DNA strand break

DNA strand breaks refer to physical interruptions in the continuity of one (single-strand break) or both (double-strand break) strands of the DNA double helix. These lesions are not proteins, receptors, enzymes, or other canonical drug targets; rather they are types of molecular damage that occur due to endogenous metabolic processes (e.g., reactive oxygen species), replication errors, ionizing radiation, and certain chemicals[5][4]. Double-strand breaks are particularly hazardous because they can lead to chromosomal rearrangements and cell death if unrepaired. Cells have evolved complex repair mechanisms—primarily non-homologous end joining (NHEJ) and homologous recombination (HR)—to resolve these lesions[2][4][5]. Failure to properly repair DNA strand breaks is implicated in cancer development and progression as well as other diseases associated with genomic instability[1][3]. Note on correctness: “DNA strand break” is **not** a canonical therapeutic target such as a receptor or enzyme. It describes a type of molecular lesion rather than a discrete protein/gene product amenable to direct pharmacological modulation. While many drugs act by inducing these lesions (e.g., topoisomerase inhibitors), “DNA strand break” itself does not meet criteria for inclusion as a structured drug target entity. If you require information about specific proteins involved in sensing or repairing these lesions—such as ATM kinase, PARP1/2 enzymes for single-strand breaks, or components like BRCA1/2 for double-strand repairs—please specify those targets.

Other names

DNA breaksSingle-strand break (SSB)Double-strand break (DSB)

Drugs may cause or exploit DNA strand breaks, but there is no direct mechanism of action for targeting the lesion itself.