions... This is irreversible and leads to cell apoptosis.[1] Phosphoramide mustard induces DNA crosslinking, alkylates guanine in DNA...[4] It functions as an alkylating agent...at the N7 position of guanine bases...[8]

Other names

Guanine in DNAN7-guanine of DNADNA guanine residue

Alkylation at the N7 position of guanine by phosphoramide mustard, leading to interstrand and intrastrand crosslinking of DNA[1][4][8]. Crosslinking prevents proper DNA replication and transcription, resulting in cell cycle arrest and apoptosis[1][4].