 | |
| Clinical data | |
|---|---|
| ATC code | |
| Legal status | |
| Legal status |
|
| Pharmacokinetic data | |
| Protein binding | 96 to 98% |
| Eliminationhalf-life | 8–9 hours |
| Identifiers | |
| |
| CAS Number | |
| PubChemCID | |
| DrugBank |
|
| ChemSpider |
|
| UNII | |
| KEGG |
|
| ChEBI | |
| ChEMBL |
|
| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.051.887 |
| Chemical and physical data | |
| Formula | C21H19N3O3S |
| Molar mass | 393.46 g·mol−1 |
| 3D model (JSmol) | |
| |
| |
| (verify) | |
Amsacrine (synonyms:m-AMSA,acridinyl anisidide) is anantineoplastic agent.
It has been used inacute lymphoblastic leukemia.[1]
Its planar fused ring system canintercalate into theDNA oftumor cells, thereby altering the major and minor groove proportions. These alterations to DNA structure inhibit both DNA replication and transcription by reducing association between the affected DNA and: DNA polymerase, RNA polymerase and transcription factors.
Amsacrine also expressestopoisomerase inhibitor activity, specifically inhibiting topoisomerase II.[2] In contrast, the structurally similar o-AMSA, which differs only in the position of the methoxy substituent on the anilino ring, exhibits limited ability to poison topoisomerase II despite its intercalative properties. This suggests that intercalation alone is insufficient to stabilize topoisomerase II as a covalent complex on DNA.[3][4][5]
 | Thisantineoplastic orimmunomodulatorydrug article is astub. You can help Wikipedia byexpanding it. |
