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Amsacrine

Amsacrine
Systematic (IUPAC) name
N-(4-(acridin-9-ylamino)-3-methoxyphenyl)methanesulfonamide
Pharmacokinetic data
Protein binding 96 to 98%
Biological half-life 8-9 hours
Identifiers
CAS Registry Number  Y
ATC code L01
PubChem CID:
DrugBank  Y
ChemSpider  Y
UNII  Y
KEGG  Y
ChEBI  Y
ChEMBL  Y
Chemical data
Formula C21H19N3O3S
Molecular mass 393.46 g/mol
 Y   

Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent.

It has been used in acute lymphoblastic leukemia.[1]

Mechanism

Its planar fused ring system can intercalate into the DNA of tumor 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 expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better known agent etoposide).[2] In contrast, the structurally similar o-AMSA differing in the position of the methoxy substituent group on the anilino-ring have little ability to poison topoisomerase II despite of its intercalative behavior, suggesting that intercalation of the molecule in itself is insufficient to trap topoisomerase II as a covalent complex on DNA. [3] [4] [5]

References

  1. ^ "Amsacrine combined with etoposide and high-dose methylprednisolone as salvage therapy in acute lymphoblastic leukemia in children". Haematologica 90 (12): 1701–3. December 2005.  
  2. ^ Genetic Response to Metals. Sarkar, Bibudhendra. CRC Press, 1995. ISBN 978-0-8247-9615-0
  3. ^ "Thermodynamics of the interactions of m-AMSA and o-AMSA with nucleic acids: influence of ionic strength and DNA base composition". Nucleic Acids Res. 17 (23): 9933–46. December 1989.  
  4. ^ "Mutagenicity of m-AMSA and o-AMSA in mammalian cells due to clastogenic mechanism: possible role of topoisomerase". Mutagenesis 2 (5): 349–55. September 1987.  
  5. ^ "Targeting DNA topoisomerase II in cancer chemotherapy". Nat. Rev. Cancer 9 (5): 338–50. May 2009.  



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